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 The  International Journal of Cardiology  is devoted to cardiology in the broadest sense. Both 
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 Institutional subscribers  can access the journal online via ScienceDirect. For more information, please go to:    http://www.sciencedirect.com .   </description><link>http://www.internationaljournalofcardiology.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2011 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:issn>0167-5273</prism:issn><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:publicationDate>9 February 2012</prism:publicationDate><prism:copyright> © 2011 Published by Elsevier Inc. 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rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311022868/abstract?rss=yes"><title>Editorial Board</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311022868/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0167-5273(11)02286-8</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2012-02-09</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2012-02-09</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IFC</prism:startingPage><prism:endingPage>IFC</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311019279/abstract?rss=yes"><title>Double right coronary artery or split right coronary artery?</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311019279/abstract?rss=yes</link><description>Abstract: The prevalence of congenital anomalies of the coronary arteries (CAAs) is reported to be approximately 0.2–1.4% of the general population. Of them, The double right coronary artery (RCA) is one of the rarest coronary anomalies. Nonetheless, there is no consensus of the definition of a double RCA until now. Several concepts have been proposed in order to define what is and is not a double RCA. So far, it was been reported 37 times and in 44 cases after a comprehensive literature search through the PubMed database, using the keywords “double right coronary artery,” “duplicated right coronary artery,” “dual right coronary artery” and “split right coronary artery.” Most of the published articles (28 of 37 articles) used the name “double right coronary artery.” Nevertheless, some investigators contended that a split RCA is anatomically the same anomaly as the improperly named “double right coronary artery”. The debate between those who favor “double RCA” and those who favor “split RCA” indicate the need for a consensus regarding the nomenclature as well diagnostic criteria of such coronary anomalies. It is the time we need to reach a consensus of the nomenclature of this congenital coronary anomaly.</description><dc:title>Double right coronary artery or split right coronary artery?</dc:title><dc:creator>Ying-Fu Chen, Tsu-Ming Chien, Chih-Wei Chen, Ching-Cheng Lin, Chee-Siong Lee</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.053</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-11</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-11</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>243</prism:startingPage><prism:endingPage>245</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311004864/abstract?rss=yes"><title>Ultrafiltration for acute decompensated heart failure: Financial implications</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311004864/abstract?rss=yes</link><description>Abstract: Heart failure is the leading cause of hospitalization in older patients and is considered a public health problem with a significant financial burden on the health care system. Ultrafiltration represents an emerging therapy for patients with heart failure with a number of advantages over the conventional therapy. In this article, a summary of the relevant pathophysiological mechanisms such as removal of inflammatory cytokines are provided that might indeed be associated with a number of financial implications for ultrafiltration. Then practical points such as training of physicians and staff that need to be considered by physicians and medical centers with regards to financial implications of this therapy are reviewed.</description><dc:title>Ultrafiltration for acute decompensated heart failure: Financial implications</dc:title><dc:creator>Amir Kazory, Frank B. Bellamy, Edward A. Ross</dc:creator><dc:identifier>10.1016/j.ijcard.2011.05.073</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-06-03</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-06-03</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Review</prism:section><prism:startingPage>246</prism:startingPage><prism:endingPage>249</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007394/abstract?rss=yes"><title>The relationship between early left ventricular myocardial alterations and reduced coronary flow reserve in non-insulin-dependent diabetic patients with microvascular angina</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007394/abstract?rss=yes</link><description>Abstract: Aims: To evaluate left ventricular (LV) systolic and diastolic myocardial function, and their relation to coronary flow reserve in patients with non-insulin-dependent diabetes mellitus (DM) and microvascular angina.Methods and results: We selected a population of 45 normotensive patients with DM (56.3±8.2years; 25 males) with LV ejection fraction &gt;50% and microvascular angina (anginal pain, positive imaging stress test and normal coronary angiography). Thirty-five age- and sex-matched healthy controls were also enrolled. All the patients underwent standard echocardiography, Tissue Doppler (TDI), two-dimensional strain (2DSE) imaging, and coronary flow reserve (CFR) measurement. LV myocardial early diastolic peak velocities (Em) and peak systolic 2DSE were reduced in both interventricular septum (IVS) and LV lateral wall (p&lt;0.01) in DM, as well as CFR (1.89±0.7 vs 2.55±0.56, p&lt;0.0001) compared with controls. By multivariate analysis, the independent determinants of Em were glycated haemoglobin (β coefficient=−0.36; p&lt;0.01) and age (β=−0.46, p&lt;0.001), while global longitudinal strain was predicted by glycated haemoglobin (β=0.48, P&lt;0.001) and by the duration of the disease (β=0.38, P&lt;0.005). An independent association between LV global longitudinal strain and CFR (β coefficient=−0.47, p&lt;0.001) in DM patients was also evidenced.Conclusions: TDI, 2DSE and CFR are valuable non-invasive and easy-repeatable tools for detecting LV myocardial and coronary function in DM patients with microvascular angina.</description><dc:title>The relationship between early left ventricular myocardial alterations and reduced coronary flow reserve in non-insulin-dependent diabetic patients with microvascular angina</dc:title><dc:creator>Antonello D'Andrea, Stefano Nistri, Francesca Castaldo, Maurizio Galderisi, Donato Mele, Eustachio Agricola, Maria Angela Losi, Sergio Mondillo, Paolo Nicola Marino, on behalf of the Working Group Nucleus on Echocardiography of the Italian Society of Cardiology</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.044</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-11-01</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-11-01</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>250</prism:startingPage><prism:endingPage>255</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007291/abstract?rss=yes"><title>Clinical impact of screening for sleep related breathing disorders in atrial fibrillation</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007291/abstract?rss=yes</link><description>Abstract: Objective: The aim of this study was to quantify daytime symptoms in atrial fibrillation (AF) patients with and without sleep related breathing disorders (SRBD).Background: SRBD are common in patients with AF but little is known about daytime symptoms among those with SRBD.Methods: Patients with AF admitted to clinics of two tertiary referral hospitals for a variety of different cardiovascular diseases were screened with a trans-nasal airflow measurement device allowing measurement of the apnea–hypopnea-index. Data on cardiac risk factors, left ventricular ejection fraction (LVEF) and cardiac medication were collected. Presence of SRBD was defined as an AHI≥15/h. The Epworth sleepiness scale (ESS) was used to quantify daytime symptoms.Results: Of 102 screened patients 8 were excluded due to device malfunction (n=1), dislocation of nasal cannula (n=6), or hyperthyroidism (n=1). Among the remaining 94 patients, 40 (43%) were diagnosed with SRBD. Patients with and without SRBD had similar age, body mass index, LVEF and cardiac medication. The prevalence of coronary artery disease was higher in patients with SRBD than in those without (50 vs. 17%; p=0.0007). ESS score was low and similar in both groups (no SRBD: median 4, interquartile range (IQR) 2–4 vs. SRBD: 5, IQR 3–8; p=0.14). Only 6/40 (5%) of the patients underwent overnight polysomnography and 2 (5%) started CPAP ventilation during follow-up.Conclusions: Even though SRBD are common in patients with AF, the prevalence of daytime symptoms is rare. Consequently, most patients will not initiate CPAP ventilation after positive SRBD screening.</description><dc:title>Clinical impact of screening for sleep related breathing disorders in atrial fibrillation</dc:title><dc:creator>David R. Altmann, Elke Ullmer, Hans Rickli, Micha T. Maeder, Christian Sticherling, Beat A. Schaer, Stefan Osswald, Peter Ammann</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.034</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-14</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-14</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>256</prism:startingPage><prism:endingPage>258</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007266/abstract?rss=yes"><title>Right ventricular–left ventricular interaction in adults with Tetralogy of Fallot: A combined cardiac magnetic resonance and echocardiographic speckle tracking study</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007266/abstract?rss=yes</link><description>Abstract: Objectives: To assess ventricular dysfunction and ventricular interaction after repair of Tetralogy of Fallot (ToF) employing echocardiography speckle-tracking and cardiac magnetic resonance imaging (CMR).Background: Severe pulmonary regurgitation and right ventricular (RV) dysfunction are common after repair of ToF and may also affect the shape and function of the left ventricle (LV). Recent studies suggest that LV dysfunction may be of particular prognostic value.Methods and results: Twenty-one consecutive adults with repaired ToF (15 male, mean age 38±11years, 7 with severe PR) underwent a comprehensive echocardiographic exam including speckle-tracking analysis, CMR and cardiopulmonary exercise testing. Twenty-one subjects without relevant heart disease served as controls. Echocardiographically measured RV diameters correlated with RV volumes obtained from CMR (r=0.63; p=0.006). In addition, a close correlation was found between RV and LV function on CMR (r=0.74, p=0.002), speckle-tracking LV and RV peak longitudinal 2D strain (r=0.66, p=0.003) and mitral and tricuspid annular plain systolic excursion (r=0.71, p=0.0003). While LV ejection fraction was normal in the majority of patients and not different from controls, LV longitudinal strain was significantly reduced in ToF patients (−16.5±3.3 vs. -20.5±2.7%, p=0.0001).Conclusion: Left and right ventricular function both by CMR and speckle-tracking is interrelated in adults with repaired ToF. Despite normal LV ejection fraction, 2D longitudinal strain is significantly reduced in ToF patients, suggesting subclinical LV myocardial damage. Considering the potential prognostic value of LV dysfunction in ToF, this measurement may gain importance and should be included in future outcome studies.</description><dc:title>Right ventricular–left ventricular interaction in adults with Tetralogy of Fallot: A combined cardiac magnetic resonance and echocardiographic speckle tracking study</dc:title><dc:creator>Aleksander Kempny, Gerhard-Paul Diller, Stefan Orwat, Gerrit Kaleschke, Gregor Kerckhoff, Alexander Ch. Bunck, David Maintz, Helmut Baumgartner</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.031</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-11</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-11</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>259</prism:startingPage><prism:endingPage>264</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007230/abstract?rss=yes"><title>Minor symptoms of depression in patients with congenital heart disease have a larger impact on quality of life than limited exercise capacity</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007230/abstract?rss=yes</link><description>Abstract: Objective: In patients with congenital heart disease quality of life is only marginally associated with exercise capacity. The aim of this study was to determine the prevalence of depression and its impact on quality of life and exercise capacity.Patients and methods: From November 2007 to October 2009 a total of 767 patients (352 female, 14–67years) with various congenital heart diseases (37 palliated/native cyanotic, 57 Fontan, 74 Transposition of the Great Arteries (TGA) after atrial switch, 50 other TGA, 136 Fallot, 38 Ebstein, 47 Pulmonic stenosis/regurgitation, 68 aortic coarctation, 103 aortic stenosis, 90 isolated shunts, 67 other) completed the health-related quality of life questionnaire SF-36 and the German translation of the “Center for Epidemiologic Studies Depression Scale” (CES-D) to assess depressive symptoms. Afterwards a cardiopulmonary exercise test was performed.Results: Only 66 patients (8.6%) showed depressive symptoms fulfilling the CES-D definition for depression. The total prevalence of depression was lower than in the general population (Wilcoxon test, p&lt;0.001) and did not differ substantially in between the diagnostic subgroups (Kruskal–Wallis test, p=0.195). CES-D score was correlated to all of the nine dimensions of quality of life (r=−0.170 to r=−0.740, p&lt;0.001) and less pronounced to exercise capacity (r=−0.164, p&lt;0.001). Correlation of peak oxygen uptake to quality of life was weaker than the CES-D scores in all subscales of life quality.Conclusions: Patients with congenital heart disease are rarely depressive. However, even minor depressive symptoms have a stronger impact on quality of life than limited exercise capacity as seen in many patients.</description><dc:title>Minor symptoms of depression in patients with congenital heart disease have a larger impact on quality of life than limited exercise capacity</dc:title><dc:creator>Jan Müller, John Hess, Alfred Hager</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.029</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-06</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-06</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>265</prism:startingPage><prism:endingPage>269</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007229/abstract?rss=yes"><title>Outcome of direct current cardioversion for atrial arrhythmias in adults with congenital heart disease</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007229/abstract?rss=yes</link><description>Abstract: Objectives: We sought to evaluate safety, efficacy, and outcome of direct current cardioversion (DCCV) for atrial arrhythmias in adults with congenital heart disease (CHD).Background: Atrial arrhythmias are increasingly noted in adults with CHD. The outcome of DCCV for atrial arrhythmias in this population is unknown.Methods: Our study was a retrospective review of patients 18years or older with CHD who underwent DCCV between June 2000 and July 2003. This constituted the CHD group. Patient characteristics reviewed included the specific cardiac diagnosis and arrhythmia history. A subset of patients had transesophageal echocardiography (TEE) before DCCV; this subset was reviewed to evaluate spontaneous echocardiographic contrast. The outcome data evaluated included success of DCCV, complications, recurrence of arrhythmia, antiarrhythmic medication use, electrophysiology or pacemaker procedure in follow-up, and all-cause mortality. The recurrence rate of the arrhythmia was compared to a control group consisting of an age, gender, and rhythm matched group of patients who have no CHD and who underwent DCCV for atrial arrhythmias.Results: Sixty-three patients in the CHD group underwent 80 DCCVs, 59 of which were TEE-guided. Atrial flutter was more common in the CHD group (37 of 80 DCCV, 46%) than in the control group (13 of 56, 23%) (p&lt;0.001). DCCV was successful in 75 (94%). Mean follow-up was 387days. No thromboembolic events were noted. All-cause mortality on follow-up was 11%. There was no death related to DCCV. Twenty-five patients in the CHD group (40%) remained in sinus rhythm throughout follow-up. This was similar to that observed in the control group (30/56, 54%, p=0.13). Recurrent arrhythmia in the CHD group was predicted by the presence of atrial fibrillation (p=0.009) and less so spontaneous echo contrast in the left atrium (p=0.05).Conclusions: DCCV with appropriate anticoagulation is safe and effective for patients with CHD, even in the presence of an intracardiac shunt and spontaneous contrast on TEE. However, the recurrence rate is substantial. Spontaneous echo contrast in the left atrium along with atrial fibrillation predicts arrhythmia recurrence following DCCV in patients with CHD.</description><dc:title>Outcome of direct current cardioversion for atrial arrhythmias in adults with congenital heart disease</dc:title><dc:creator>Naser M. Ammash, Sabrina D. Phillips, David O. Hodge, Heidi M. Connolly, Martha A. Grogan, Paul A. Friedman, Carole A. Warnes, Samuel J. Asirvatham</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.028</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-11</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-11</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>270</prism:startingPage><prism:endingPage>274</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007370/abstract?rss=yes"><title>Timing of events in STEMI patients treated with immediate PCI or standard medical therapy: Implications on optimisation of timing of treatment from the CARESS-in-AMI trial</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007370/abstract?rss=yes</link><description>Abstract: Objectives: Early angioplasty after thrombolysis is now recommended for ST-elevation myocardial infarction, but the current guidelines propose a wide time-window ranging between 3 and 24h after lytic administration. To identify the optimal timing for PCI after thrombolysis, we analyzed frequency and time course of the adverse events in patients randomized in the multicenter CARESS-in-AMI trial.Methods: 598 high-risk patients with STEMI recruited in the CARESS-in-AMI study, were divided into the Immediate PCI group (IMM, n=298), Rescue PCI group (RES, n=107) and Standard Treatment Arm without rescue PCI (STA, n=193).Results: RES patients had worse pre-procedural TIMI flow and post-procedural blush grade. At 30days, there were 23 deaths: 11 (10.3%) in RES, 9 (3%) in IMM and 3 (1.6%) in STA (p&lt;0.001). There were 22 episodes of refractory ischemia or re-infarction: 17 (8.8%) in the STA group, 4 (1.6%) in IMM and 1 (0.9%) in RES (p&lt;0.001). In the RES group 10/11 (90.9%) deaths occurred before day 5. In the STA group, all deaths and the majority of ischemic events occurred after day 3. A reduction of risk of death was observed if PCI after thrombolysis was performed within 3.35h from initial hospitalization.Conclusions: The mortality benefit of immediate referral to PCI after pharmacological treatment for STEMI derives from a reduction in the time to reperfusion of patients with failed thrombolysis in need of rescue PCI. In patients with evidence of successful reperfusion, “elective” PCI within 3days may be sufficient to reduce the recurrent ischemic events.</description><dc:title>Timing of events in STEMI patients treated with immediate PCI or standard medical therapy: Implications on optimisation of timing of treatment from the CARESS-in-AMI trial</dc:title><dc:creator>Konstantinos Dimopoulos, Dariusz Dudek, Federico Piscione, Waldemar Mielecki, Stefano Savonitto, Francesco Borgia, Ernesto Murena, Antonio Manari, Achille Gaspardone, Andrzej Ochala, Krzysztof Zmudka, Leonardo Bolognese, Philippe Gabriel Steg, Marcus Flather, Carlo Di Mario, on behalf of the CARESS-in-AMI (Combined Abciximab RE-teplase Stent Study in Acute Myocardial Infarction) Investigators (All Investigators and Committees are listed in the Appendix)</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.042</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-21</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-21</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>275</prism:startingPage><prism:endingPage>281</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS016752731000759X/abstract?rss=yes"><title>Clinical and genetic determinants of anthracycline-induced cardiac iron accumulation</title><link>http://www.internationaljournalofcardiology.com/article/PIIS016752731000759X/abstract?rss=yes</link><description>Abstract: Background: The involvement of iron in anthracycline cardiotoxicity is supported by extensive experimental data, and by the preventive efficacy of dexrazoxane, an iron chelator. However, no clinical evidence of anthracycline-induced cardiac iron accumulation is available and the influence of previous iron overload or of genetic factors in human-induced heart disease is largely unknown. Our aim was to test the hypothesis that anthracyclines increase iron heart concentration and that HFE genotype modulates this iron deposit.Methods: We retrospectively evaluated cardiac events, cardiac iron and HFE genotype in 97 consecutive necropsies from patients with solid and hematological neoplasms. Heart and liver iron concentration was determined by atomic absorption spectroscopy. HFE gene mutations (C282Y and H63D) linked to hereditary hemochromatosis were analyzed by Fluorescence Resonance Energy Transfer (FRET) genotyping.Results: Heart iron concentration was increased in cases treated with a cumulative doxorubicin dose greater than 200mg/m2 (490 vs 240μg/g; p=0.01), independently of liver iron load or transfusion history. HFE mutated haplotypes 282C/63D (p=0.049) and 282Y/63H (p=0.027) were associated to higher cardiac iron deposits. The haplotype C282Y-Y/H63D-H interacted with anthracyclines for increasing cardiac iron load. In a multivariate linear regression analysis both HFE genotypes and anthracyclines contributed to heart iron concentration (R2=0.284).Conclusions: Our data support the occurrence of an HFE-modulated heart iron accumulation in individuals treated with anthracyclines, independently of systemic iron load. If prospectively confirmed, iron-related parameters might be useful as predictive factors for anthracycline cardiotoxicity.</description><dc:title>Clinical and genetic determinants of anthracycline-induced cardiac iron accumulation</dc:title><dc:creator>Almudena Cascales, Beatriz Sánchez-Vega, Noelia Navarro, Francisco Pastor-Quirante, Javier Corral, Vicente Vicente, Francisco Ayala de la Peña</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.046</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-25</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-25</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>282</prism:startingPage><prism:endingPage>286</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007746/abstract?rss=yes"><title>Inflammatory markers and plaque morphology: An optical coherence tomography study</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007746/abstract?rss=yes</link><description>Abstract: Background: OCT with its unique image resolution is the ideal method to detect culprit lesion characteristics in different clinical presentations. The identification of inflammatory markers related to plaque characteristics may be of clinical importance.Methods: Thirty-two patients with acute coronary syndromes (ACS) and fourteen patients with stable angina pectoris (SAP) were enrolled in this study. Culprit lesion morphology was assessed by optical coherence tomography (OCT) in patients with ACS and SAP. The possible relations between serum levels of high sensitivity-C reactive protein (hs-CRP) and interleukin-18 (IL-18) with plaque characteristics were investigated in those patients.Results: Plaque rupture and thin-cap fibroatheroma (TCFA) were detected more frequently in ACS patients compared with SAP patients, (78.6% vs. 14.3%, p&lt;0.001, 92.9% vs. 14.3%, p&lt;0.001, respectively). Higher levels of serum hs-CRP and IL-18 were found in patients with plaque rupture vs. those with no plaque rupture (median value: 19.2mg/L vs. 1.6mg/L, p&lt;0.001 and 219.5pg/ml vs. 127.5pg/ml, p=0.001 respectively), and TCFA vs. those without TCFA (median value: 15.2mg/L vs. 1.6mg/L, p=0.004 and 209.0pg/ml vs.153.2pg/ml, p=0.03 respectively). Serum hs-CRP was the only independent predictor of plaque rupture (p=0.02, odds ratio 1.1, 95% confidence interval 1.0 to 1.2). A cut-off value of hs-CRP&gt;4.5mg/L could detect ruptured plaque with a sensitivity of 91.7% and a specificity of 77.8%.Conclusions: OCT detected plaque rupture and TCFA more frequent in ACS patients compared with SAP. Elevated hs-CRP and IL-18 were positively related to plaque instability and rupture.</description><dc:title>Inflammatory markers and plaque morphology: An optical coherence tomography study</dc:title><dc:creator>Konstantina P. Bouki, Mihail G. Katsafados, Dionissios N. Chatzopoulos, Stavroula N. Psychari, Konstantinos P. Toutouzas, Athanasios F. Charalampopoulos, Eleni N. Sakkali, Antonia A. Koudouri, Georgios K. Liakos, Thomas S. Apostolou</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.059</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-25</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-25</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>287</prism:startingPage><prism:endingPage>292</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007734/abstract?rss=yes"><title>Intra-aortic balloon pumping recruits graft flow reserve by lowering coronary resistances</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007734/abstract?rss=yes</link><description>Abstract: Background: The intra-aortic balloon pump (IABP) is used worldwide as an anti-ischemic strategy and to reduce myocardial workload. However, whether IABP augments coronary flow after coronary bypass via a passive increase in diastolic pressure or an active response of the coronary bed remains uncertain.Methods: We analyzed transit-time flow measurements and the contemporary changes in coronary resistances obtained during 1:1 IABP and during its cessation in 144 consecutive patients receiving prophylactic IABP before isolated coronary artery bypass grafting (n=340 graft segments).Results: Normally functioning grafts showed lower coronary resistances, greater percentage decrease in resistance, and greater increases in average maximum diastolic and mean flow during 1:1 IABP compared with IABP cessation (P 1) during 1:1 IABP in all normally functioning grafts, with higher values in single arterial or sequential saphenous vein grafts than in single venous grafts (both P&lt;.001). Coronary resistances were higher in 7 failed grafts versus normal-functioning grafts at baseline; these did not decrease during 1:1 IABP and showed worse transit-time flow results.Conclusions: IABP recruits graft flow reserve by lowering coronary resistance in functioning grafts. Arterial and sequential venous grafts showed greater reduction in coronary resistance compared with single saphenous grafts.</description><dc:title>Intra-aortic balloon pumping recruits graft flow reserve by lowering coronary resistances</dc:title><dc:creator>Antonino S. Rubino, Francesco Onorati, Cristian Scalas, Giuseppe F. Serraino, Roberto Marsico, Sandro Gelsomino, Roberto Lorusso, Attilio Renzulli</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.058</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-25</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-25</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>293</prism:startingPage><prism:endingPage>298</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007722/abstract?rss=yes"><title>Randomised trial of ramipril in repaired tetralogy of Fallot and pulmonary regurgitation: The APPROPRIATE study (Ace inhibitors for Potential PRevention Of the deleterious effects of Pulmonary Regurgitation In Adults with repaired TEtralogy of Fallot)</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007722/abstract?rss=yes</link><description>Abstract: Background: Optimal treatment for stable repaired tetralogy of Fallot (rTOF) patients with pulmonary regurgitation (PR) and related right ventricular (RV) dilatation, including timing of valve implantation, remains uncertain. We sought to study tolerability of the angiotensin-converting-enzyme (ACE) inhibitor ramipril and its effects on cardiovascular function in these patients.Methods: Clinically stable rTOF patients with moderate/severe PR were included. A double-blinded, placebo-controlled study of 6months of ramipril vs placebo was performed. All patients underwent cardiovascular magnetic resonance (CMR), echocardiography, neurohormonal analysis, and objective cardiopulmonary exercise testing at baseline and follow-up.Primary endpoint: The main aim was to detect changes in RV function (primary endpoint CMR-derived RV ejection fraction).Results: Seventy-two patients were enrolled and 64 qualified for the final analysis.There was no difference in the primary endpoint RV ejection fraction. RV long-axis shortening significantly improved in the ramipril group compared to placebo (RV: 2.3±3.8 vs 0.02±2.7mm; P=0.017) as did LV long-axis shortening (1.9±4.5 vs −0.2±3.7mm respectively; P=0.030). No clear differences were detected between ramipril and placebo for other measures. In a subgroup of patients with restrictive RV physiology, ramipril resulted in decrease in LV end-systolic volume index and increase in LVEF (−2.4±5.0 vs 2.7±3.6mL/m2; P=0.005, 2.5±5.0 vs −1.3±3.5%; P=0.03). Ramipril did not cause adverse events and was well tolerated.Conclusions: Ramipril is a well tolerated therapy, improves biventricular function in patients with rTOF and may have a particular role in patients with restrictive RV physiology. Larger, longer-term studies are needed to determine if ACE inhibitors can improve both ventricular remodelling and clinical outcomes. (ISRCTN: 97515585)</description><dc:title>Randomised trial of ramipril in repaired tetralogy of Fallot and pulmonary regurgitation: The APPROPRIATE study (Ace inhibitors for Potential PRevention Of the deleterious effects of Pulmonary Regurgitation In Adults with repaired TEtralogy of Fallot)</dc:title><dc:creator>Sonya V. Babu-Narayan, Anselm Uebing, Periklis A. Davlouros, Michael Kemp, Simon Davidson, Konstantinos Dimopoulos, Stephanie Bayne, Dudley J. Pennell, Derek G. Gibson, Marcus Flather, Philip J. Kilner, Wei Li, Michael A. Gatzoulis</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.057</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-25</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-25</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>299</prism:startingPage><prism:endingPage>305</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007710/abstract?rss=yes"><title>A 14-year follow-up study of chest pain patients including stress hormones and mental stress at index event</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007710/abstract?rss=yes</link><description>Abstract: Background: Knowledge of long-term outcome in chest pain patients is limited. We reinvestigated patients who 14years earlier had visited the emergency department due to chest pain, and were discharged without hospitalization. Extensive examinations were made at that time on 484 patients including full medical history, exercise test, a battery of stress questions and stress hormone sampling.Methods: From a previously conducted chest pain study patients still alive after 14years were approached. Hospitalization or deaths with a diagnosis of ischemic heart disease or cerebrovascular disease were used as end point.Results: During the follow-up period 24 patients had died with a diagnosis of ischemic heart or cerebrovascular disease, and 50 patients had been given such a diagnosis at hospital discharge. Age (OR 1.12, CI 1.06–1.19), previous history of angina pectoris (OR 9.69, CI 2.06–71.61), pathological ECG at emergency department visit (OR 3.27, CI 1.23–8.67), hypertension (OR 5.03, CI 1.90–13.76), smoking (OR 3.04, CI 1.26–7.63) and lipid lowering medication (OR 14.9, CI 1.60–152.77) were all associated with future ischemic heart or cerebrovascular events. Noradrenalin levels were higher in the event group than in the non-event group, mean (SD) 2.44 (1.02) nmol/L versus 1.90 (0.75) nmol/L. When noradrenalin was included in the regression model high maximal exercise capacity was protective of an event (OR 0.986, CI 0.975–0.997).Conclusion: In chest pain patients previous history of angina pectoris, hypertension, smoking, pathological ECG at primary examination, and age were the main risk factors associated with future cardiovascular or cerebrovascular events.</description><dc:title>A 14-year follow-up study of chest pain patients including stress hormones and mental stress at index event</dc:title><dc:creator>Inger Bengtsson, Björn W. Karlson, Johan Herlitz, Maria Haglid Evander, Peter Währborg</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.056</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-21</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-21</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>306</prism:startingPage><prism:endingPage>311</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310007709/abstract?rss=yes"><title>“The heart is simply a muscle” and first description of the tetralogy of “Fallot”. Early contributions to cardiac anatomy and pathology by bishop and anatomist Niels Stensen (1638–1686)</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310007709/abstract?rss=yes</link><description>Abstract: Background: Many are familiar with the parotid duct and the Danish physician/anatomist's name associated with it. However, most are unaware of Niels Stensen's life and his significant contributions to the early study of the heart. For example, he found that the heart is simply muscle and was the first to describe what we now refer to as the tetralogy of Fallot.Methods: A review of germane literature regarding this pioneer of cardiac anatomy was performed.Conclusions: This physician of the Medici court was clearly ahead of his time and found errors in the publications of such giants as Varolius and Willis. The tetralogy of Fallot should rightfully, be termed the tetralogy of Stensen. The present review discusses the life of this 17th century anatomist, physician and priest/bishop and highlights his contributions to cardiac anatomy and pathology.</description><dc:title>“The heart is simply a muscle” and first description of the tetralogy of “Fallot”. Early contributions to cardiac anatomy and pathology by bishop and anatomist Niels Stensen (1638–1686)</dc:title><dc:creator>R. Shane Tubbs, Nicholas Gianaris, Mohammadali M. Shoja, Marios Loukas, Aaron A. Cohen Gadol</dc:creator><dc:identifier>10.1016/j.ijcard.2010.09.055</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2010-10-21</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-10-21</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>312</prism:startingPage><prism:endingPage>315</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311005808/abstract?rss=yes"><title>Hyperuricemia and increased risk of ischemic heart disease in a large Chinese cohort</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311005808/abstract?rss=yes</link><description>Abstract: Aims: There is an ongoing discussion on whether serum uric acid (SUA) predicts ischemic heart disease (IHD) independently of other metabolic factors, which, if confirmed, would signify a role for uric acid in the pathogenesis of cardiovascular disease. We investigated whether such a relation exists for ethnic Chinese with low CVD risk.Methods and results: Enrolled, between 1994 and 1996, were 128,569 adults ≥20years from four ‘MJ’ Health Check-up Clinics in Taiwan. Excluded were those with heart disease, previous stroke(s), renal disease, and/or cancer. Physical examinations, biospecimen collections, and structured questionnaires were executed according to standardised protocols. We identified IHD events according to the ICD-9-CM codes 410–414 using hospitalisation records obtained from the National Health Insurance and the Death Certification Registry databases. The Cox proportional hazard model was used to estimate the hazard ratios (HRs) between SUA and IHD events. A total of 2049 subjects (1239 men, 810 women) developed IHD from baseline to Dec. 31, 2002. Men had a higher IHD incidence than did women (2.84 vs. 1.61 1/1000person-years; p&lt;0.0001). The risk-factor-adjusted HRs (95% confidence-interval [CI]) for hyperuricemiae (SUA ≥7.0/≥6.0mg/dL) were 1.25 (1.11–1.40) for men and 1.19 (1.02–1.38) for women. In the low-risk population (lacking the NCEP-ATPIII metabolic syndrome components), a significant association was still observed (adjusted HR: 1.54 [1.09–2.17]).Conclusion: The hyperuricemia was independently associated with the development of IHD not only in the general population but also in those without any metabolic risk factor for NCEP ATPIII. Hyperuricemia may be considered as a potential risk factor for IHD.</description><dc:title>Hyperuricemia and increased risk of ischemic heart disease in a large Chinese cohort</dc:title><dc:creator>Shao-Yuan Chuang, Jiunn-Horng Chen, Wen-Ting Yeh, Chih-Cheng Wu, Wen-Harn Pan</dc:creator><dc:identifier>10.1016/j.ijcard.2011.06.055</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-08-22</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-08-22</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>316</prism:startingPage><prism:endingPage>321</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311006735/abstract?rss=yes"><title>Erythrocyte aggregation as a cause of slow flow in patients of acute coronary syndromes</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311006735/abstract?rss=yes</link><description>Abstract: Background: There are multiple lines of evidence to suggest the role of erythrocyte aggregation (EA) in microcirculatory dysfunction during conditions of very slow flow. Such conditions might develop in the myocardium of patients with acute coronary syndromes (ACS).Methods: EA as a function of shear stress was evaluated by using a cell flow properties analyzer (CFA) in a cohort of 91 ACS patients and in 36 patients with non specific chest pain or heart failure at the time of cardiac catheterization.Results: The ACS group included 34 patients with acute myocardial infarction and 57 patients with unstable angina. In addition, we examined 36 patients who underwent angiography for non specific chest pain or heart failure. A significant (r=0.44, p&lt;0.0005) correlation was found between the concentration of fibrinogen and the average aggregate size (AAS) only when using conditions of very slow flow and applying relatively low (0.15dyn/cm2) shear stress in the ACS group. This correlation decreased and became insignificant when applying shear stress forces of 1dyn/cm2 and more. This correlation was nonsignificant for all the 5 shear stress forces (between 0.15 and 4dyn/cm2) in the samples obtained from the non-ACS group.Conclusion: Erythrocytes that are suspended in autologous plasma obtained from patients with ACS tend to aggregate in conditions of very slow flow. These findings might be detrimental in terms of microcirculatory flow in ACS patients and might open new therapeutic options such as the use of low dose thrombolysis following PCI.</description><dc:title>Erythrocyte aggregation as a cause of slow flow in patients of acute coronary syndromes</dc:title><dc:creator>Yaron Arbel, Shmuel Banai, Jessia Benhorin, Ariel Finkelstein, Itzhak Herz, Amir Halkin, Gad Keren, Saul Yedgar, Gershon Barashtein, Shlomo Berliner</dc:creator><dc:identifier>10.1016/j.ijcard.2011.06.116</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-07-25</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-07-25</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>322</prism:startingPage><prism:endingPage>327</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311018067/abstract?rss=yes"><title>Takotsubo cardiomyopathy has a unique cardiac biomarker profile: NT-proBNP/myoglobin and NT-proBNP/troponin T ratios for the differential diagnosis of acute coronary syndromes and stress induced cardiomyopathy</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311018067/abstract?rss=yes</link><description>Abstract: Background: Takotsubo cardiomyopathy (TC) usually is not recognized until heart catheterization reveals typical wall motion abnormalities in the absence of significant coronary artery disease. It was our aim to identify TC by its unique cardiac biomarker profile at an early stage and, preferably, with non-invasive procedures only.Methods: Ratios of N-terminal prohormone of brain natriuretic peptide (NT-proBNP) and myoglobin, NT-proBNP and troponin T (TnT), NT-proBNP and creatinekinase-MB (CK-MB) were compared in patients with TC (n=39), patients with ST-elevation myocardial infarction (STEMI, n=48) and patients with non-ST-elevation myocardial infarction (NSTEMI, n=34). Biomarkers were recorded serially at admission and at the three consecutive days. Optimal cut-off values to distinguish TC from STEMI and NSTEMI were calculated with receiver operator characteristic (ROC) curves.Results: At admission a NT-proBNP (ng/l)/myoglobin (μg/l) ratio of 3.8, distinguished TC from STEMI (sensitivity: 89%, specificity: 90%), while a NT-proBNP (ng/l)/myoglobin (μg/l) ratio of 14 separated well between TC and NSTEMI (sensitivity: 65%, specificity: 90%). Best differentiation of TC and ACS was possible with the ratio of peak levels of NT-proBNP (ng/l)/TnT (μg/l). A cut-off value of NT-proBNP (ng/l)/TnT (μg/l) ratio of 2889, distinguished TC from STEMI (sensitivity: 91%, specificity: 95%), while a NT-proBNP (ng/l)/TnT (μg/l) ratio of 5000 separated well between TC and NSTEMI (sensitivity: 83%, specificity: 95%).Conclusions: TC goes along with a singular cardiac biomarker profile, which might be useful to identify patients with TC among patients presenting with acute coronary syndromes (ACS).</description><dc:title>Takotsubo cardiomyopathy has a unique cardiac biomarker profile: NT-proBNP/myoglobin and NT-proBNP/troponin T ratios for the differential diagnosis of acute coronary syndromes and stress induced cardiomyopathy</dc:title><dc:creator>Georg M. Fröhlich, Boris Schoch, Florian Schmid, Philipp Keller, Isabella Sudano, Thomas F. Lüscher, Georg Noll, Frank Ruschitzka, Frank Enseleit</dc:creator><dc:identifier>10.1016/j.ijcard.2011.09.077</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-01</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-01</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>328</prism:startingPage><prism:endingPage>332</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS016752731101905X/abstract?rss=yes"><title>Variability and treatment of high on-prasugrel platelet reactivity in patients with initial high on-clopidogrel platelet reactivity</title><link>http://www.internationaljournalofcardiology.com/article/PIIS016752731101905X/abstract?rss=yes</link><description>High on-treatment platelet reactivity (HTPR) following clopidogrel is a well studied phenomenon associated with prognostic significance post percutaneous coronary angioplasty (PCI). Platelet reactivity variability over time while on clopidogrel is also well appreciated . Prasugrel, a newer P2Y12 inhibitor, has been shown to result in a faster, more consistent and stronger inhibition of platelet aggregation, compared to clopidogrel mainly attributed to its more efficient metabolic activation. Cases of HTPR while on prasugrel have scarcely been reported, with minimal data on its variability over time and ways for its treatment . We describe our experience in patients who exhibited HTPR while on 10mg maintenance dose of prasugrel, its variability over time and strategies to overcome.</description><dc:title>Variability and treatment of high on-prasugrel platelet reactivity in patients with initial high on-clopidogrel platelet reactivity</dc:title><dc:creator>Dimitrios Alexopoulos, Theodora-Eleni Plakomyti, Ioanna Xanthopoulou</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.031</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-10</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-10</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>333</prism:startingPage><prism:endingPage>334</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311019048/abstract?rss=yes"><title>Large and small artery endothelial dysfunction in chronic fatigue syndrome</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311019048/abstract?rss=yes</link><description>There is accumulating evidence that myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is associated with cardiovascular symptoms including autonomic dysfunction , impaired blood pressure regulation  and loss of beat-to-beat heart rate control . A number of recent studies reporting raised levels of oxidative stress , low-grade inflammation  and increased arterial stiffness contribute to a picture of increased cardiovascular risk in ME/CFS. One potential site of oxidative injury is the vascular endothelium, and such damage would be expected to lead to endothelial cell dysfunction and diminished vasodilator capacity. The primary aim of the current study was to investigate large-vessel endothelial function in ME/CFS using flow-mediated dilatation (FMD), and to assess microvascular endothelial function using post-occlusive reactive hyperaemia, both of which have been shown to be related to cardiovascular risk and outcome .</description><dc:title>Large and small artery endothelial dysfunction in chronic fatigue syndrome</dc:title><dc:creator>David J. Newton, Gwen Kennedy, Kenneth K.F. Chan, Chim C. Lang, Jill J.F. Belch, Faisel Khan</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.030</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-14</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-14</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>335</prism:startingPage><prism:endingPage>336</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311018997/abstract?rss=yes"><title>Winning the war, far, in developing countries. Novel anticoagulants as a new weapon against stroke</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311018997/abstract?rss=yes</link><description>I have just returned from an African mission in Zimbabwe. I am now in the university hospital in Bologna where I work. In the waiting room of the anticoagulation therapy center I see a silent mass of people, mostly elderly, waiting for a blood sample to be taken. The expression on the faces of these men and women is generally sad and resigned; I know this ritual well, it can happen from two to four times a month. The queue, the nurse, the needle and the wait for the verdict – INR – that will decide the dose of the medicine to be taken in the evening, a few hours after meals. Meals that in turn are limited by the countless interferences of warfarin/Coumadin, the infamous rat poison that has become a life-saver for heart disease patients. This image takes me back irresistibly to Africa. Some go to Black Africa with their world-class Reflex to look for the “Big Five” on safari, some go with a portable echocardiograph to look for the many “big African hearts” in the improvized clinics between the wards where people are dying of HIV and TBC, as was my case last week. In just a few days I saw around a hundred people with heart disease, some with rheumatic valvulopathy, some with congenital heart disease; I did the follow-up on those who had already been operated on in Italy and screened those scheduled for surgery. The great majority of these patients are being treated with Coumadin due to the presence of a valvular prosthesis or atrial fibrillation. In the last year, among the young cardiopathic patients with valvular disease being followed up there were 6 deaths; in 3 of them the suspected cause was an acute malfunction of the prosthesis and in the other 3 it was stroke (both of these had chronic atrial fibrillation). In all these cases, inappropriate anticoagulant therapy seems to have been the cause of death. It is not difficult to imagine how prohibitive anticoagulant therapy can be in third world countries. The reagent is expensive and the test is inaccessible to most patients, never mind the unreliability of the test results due to laboratory errors; on top of all this lack of compliance and dietary errors complete the disastrous scenario. Finding a drug to replace warfarin would be enormously significant for a number of reasons, including its possible use in developing countries.</description><dc:title>Winning the war, far, in developing countries. Novel anticoagulants as a new weapon against stroke</dc:title><dc:creator>G.K. Bronzetti, A. Corzani, C. D'Angelo, M. Bonvicini, G.D. Gargiulo, G. Boriani</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.025</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-16</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-16</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>336</prism:startingPage><prism:endingPage>337</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311018985/abstract?rss=yes"><title>Interaction of anemia and decrease in renal function on survival of patients with heart failure</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311018985/abstract?rss=yes</link><description>Anemia and renal dysfunction are comorbidities commonly associated with heart failure (HF) and appear to be associated with unfavorable outcomes . Despite evidence demonstrating worse prognosis in patients with anemia and reduced renal function when analyzed independently, the interaction between these variables has not been well studied. We sought to evaluate the longitudinal impact and interaction of these factors on survival of patients that have been once hospitalized because of HF and were discharged alive.</description><dc:title>Interaction of anemia and decrease in renal function on survival of patients with heart failure</dc:title><dc:creator>Márcia Olandoski, Raphael Rodrigues de Lima, Miguel Morita Fernandes da Silva, Roberto Pecoits-Filho, Angela Olandoski Barboza, Bruna Olandoski Erbano, Lidia Zytynski Moura, Paulo Roberto Slud Brofman, José Rocha Faria-Neto</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.024</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-21</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-21</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>338</prism:startingPage><prism:endingPage>340</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311018973/abstract?rss=yes"><title>Myocardial infarction-stroke association</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311018973/abstract?rss=yes</link><description>I have read the interesting article by Sidler et al. regarding post myocardial infarction (MI) basilar artery occlusion and congratulate them for their observation . We have previously demonstrated the association of basilar artery ischemic stroke and MI as was evident in our case by massive infarction involving the brain stem, both cerebellar hemispheres and both occipital lobes following acute infero-posterior MI and we labeled this association as “cardio-cerebral infarction” . However, our observation was not recognized by the authors. We have developed several explanations for this association. First, left ventricular systolic dysfunction can be complicated by formation of a left ventricular thrombus and subsequent embolization. Second, if the underlying pathological mechanism for the MI is dissection of the ascending aorta involving the coronary ostium, then an extension of the dissection process to involve the basilar artery might explain the association. Third, the sudden development of severe hypotension (after acute MI) in patients with long standing hypertension and the initial failure of the auto-regulatory mechanisms will cause a sudden reduction in the cerebral blood flow and subsequent infarction. This is evident in the brainstem because of its relative inability to auto-regulate intravascular pressures. However, these types of infarcts are more likely to occur in water-shed areas. Another possibility is a paradoxical embolus due to a right ventricular thrombus (in cases of right ventricular infarction) through a patent foramen ovale which is present in approximately 20% f the population. However, we demonstrated that the later explanation can be valid only for small strokes as the diameter of the foramen ovale will not allow the passage of large emboli sufficient to cause a basilar artery occlusion. Another group of possibilities include post coronary angiography stroke which is likely a procedure related complication due to atheroemboli, air embolism or thromboembolism from a thrombus formed on the catheter surface . New onset atrial fibrillation is an independent predictor of stroke after acute MI but is likely to be a more delayed presentation than the previously mentioned causes. A question to be answered is whether alteplase therapy would be favored in patients with concomitant presentation of transmural MI and embolic cerebrovascular stroke for the benefit of curing both pathologies.</description><dc:title>Myocardial infarction-stroke association</dc:title><dc:creator>Hesham R. Omar</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.023</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-10</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-10</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>340</prism:startingPage><prism:endingPage>340</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311019905/abstract?rss=yes"><title>Systemic administration of bevacizumab increases the risk of cardiovascular events in patients with metastatic cancer</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311019905/abstract?rss=yes</link><description>Bevacizumab, a recombinant humanized monoclonal antibody targeting vascular endothelial growth factor (VEGF), is an anti-angiogenic agent used widely in the treatment of renal, colorectal, lung and breast cancers . A limited number of studies have investigated the impact of systemic administration of bevacizumab on the cardiovascular system. A recent meta-analysis demonstrated an increase of the thrombotic events in patients receiving bevacizumab . The exact pathway, however, through which bevacizumab provokes the thromboembolic events is not well determined, but several pathophysiological mechanisms have been proposed . We have previously shown in an experimental model that local administration of bevacizumab in atheromatic animals was safe, and inhibited the vessel wall neovascularization without affecting the endothelialization procedure . Similarly in patients with coronary artery disease, the implantation of a bevacizumab-eluting stent that exhibited the anti-neovascularization effect locally, was associated with limited neointimal hyperplasia and excellent long term clinical results . The aim of the present study was firstly to evaluate the incidence of cardiovascular events in patients with cancer treated with bevacizumab, and secondly to identify possible prognostic clinical, electrocardiographic, and echocardiographic factors of the effect of bevacizumab on cardiovascular system.</description><dc:title>Systemic administration of bevacizumab increases the risk of cardiovascular events in patients with metastatic cancer</dc:title><dc:creator>Christodoulos Stefanadis, Andreas Synetos, Dimitris Tousoulis, Eleftherios Tsiamis, Archontoula Michelongona, Flora Zagouri, Aristotle Bamias, Meletios Athanasios Dimopoulos, Stella Kyvelou, Ioannis Kapelakis, Konstantinos Toutouzas</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.115</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-11</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-11</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>341</prism:startingPage><prism:endingPage>344</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020262/abstract?rss=yes"><title>Relationship of aortic stiffness, central systolic blood pressure and left atrium enlargement in general middle and aged population</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020262/abstract?rss=yes</link><description>Left atrial enlargement has been proposed as a predictor of atrial fibrillation, stroke, congestive heart failure, and cardiovascular death . Recently, it is reported that left atrial diameter (LAD) is increased and independently associated with arterial stiffness in patients with obstructive sleep apnea .</description><dc:title>Relationship of aortic stiffness, central systolic blood pressure and left atrium enlargement in general middle and aged population</dc:title><dc:creator>Sheng Kang, Hui-min Fan, Jue Li, Lie-ying Fan, Ming Chen, Zhong-min Liu, Heart Failure Risk Factors Investigation Project collaborative group (HFRFIP collaborative group)</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.135</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-24</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-24</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>344</prism:startingPage><prism:endingPage>347</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020213/abstract?rss=yes"><title>No evidence for an association of AB0 blood group and manifestation of thrombotic microangiopathies</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020213/abstract?rss=yes</link><description>Since many years, AB0 blood group has been known to influence on the manifestation of arterial and venous thrombotic disease . In particular, individuals carrying a Non-0-blood group (A, B, AB) appeared to have a higher risk for thrombotic events compared to those with A, B, or AB blood groups. This effect was attributed to higher factor VIII and von Willebrand factor (vWF) plasma levels compared to individuals with the 0 blood group . In a study enrolling 1117 healthy individuals, plasma vWF levels were lowest in group O (mean vWF antigen [vWF:Ag] 75IU/dl) and highest in group AB subjects (mean vWF:Ag 123IU/dl) . The cause for blood group-related differences in vWF plasma levels has been investigated by different groups and an expression of ABH oligosaccharide structures on the N-linked oligosaccharide chains of vWF located in the A1 domain that contains the binding site for the platelets' von Willebrand factor receptor, glycoprotein (GP) Ib-V-IX, has been identified as the missing link . In a murine model, the important effect of glycosylation on vWF plasma levels could be shown by demonstrating a heightened clearance of this adhesive protein in mice by induced aberrant endothelial expression of N-acetylgalactosaminyltranferase . A and B antigens expressed on vWF were found to explain about 18% of the variation in vWF plasma levels, but the exact mechanism has not yet been totally clarified . While the in vitro removal of A and B antigens from purified plasma vWF reduces activity but not its antigenic level , the detection of lower antigen levels and activity of plasmic vWF in type O individuals suggests an effect of AB0 antigens on the in vivo clearance of the whole vWF molecule . As the most likely explanation, the expression of AB0 determinants on vWF appears to modulate its susceptibility to proteolysis by a specific metalloprotease, ADAMTS13 (a disintegrin-like and metalloproteinase with thrombospondin type-1 repeats-13) . Incubating purified vWF from individuals with different AB0 blood groups with human plasma-derived ADAMTS13, a significantly faster vWF proteolysis in blood group 0 samples compared to non-O vWF could be detected . Individuals with the rare Bombay phenotype (lack of AB0 blood group antigens) have a significantly increased clearance of vWF by ADAMTS 13 . Summing up, carbohydrate structure protects vWF from enzymatic degradation in plasma  and a reduced amount of oligosaccharide chains on vWF results in increased susceptibility of vWF to cleavage by ADAMTS 13 . In particular, two N-linked potential glycosylation sites (asparagines 1515 and 1574) are located in close proximity to the ADAMTS13 cleavage site (Tyr1605-Met1606 bond within the A2 domain) and are likely to modulate vWF cleavage by the enzyme.</description><dc:title>No evidence for an association of AB0 blood group and manifestation of thrombotic microangiopathies</dc:title><dc:creator>Christoph Sucker, Andreas Fusshoeller, Firuseh Dierkes, Bernd Grabensee, Rüdiger E. Scharf, Rainer B. Zotz, Jens Litmathe</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.130</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-18</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-18</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>347</prism:startingPage><prism:endingPage>348</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020201/abstract?rss=yes"><title>Very late stent thrombosis after drug eluting stent: Management therapy guided by intravascular ultrasound imaging</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020201/abstract?rss=yes</link><description>Very late stent thrombosis (VLST) is a very serious complication of drugs eluting stent (DES) implantation . Several factors triggering DES thrombosis have recently been identified , especially stent underexpansion or malapposition . However the management strategy of these mechanical stent failures still remains debated.</description><dc:title>Very late stent thrombosis after drug eluting stent: Management therapy guided by intravascular ultrasound imaging</dc:title><dc:creator>Estelle Vautrin, Gilles Barone-Rochette, Benoit Berthoud, Stéphanie Marlière, Hélène Bouvaist, Bernard Bertrand, Olivier Ormezzano, Jacques Machecourt, Gérald Vanzetto</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.129</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-30</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-30</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>349</prism:startingPage><prism:endingPage>351</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020171/abstract?rss=yes"><title>Red Cell Distrubition Width (RDW): A novel risk factor for cardiovascular disease</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020171/abstract?rss=yes</link><description>The red cell distribution width (RDW) is a marker of variation of the size of the circulating red blood cells (anisocytosis) and is routinely reported as a part of routine complete blood count (CBC). Thus, elevated RDW levels are observed in many clinical setting such as hemolysis, after blood transfusions and in the setting of an ineffective red cell production such as that of iron deficiency, vitamin B12 or folate. RDW is also increased in clinical states such as pregnancy, thrombotic thrombocytopenic purpura and inflammatory bowel diseases. Because of the lack of knowledge about prognostic significance, RDW was ignored previously except anemia evaluation.</description><dc:title>Red Cell Distrubition Width (RDW): A novel risk factor for cardiovascular disease</dc:title><dc:creator>Huseyin Uyarel, Turgay Isik, Erkan Ayhan, Mehmet Ergelen</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.126</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-21</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-21</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>351</prism:startingPage><prism:endingPage>352</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020110/abstract?rss=yes"><title>C-reactive protein and endothelial dysfunction: The clinicians should have in mind diurnal variations</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020110/abstract?rss=yes</link><description>We read the article by Forte et al.  that the increase in C-reactive protein (CRP) plasma levels across the coronary circulation is associated with a profound impairment in coronary endothelial-dependent function, outlining a novel pathophysiological mechanism linking CRP to acute coronary syndrome (ACS). However, in the present article we saw an additional potential limitation of the study: the authors have not measured CRP during a 24-hour period.</description><dc:title>C-reactive protein and endothelial dysfunction: The clinicians should have in mind diurnal variations</dc:title><dc:creator>Alberto Dominguez-Rodriguez, Pedro Abreu-Gonzalez</dc:creator><dc:identifier>10.1016/j.ijcard.2011.10.120</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-21</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-21</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>353</prism:startingPage><prism:endingPage>353</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020614/abstract?rss=yes"><title>Left ventricular functional recovery after intracoronary injection of autologous bone marrow-derived stem cells in patients with acute myocardial infarction: A dose–response pilot study</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020614/abstract?rss=yes</link><description>Cell therapy based on autologous stem cell transplantation and hope for myocardial regeneration after acute myocardial infarction (AMI) has been the focus of many clinical trials for more than a decade. Most of the trials have used bone marrow mononuclear cell fraction (BMC) for the treatment of AMI patients but the cell doses have varied greatly between the different studies (reviewed by George et al.) . Based on a meta-analysis of several trials it has been suggested that the smallest effective dose to significantly improve left ventricular ejection fraction (LVEF) after cell administration is 108 BMCs . However, one later study reported statistically significant effects also with a smaller cell dose (6×107) . An actual dose–response study comparing the effect of two different cell doses on the functional recovery of the heart after AMI and stem cell transplantation has only been performed by one study group . Meluzin et al. reported that the recovery of the regional myocardial function of the infarcted wall seems to be dose dependent [].</description><dc:title>Left ventricular functional recovery after intracoronary injection of autologous bone marrow-derived stem cells in patients with acute myocardial infarction: A dose–response pilot study</dc:title><dc:creator>Johanna A. Miettinen, Kari V. Ylitalo, Matti Niemelä, Kari Kervinen, Marjaana Säily, Pirjo Koistinen, Eeva-Riitta Savolainen, Timo H. Mäkikallio, Heikki V. Huikuri</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.012</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-02</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-02</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>354</prism:startingPage><prism:endingPage>356</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020602/abstract?rss=yes"><title>What is the acceptable rate of false positives for STEMI within a primary PCI network? Insights from a metropolitan system with direct ambulance-based access</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020602/abstract?rss=yes</link><description>In recent years percutaneous coronary intervention (PCI) has become the preferred treatment for patients with ST elevation acute myocardial infarction (STEMI) and regional PCI networks have been widely developed in many countries . In this context, the problem of “false-positive” (FP) cardiac catheterization laboratory activations is emerging as a relevant issue (average rate of 12.7%, ranging from 6.4% to 22.7%) potentially leading to resource wasting . The extent to which the type of network organization influences the prevalence of FP is currently unknown and minimum and maximum acceptable FP rates have yet to be established. Direct ambulance-based access to the catheterization lab for example, which has been shown to reduce pre-balloon time on one hand , on the other may increase the risk of FP. We designed this study to determine prevalence (including secular trend), causes and possible determinants of electrocardiographic FP for STEMI within a large regional PCI Hub and Spoke network offering both emergency department (ED) hospital access and direct ambulance-based access with facilities allowing pre-hospital ECG transmission.</description><dc:title>What is the acceptable rate of false positives for STEMI within a primary PCI network? Insights from a metropolitan system with direct ambulance-based access</dc:title><dc:creator>Enrica Perugini, Giuseppe Di Pasquale, Lara Di Diodoro, Paolo Ortolani, Gianni Casella, Nevio Taglieri, M. Letizia Bacchi Reggiani, Antonio Marzocchi, Massimiliano Lorenzini, Angelo Branzi, Claudio Rapezzi</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.011</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-02</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-02</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>356</prism:startingPage><prism:endingPage>358</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020560/abstract?rss=yes"><title>Decreased scale-specific heart rate variability after multiresolution wavelet analysis predicts sudden cardiac death in heart failure patients</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020560/abstract?rss=yes</link><description>In the present study, we aimed to assess whether multiresolution wavelet analysis (MWA)  of heart rate variability (HRV)  carries significant prognostic information independently from other well established stratifiers in the field of sudden cardiac death (SCD) prediction . All 231 HF patients gave informed consent and the study was approved by our institution's ethics committee. They underwent physical examination, personal and family history, medications recording, chest X ray, blood and biochemical tests, 12 leads-ECG (25mm/s, MAC 5000, GE Marquette Medical, Milwaukee, USA), ECHO (SONOS 5500, Hewlett Packard, Andover, MA, USA), signal averaged ECG (SAECG/MAC 5000 GE Medical, Milwaukee, USA) and Holter Monitoring (HM/Spider View-1000Hz and SyneScope 3.10 software, Sorin Group, Ela Medical, Clamart, France). Patients with NSVT episodes (n=87) were further risk stratified by electrophysiological study (EPS). The patients with clinical (n=12) or inducible ventricular tachycardia/ventricular fibrillation (VT/VF) on EPS (n=50) received an ICD (n=62). The sample size was divided into the high risk (n=46) and the low risk (n=185) groups, according to three SCD events/surrogates: 1. clinical VT/VF (n=12), 2. ICD's appropriate activation (n=22), 3. confirmed SCD (n=12). MWA was performed using Matlab software . The Haar wavelet was used and the final index σwav was extracted as the standard deviation of the detailed coefficients of scale 8. Statistical results are presented as hazard ratios (HR) and the 95% confidence intervals (CI). A p value &lt;0.05 was considered statistically significant. Arrhythmic events rate was tabulated with Kaplan–Meier curve. STATA 8.0 software (Stata Corporation 2003, TX, USA) was used for all statistical calculations. Baseline clinical characteristics are presented in . Univariate analysis searched with log rank test () and a Cox proportional hazard survival model was used to determine whether σwav predicted SCD independently from other risk stratifiers. The model was adjusted for LVEF, fQRS from SAECG, heart rate, VPBs &gt;10/hour, NSVT episodes &gt;1/24hours, mean QTc, age, gender, and σwav (). In this model σwav was a statistically significant arrhythmia predictor, with hazard ratio of 0.991 (p&lt;0.001, 95% CI: 0.987–0.996). Furthermore σwav values were dichotomized at 25th percentile (cutoff point=181) for tabulating Kaplan Meier arrhythmia events (). The σwav (continuous values) was replaced by cutoff σwav &lt;181 at the previous multivariable Cox model. The analysis revealed that patients with σwav values below 181 had hazard ratio 2.526 (p=0.01), 95% CI: 1.213–5.259 for SCD surrogate end points.().The most interesting finding of our study was that in heartbeat time series of SCD high risk patients was indentified a specific scale with decreased HRV. That means that HRV reflected by σwav at segments with a periodicity of 256 RR duration was found diminished in SCD patients. Thurner first analyzed heart beat time series with MWA method and reported correct classification of a small number of ECG signals retrieved from two different groups: a heart failure patients group and a group of healthy subjects . These results were confirmed by Ashkenazy at 1998  and again at 2001 in a sample of 116 patients . Wavelets were used to quantify HRV and assess its instantaneous changes during atropine and propanolol administration , during four classical autonomic tests , for studying HRV during myocardial ischemia  and for studying reperfusion-dependent autonomic changes during thrombolysis . In our study the scale which was proved most significant was scale 8, corresponding to 256 beat intervals and not scales 4 and 5 as in Thurners' experiments (scale 4 was also highly predictive in our analysis). The incompatibility in predictive scales reported by Thurner and our team is abolished after a deeper study of Thurner's article. He demonstrated that scales m=4 and m=5 (16–32 heartbeat intervals) were proved important for the separation of normal from heart failure patients. This was the main conclusion of his article, which was also reflected in its title. The separation between controls and the patient experiencing SCD that was included into the total patient's sample has not been discussed. After a deeper look at Fig. 2 page 1546 of this article, where σwav is presented as a function of scale , it is obvious that the σwav values for the SCD subject decrease significantly and progressively from scales 6 and 7 to scale 8. This finding is in accordance with our results. In fact both studies, Thurner's and ours, demonstrate that HF patients with increased risk for SCD exhibit a reduced scale specific (m=8) σwav variability after Haar wavelet analysis in comparison to their control group. The next question that appears is why in the case of SCD candidates the HRV is affected and reduced in this specific scale (m=8 corresponding to 256 RR duration segments), an issue for future investigation. From the electrophysiological point of view σwav represents variability. Since the signal fluctuates in time, so too does the sequence of wavelet coefficients; a natural measure for this variability is the wavelet coefficient standard deviation, as a function of scale . In our univariate analysis the σwav index outperformed the conventional SDNN in SCD prediction. It is possible that the σwav/scale 8 index carried more crucial information for the variability status than the general statistical index SDNN calculated in the time domain. If this signal has been analyzed with a general statistical time domain method, for example the SDNN for the entire 24hour time series, this sensitive information concealed in scale 8 and representing diminished HRV in segments with 256 RR duration periodicity has been lost. Thus, MWA extracts different information than that extracted from SDNN. From the other point of view, the scale 8 and the 256 RR interval duration periodicity (our patients presented mean heart rate 70beats/min and mean RR=857ms) correspond to 0.004Hz and belong in the Very Low Frequencies band after signal FFT analysis (VLF: 0.0033Hz–0.04Hz). According our study's log rank results presented in , σwav index outperforms the rest HRV indices analyzed in the frequency domain after FFT. This may happen because Haar wavelet and the wavelet mother function fit better the shape of the analyzed signal, allowing a better quantitative measurement .</description><dc:title>Decreased scale-specific heart rate variability after multiresolution wavelet analysis predicts sudden cardiac death in heart failure patients</dc:title><dc:creator>Petros Arsenos, Konstantinos Gatzoulis, George Manis, Theodoros Gialernios, Polychronis Dilaveris, Dimitrios Tsiachris, Stefanos Archontakis, Efstathios Kartsagoulis, Dimitrios Mytas, Christodoulos Stefanadis</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.007</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-02</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-02</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>358</prism:startingPage><prism:endingPage>360</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020559/abstract?rss=yes"><title>Thinking more before deciding to implant an ICD in LQT3 patients</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020559/abstract?rss=yes</link><description>Congenital long-QT syndrome (LQTS) is a clinically and genetically heterogeneous syndrome, which is characterized by abnormal QT-interval prolongation on the surface ECG and an increased risk of sudden cardiac death (SCD), usually due to ventricular fibrillation. Mutations in potassium-channel genes KCNQ1 (LQT1 locus) and KCNH2 (LQT2 locus) and the sodium-channel gene SCN5A (LQT3 locus) are the most common causes of the long-QT syndrome . Zareba et al.  in 1999 were the first to call attention to the excess lethality of cardiac events among LQT3 patients because they seemed to have less frequent arrhythmic events but a greater propensity to die; disturbingly, sudden death often seemed to be the first symptom. In 2001, Schwartz et al.  observed a disquieting number of cardiac arrests and sudden deaths among symptomatic LQT3 patients despite β-blocker therapy, a finding later confirmed by Priori et al. . Then implantable cardioverter defibrillators (ICDs) increasingly were used to treat LQT3 patients, although not always with compelling indications . ICD implantation is undeniably the most effective way to prevent arrhythmic death; however, the risks of complications inherent in this procedure, which are especially common and troublesome in patients undergoing ICD implantation at a young age , are not always appreciated. Moreover, a recent single-center study  suggests that carefully selected patients with LQT3 (excluding infants with arrhythmias during the first year of life and patients with excessive bradycardia or marked QT prolongation) may be safely treated with β-blockers without ICD backup. Thus, it is fair to think more before deciding to implant an ICD in all LQT3 patients.</description><dc:title>Thinking more before deciding to implant an ICD in LQT3 patients</dc:title><dc:creator>Zhong-le Bai, Sheng-hua Zhou, Qi-ming Liu</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.006</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-11-28</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-11-28</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>360</prism:startingPage><prism:endingPage>362</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020547/abstract?rss=yes"><title>Impact of long-term Xuezhikang therapy on cardiovascular events in high-risk patients with nonspecific, preexisting abnormal liver tests: A post-hoc analysis from Chinese Coronary Secondary Prevention Study (CCSPS)</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020547/abstract?rss=yes</link><description>The use of 3-hydroxy-3-methyglutaryl coenzyme A (HMG-CoA) reductase inhibitor, or statins has extensively been shown to reduce both primary and secondary cardiovascular risk in the general population . However, the concern about hepatotoxity acts as a barrier in real world clinical practice to prescribing statins with elevated liver transaminase values such as alanine aminotransferase (ALT) or aspartate aminotrans-ferase (AST) . Several small sample size studies of patients with raised serum or glutamic-pyruvic transaminase (GPT) activity because of non-alcohol fatty liver disease (NAFLD) showed that statins are safe and improve liver history and liver tests . A recent post-hoc analysis from GREACE study demonstrated that statin therapy was safe and could improve liver test and reduced cardiovascular morbidity in patients with mild-to-moderately abnormal liver tests that are potentially attributable to NAFLD . However, this impact may be different in different statins in different larger clinical trials, and needs to confirm in more robust, larger cohort, prospective clinical trials due to different cause, ethnic, clinical and pharmacological background.</description><dc:title>Impact of long-term Xuezhikang therapy on cardiovascular events in high-risk patients with nonspecific, preexisting abnormal liver tests: A post-hoc analysis from Chinese Coronary Secondary Prevention Study (CCSPS)</dc:title><dc:creator>Jian-Jun Li, Zong-Liang Lu, Wen-Rong Kou, Roberto Bolli, Zuo Chen, Yang-Feng Wu, Xue-Hai Yu, Yu-Cheng Zhao</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.005</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-02</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-02</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>362</prism:startingPage><prism:endingPage>365</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020936/abstract?rss=yes"><title>Normalization of ejection fraction in subjects with systolic heart failure. Is it really normal? A myocardial deformation study</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020936/abstract?rss=yes</link><description>Left ventricular ejection fraction (LVEF) has been the main parameter used to guide pharmacological and device based treatment for systolic heart failure (SHF). With advancement of medical treatment for SHF, normalisation of LVEF is not infrequently seen . As normalised LVEF may occur even in the presence of histological irreversible myocyte damage , it remains unclear if heart failure medications can be safely reduced or even ceased in these patients. However, whilst LVEF is typically used for assessment of global ventricular function it is not a sensitive measure of left ventricular (LV) systolic function. Direct measurement of myocardial contraction with strain and strain rate enables quantification of the amount and rate of myocardial deformation and is seen as a more sensitive marker of myocardial systolic function . Systolic strain is expressed as the percentage change in myocardial deformation during systole. Segmental shortening is represented by negative strain (longitudinal and circumferential) and segmental thickening by positive strain (radial strain). Strain rate measures the rate of segmental deformation over time. In this study we aimed to investigate for the presence of abnormal myocardial deformation with speckle tracking echocardiography in patients with systolic heart failure who had normalised their LV ejection fraction.</description><dc:title>Normalization of ejection fraction in subjects with systolic heart failure. Is it really normal? A myocardial deformation study</dc:title><dc:creator>Bryan Wai, Leighton G. Kearney, Louise M. Burrell, Michelle Ord, Piyush M. Srivastava</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.036</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-19</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-19</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>365</prism:startingPage><prism:endingPage>367</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311021231/abstract?rss=yes"><title>The role of Emergency Medical Services in the assessment and management of syncope</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311021231/abstract?rss=yes</link><description>Syncope is defined as a transient loss of consciousness and postural tone followed by prompt spontaneous recovery and is caused by a transient reduction in blood flow to the reticular activating system of the brain. Syncope is a common reason for calling the Emergency Medical Services (EMS) and accounts for 1–1.5% of emergency department (ED) visits with 13–83% of these resulting in hospital admission . The identification of patients at high risk and differentiating these from those who may have a more benign etiology remain a challenge for physicians assessing syncopal patients in the ED . The EMS are often the first to arrive at the scene of a syncopal patient and are involved in the preliminary assessment of these patients and offer initial medical assistance. The EMS are therefore often well placed to gain valuable clinical information which may aid in determining the cause of syncope. However, the assessment findings of the EMS may not always be taken into account in determining the potential cause of syncope. The value of this initial first response assessment, and the impact it has on decision making in the ED have not been previously evaluated. This retrospective study was aimed to analyze the findings of the EMS and to determine their contribution in the management of syncopal patients.</description><dc:title>The role of Emergency Medical Services in the assessment and management of syncope</dc:title><dc:creator>Riyaz Somani, Adrian Baranchuk, Juan Camilo Guzman, Carlos A. Morillo</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.066</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-22</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-22</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>368</prism:startingPage><prism:endingPage>369</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS016752731102122X/abstract?rss=yes"><title>Disrupted circadian rhythm in night shift workers: What can we do?</title><link>http://www.internationaljournalofcardiology.com/article/PIIS016752731102122X/abstract?rss=yes</link><description>Recently, Manfredini et al. commented that disruption of circadian rhythm and clocks would account for the decreased flow-mediated dilation (FMD) and nitric oxide (NO) level in the night-shift workers . This comment is applicable to another study which also reported the greatest decrease in endothelial function in physicians with fewer sleeping hours, reflecting greater disturbance of the circadian rhythm .</description><dc:title>Disrupted circadian rhythm in night shift workers: What can we do?</dc:title><dc:creator>Weon Kim, Jong-Shin Woo, Wan Kim</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.065</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-22</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-22</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>369</prism:startingPage><prism:endingPage>370</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311021218/abstract?rss=yes"><title>Left ventricular dynamic gradient and pericardial effusion. A life threatening combination in patients with apical ballooning syndrome</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311021218/abstract?rss=yes</link><description>Although most complications of apical ballooning syndrome (ABS) are known, data regarding its incidence in series of patients is scanty . More accurate knowledge is pertinent, however, to optimize monitoring requirements and patient management. In addition, there is also little information regarding incidence and nature of follow up events . Thus, our goal was to analyze, prospectively, the in-hospital complications and follow-up of 50 consecutive patients admitted to our center from February 2002 to November 2010. They all met the criteria for ABS: a) transient hypokinesia, akinesia or dyskinesia of mid and apical segments of the left ventricle corresponding to ≥2 main coronary arteries; b) absence of significant stenosis (≥50%); c) ST elevation and/or negative T waves in anterior precordial leads; and d) absence of cerebral hemorrhage, pheocromocytoma, craneal trauma or myocarditis. A 2D echocardiogram was performed on admission to assess ejection fraction in the parasternal short-axis and apical 4-chamber long-axis views (Simpson method), septal and posterior wall thickness, regional contractility, and the presence of mitral regurgitation or intraventricular dynamic gradient ≥10mmHg. The echocardiogram was repeated prior to discharge and in the follow-up if recovery of systolic function did not occur. In patients with a dynamic gradient, pericardial effusion or heart failure, additional echocardiograms were performed during hospitalization. Coronary angiography was carried out within 12h of symptom onset in 17 patients with persistent ST elevation, within 4days in 31, and prior to discharge in 2. Contrast left ventriculogram was performed in 45 patients and cardiac magnetic resonance in the last 19. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [].</description><dc:title>Left ventricular dynamic gradient and pericardial effusion. A life threatening combination in patients with apical ballooning syndrome</dc:title><dc:creator>Josefa Cortadellas, Jaume Figueras, Cinta Llibre, José Rodriguez Palomares, Gerard Martí, Rosa M. Lidon, José A. Barrabés, David García Dorado</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.064</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-22</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-22</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>370</prism:startingPage><prism:endingPage>372</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311021127/abstract?rss=yes"><title>Does hypoxia directly regulate the natriuretic peptide system?</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311021127/abstract?rss=yes</link><description>We read with great interest the letter by Costantino et al.  published recently in International Journal of Cardiology. In the paper they reported the time course of B-type natriuretic peptides after ventricular fibrillation (VF) and showed that the levels of both B-type natriuretic peptides increased after VF. Based on the previously published results they refer to that the mechanisms behind VF-induced increases in plasma BNP levels are cardiac myocyte stretching and arrhythmias.</description><dc:title>Does hypoxia directly regulate the natriuretic peptide system?</dc:title><dc:creator>Olli Arjamaa, Mikko Nikinmaa</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.055</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-21</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-21</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>372</prism:startingPage><prism:endingPage>372</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311021085/abstract?rss=yes"><title>Response to the letter: How to manage coronary slow flow following PCI?</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311021085/abstract?rss=yes</link><description>Dear Editor,   We read with pleasure the letter by Korkmaz et al.  regarding therapeutic options for slow flow in the coronary circulation. Their letter was in response to our recently published study showing that ACS is related to increased erythrocyte aggregation regardless of fibrinogen levels. Our results hint to the fact that interfering with fibrinogen activity might improve microcirculatory flow , and therefore suggested the use of fibrinolytic therapy.</description><dc:title>Response to the letter: How to manage coronary slow flow following PCI?</dc:title><dc:creator>Yaron Arbel, Shmuel Banai</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.051</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-22</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-22</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>373</prism:startingPage><prism:endingPage>373</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS016752731102105X/abstract?rss=yes"><title>Comparison of drug-eluting versus bare-metal stents after rotational atherectomy for the treatment of calcified coronary lesions</title><link>http://www.internationaljournalofcardiology.com/article/PIIS016752731102105X/abstract?rss=yes</link><description>Calcified coronary lesions are a well-known risk factor for short and long-term failure after both bare metal stent (BMS)  and drug eluting stent (DES) implantation . Rotational atherectomy facilitates the delivery of stents in severely calcified coronary lesions by modifying plaque anatomy and smoothing inner vascular lumen. Recent reports suggest that the use of rotational atherectomy in combination with DES implantation for the treatment of severely calcified lesions might result in high procedural success and acceptable restenosis rate . However, the long-term efficacy and safety of DES compared to BMS, in combination with rotational atherectomy in patients with calcified coronary lesions is limited.</description><dc:title>Comparison of drug-eluting versus bare-metal stents after rotational atherectomy for the treatment of calcified coronary lesions</dc:title><dc:creator>Fabio Mangiacapra, Guy R. Heyndrickx, Etienne Puymirat, Aaron J. Peace, William Wijns, Bernard De Bruyne, Emanuele Barbato</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.048</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-26</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-26</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>373</prism:startingPage><prism:endingPage>376</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311021024/abstract?rss=yes"><title>Serum copeptin/NT-proBNP ratio: A more reliable index of absolute endogenous stress and prognosis during the course of Tako-tsubo cardiomyopathy?</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311021024/abstract?rss=yes</link><description>Diagnostic approaches for the non-invasive differentiation of Tako-tsubo cardiomyopathy (TTC) and acute coronary syndromes (ACS) have drawn particular attention in the recent years.These approaches are generally based on a variety of suggested initial electrocardiographic (ECG) findings  and non-invasive imaging modalities. However, serum levels of a variety of biomarkers including copeptin (C-terminal provasopressin) (CP)  and the ratios of serum N-terminal pro-brain natriuretic peptide (NT-proBNP)/myocardial enzymes (myoglobin and troponin T)  have also been recently suggested for the differentiation of these two entities. Notwithstanding the recent progress in the non-invasive diagnosis of TTC, clinical tools for the risk stratification (serum markers, etc.) that may potentially serve as prognostic and therapeutic guides are still needed for the proper management of patients with established TTC. As described below, in comparison to a variety of serum markers, the index of serum CP/NT-proBNP ratio during the course of an established TTC may more accurately mirror endogenous stress levels, and may serve as a more independent prognostic parameter particularly with regards to duration of the disease course and risks of arrhythmogenesis, sudden cardiac death (SCD), etc. indicating its potential role as a therapeutic guide for the proper management of patients with TTC.</description><dc:title>Serum copeptin/NT-proBNP ratio: A more reliable index of absolute endogenous stress and prognosis during the course of Tako-tsubo cardiomyopathy?</dc:title><dc:creator>Kenan Yalta</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.045</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-28</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-28</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>376</prism:startingPage><prism:endingPage>377</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311021000/abstract?rss=yes"><title>Hyperglycemia in patients with hypertensive crisis: Response to “Hypertensive crisis: Comparison between diabetics and non-diabetics”</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311021000/abstract?rss=yes</link><description>Dear Editor,   Bannay and Al Husain , in a recent letter to the editor, compared the profile of hypertensive crisis (HC) in patients treated at the main hospital complex in Bahrain, highlighting the difference between those with and without diabetes mellitus (DM).</description><dc:title>Hyperglycemia in patients with hypertensive crisis: Response to “Hypertensive crisis: Comparison between diabetics and non-diabetics”</dc:title><dc:creator>Renan Oliveira Vaz-de-Melo, José Fernando Vilela-Martin</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.043</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-30</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-30</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>378</prism:startingPage><prism:endingPage>378</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020985/abstract?rss=yes"><title>Marked lipomatous hypertrophy of the right ventricular wall: A distinct clinicopathological entity from arrhythmogenic right ventricular cardiomyopathy?</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020985/abstract?rss=yes</link><description>A 21-year-old male was referred to our hospital because of palpitations due to sustained ventricular tachycardia (VT) (A) after hitting his chest hard while snow-boarding. Since the VT was resistant to antiarrhythmic drugs, it was converted to sinus rhythm by cardioversion. His 12-lead electrocardiogram (ECG) during sinus rhythm showed conduction abnormalities, with a complete right bundle branch block morphology, right axis deviation, and first degree atrioventricular block, accompanied by inverted T waves in leads V1-3 (B). Although he had remained asymptomatic by that time, he was diagnosed with a cardiac tumor of unknown pathogenesis in his right ventricle (RV) when he was three years old. Annual checkups with non-invasive imagings in a pediatrics department had demonstrated no remarkable growth of the cardiac tumor.</description><dc:title>Marked lipomatous hypertrophy of the right ventricular wall: A distinct clinicopathological entity from arrhythmogenic right ventricular cardiomyopathy?</dc:title><dc:creator>Tadashi Nakajima, Yoshiaki Kaneko, Nobuaki Fukuda, Tadanobu Irie, Tatsuya Iso, Masahiko Kurabayashi</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.041</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-28</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-28</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>379</prism:startingPage><prism:endingPage>380</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020973/abstract?rss=yes"><title>Serum uric acid and ischemic heart disease incidence</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020973/abstract?rss=yes</link><description>Chuang et al. presented a 7-year follow-up study on the effect of uric acid on the occurrence of ischemic heart disease (IHD), adjusted by age, metabolic factors, lifestyles, medication and working type . They used popular variables in the health examination targeting 128,569 subjects. Kim et al. recently overviewed and conducted meta-analysis on this association precisely, and concluded that hyperuricemia may increase the risk of IHD events, independently of traditional IHD risk factors . But sub-analysis stratified by sex presented that the significance of relative risk disappeared in men, and only Chinese cohort kept significance in case of women.</description><dc:title>Serum uric acid and ischemic heart disease incidence</dc:title><dc:creator>Tomoyuki Kawada</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.040</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-22</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-22</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>381</prism:startingPage><prism:endingPage>381</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311020961/abstract?rss=yes"><title>Safety and positive predictive value of high-dose dipyridamole stress-echocardiography with or without contrast flash-replenishment perfusion imaging in patients with suspected or known coronary artery disease</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311020961/abstract?rss=yes</link><description>A growing body of literature has demonstrated the safety of ultrasound contrast agents in conjunction with low mechanical-index imaging during echocardiography, although most studies reported on contrast use during rest echocardiography for left ventricle opacification and rarely on its use during stress-echo (SE) with flash-replenishment myocardial perfusion imaging (MPI). Flash-replenishment sequences, by means of high-mechanical index pulses, represent a specific model of interaction among ultrasound, microbubbles and myocardial tissue, which could theoretically portend specific safety concerns.</description><dc:title>Safety and positive predictive value of high-dose dipyridamole stress-echocardiography with or without contrast flash-replenishment perfusion imaging in patients with suspected or known coronary artery disease</dc:title><dc:creator>Nicola Gaibazzi, Lorena Silva, Claudio Reverberi</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.039</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-14</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-14</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>382</prism:startingPage><prism:endingPage>383</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS016752731102095X/abstract?rss=yes"><title>The relationship between minute ventilation and oxygen consumption in heart failure: Comparing peak VE/VO2 and the oxygen uptake efficiency slope</title><link>http://www.internationaljournalofcardiology.com/article/PIIS016752731102095X/abstract?rss=yes</link><description>The assessment of ventilatory efficiency during cardiopulmonary exercise testing (CPX) is now widely recognized for its prognostic value in patients with systolic heart failure (HF) . Of the various ways to quantify ventilatory efficiency, the relationship between minute ventilation (VE) and carbon dioxide production (VCO2), commonly expressed as the VE/VCO2 slope, is perhaps the most widely utilized CPX variable for this purpose. While the general linearity of the VE–VCO2 relationship allows for a slope calculation, the relationship between VE and oxygen consumption (VO2) does not follow a similar pattern. Thus, the VE–VO2 relationship has historically been expressed as a peak exercise ratio, which also demonstrates prognostic value . To accommodate for this dislinearity, the oxygen uptake efficiency slope (OUES), which is derived from the strongly linear relationship between VO2 on the y-axis and the log transformation of VE on the x-axis, was developed . Previous studies have also found the OUES to portend prognostic value in systolic HF patients . However, we are unaware of any previous investigation which has compared the relationship or the prognostic strength of the OUES and peak VE/VO2, which is the purpose of the present investigation.</description><dc:title>The relationship between minute ventilation and oxygen consumption in heart failure: Comparing peak VE/VO2 and the oxygen uptake efficiency slope</dc:title><dc:creator>Ross Arena, Marco Guazzi, Jonathan Myers, Paul Chase, Daniel Bensimhon, Lawrence P. Cahalin, Mary Ann Peberdy, Euan Ashley, Erin West, Daniel E. Forman</dc:creator><dc:identifier>10.1016/j.ijcard.2011.11.038</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-12-21</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-12-21</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>384</prism:startingPage><prism:endingPage>385</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527309004215/abstract?rss=yes"><title>Acute myocardial infarction and left bundle branch block with changing axis deviation</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527309004215/abstract?rss=yes</link><description>Abstract: Changing axis deviation has been reported also during atrial fibrillation or atrial flutter. Changing axis deviation has been also reported during acute myocardial infarction associated with atrial fibrillation too or at the end of atrial fibrillation during acute myocardial infarction. Left bundle branch block is usually associated with normal or left axis deviation. Rarely the ECG shows a LBBB with changing QRS morphology and changing axis deviation. There are several possible explanations for the intermittent shift in the QRS axis in the presence of complete left bundle branch block. The most plausible explanation is the coexistence of left posterior hemiblock and predivisional left bundle branch block. We present a case of a left bundle branch block with changing axis deviation in a 93-year-old Italian woman admitted to the Cardiology Unit with an acute myocardial infarction.</description><dc:title>Acute myocardial infarction and left bundle branch block with changing axis deviation</dc:title><dc:creator>Salvatore Patanè, Filippo Marte, Giuseppe Dattilo, Mauro Sturiale</dc:creator><dc:identifier>10.1016/j.ijcard.2009.03.128</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2009-05-08</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2009-05-08</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Online Letters to the Editor</prism:section><prism:startingPage>e47</prism:startingPage><prism:endingPage>e49</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311005651/abstract?rss=yes"><title>Regression of non-compaction in left ventricular non-compaction cardiomyopathy by cardiac contractility modulation</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311005651/abstract?rss=yes</link><description>Research highlights: ► Left ventricular non-compaction cardiomyopathy is potentially reversible. ► Cardiac Contractility Modulation may lead to regression of non-compaction.</description><dc:title>Regression of non-compaction in left ventricular non-compaction cardiomyopathy by cardiac contractility modulation</dc:title><dc:creator>Philip H.C. Wong, Jeffrey W.H. Fung</dc:creator><dc:identifier>10.1016/j.ijcard.2011.06.040</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-06-27</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-06-27</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Online Letters to the Editor</prism:section><prism:startingPage>e50</prism:startingPage><prism:endingPage>e51</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS016752731100564X/abstract?rss=yes"><title>Usefulness of tissue characterization by cardiac magnetic resonance imaging as a complementary method for evaluation of cardiac malignant lymphoma</title><link>http://www.internationaljournalofcardiology.com/article/PIIS016752731100564X/abstract?rss=yes</link><description>Research highlights: ► Cardiac mass with the manifestation of fetal arrhythmia. ► Myocardial invasion of malignant lymphoma diagnosed by cardiac MRI. ► Late gadolinium-enhanced MRI was homologous to histopathological findings. ► No past similar cases reporting both cardiac MRI and postmortem autopsy.</description><dc:title>Usefulness of tissue characterization by cardiac magnetic resonance imaging as a complementary method for evaluation of cardiac malignant lymphoma</dc:title><dc:creator>Kei Sato, Tairo Kurita, Shiro Nakamori, Yasutaka Ichikawa, Koji Mastuoka, Takashi Tanigawa, Katsuya Onishi, Hajime Sakuma, Masaaki Ito</dc:creator><dc:identifier>10.1016/j.ijcard.2011.06.039</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-07-04</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-07-04</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Online Letters to the Editor</prism:section><prism:startingPage>e52</prism:startingPage><prism:endingPage>e53</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311005626/abstract?rss=yes"><title>Rescue extracorporeal life support as a bridge to reflection in fulminant stress-induced cardiomyopathy</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311005626/abstract?rss=yes</link><description>Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is increasingly used as rescue therapy in severe cardiogenic shock refractory to medical treatment and intra-aortic balloon pump (IABP). Yet, indications and benefits of VA-ECMO in acute heart failure remain to be fully established. Importantly, it is unclear whether major clinical uncertainties related to potential reversibility of cardiac dysfunction and contraindications for bridging to transplantation justify refusal of VA-ECMO support in an emergency setting.</description><dc:title>Rescue extracorporeal life support as a bridge to reflection in fulminant stress-induced cardiomyopathy</dc:title><dc:creator>Dirk W. Donker, Elien Pragt, Patrick W. Weerwind, Johanna W.M. Holtkamp, Jindra Vainer, Bas Mochtar, Jos G. Maessen</dc:creator><dc:identifier>10.1016/j.ijcard.2011.06.037</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-06-27</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-06-27</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Online Letters to the Editor</prism:section><prism:startingPage>e54</prism:startingPage><prism:endingPage>e56</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311005596/abstract?rss=yes"><title>Repeated sudden cardiac death in coronary spasm: Is IVUS helpful to decide treatment strategy?</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311005596/abstract?rss=yes</link><description>Coronary spasm is thought to be the main pathogenic mechanism of variant angina. Despite medical treatment, ischemic events are continued in some patients, often associated with serious complications . Ventricular arrhythmias and sudden cardiac death have been predominantly reported in cases of multivessel coronary artery spasm . In medically intractable coronary spasm, coronary stent or Implantable cardioverter defibrillators (ICD) have suggested as a treatment strategy, but optimal therapy is still unknown. We report a young patient of medically intractable vasospastic angina who experienced sudden cardiac death twice and successfully treated with stent after intravascular ultrasound study.</description><dc:title>Repeated sudden cardiac death in coronary spasm: Is IVUS helpful to decide treatment strategy?</dc:title><dc:creator>Yae Min Park, Woong Chol Kang, Kwen-Chul Shin, Seung Hwan Han, Taehoon Ahn, In Suk Choi, Eak Kyun Shin</dc:creator><dc:identifier>10.1016/j.ijcard.2011.06.034</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-06-23</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-06-23</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Online Letters to the Editor</prism:section><prism:startingPage>e57</prism:startingPage><prism:endingPage>e59</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311005547/abstract?rss=yes"><title>Sinus venosus defect (SVD) identified in zebrafish Glut1 morphants by video imaging</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311005547/abstract?rss=yes</link><description>Research Highlights: ► Zebrafish is an informative vertebrate model for human cardiovascular development. ► Glut1 is required to maintain the structural integrity of sinus venosus in vivo. ► The findings may have relevance to human embryogenesis of sinus venosus.</description><dc:title>Sinus venosus defect (SVD) identified in zebrafish Glut1 morphants by video imaging</dc:title><dc:creator>Ping-Pin Zheng, Peter J. van der Spek, Clemens M.F. Dirven, Rob Willemsen, Johan M. Kros</dc:creator><dc:identifier>10.1016/j.ijcard.2011.06.029</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-07-15</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-07-15</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Online Letters to the Editor</prism:section><prism:startingPage>e60</prism:startingPage><prism:endingPage>e61</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311005869/abstract?rss=yes"><title>Cardiac rupture in a patient with an acute myocardial infarction and extensive fatty infiltration of the heart (“adipositas cordis”)</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311005869/abstract?rss=yes</link><description>Research highlights: ► Fatty heart maybe a substrate to left ventricular rupture in ischemic heart disease. ► Excessive intracardiac pressure maybe the cause of cardiac rupture in fatty heart. ► Imaging studies in ischemic heart disease must paid attention to fatty infiltration.</description><dc:title>Cardiac rupture in a patient with an acute myocardial infarction and extensive fatty infiltration of the heart (“adipositas cordis”)</dc:title><dc:creator>Victor H. Godinez-Valdez, Iris Cázares-Campos, Alberto Aranda-Fraustro, Francisco López-Jiménez, Manuel Cárdenas, Manlio F. Márquez</dc:creator><dc:identifier>10.1016/j.ijcard.2011.06.060</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-06-30</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-06-30</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Online Letters to the Editor</prism:section><prism:startingPage>e62</prism:startingPage><prism:endingPage>e64</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527311006139/abstract?rss=yes"><title>Left ventricular noncompaction presenting as peripartum cardiomyopathy</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527311006139/abstract?rss=yes</link><description>A 23year-old pregnant female (G1P0) at 40weeks and 5days gestation presented with uterine contractions. Her past medical history was unremarkable as was her prenatal course. She complained of shortness of breath and cough during labor. Vaginal delivery was uncomplicated; however, shortness of breath worsened over the next several hours. Physical examination and chest x-ray were consistent with congestive heart failure. Presumptive diagnosis was peripartum cardiomyopathy. Transthoracic echocardiogram revealed a dilated left ventricle with end-diastolic dimension of 7.2cm and ejection fraction of 15–20%. Prominent trabeculations and deep intratrabecular recesses in the left ventricle were visualized, consistent with left ventricular noncompaction cardiomyopathy (LVNC; ). She responded well to diuresis and medical therapy. Given the unexpected finding of LVNC in setting of peripartum cardiomyopathy, we performed cardiac magnetic resonance imaging (CMR) to confirm the diagnosis. CMR showed pronounced trabeculations and deep recesses in the left ventricle and a noncompacted endothelial layer surrounded by a thin compact layer (). These findings were all consistent with LVNC. Following clinical improvement, she was discharged home, but she was readmitted within 2weeks with decompensated heart failure. She continued to worsen and required listing for cardiac transplantation. The patient was subsequently transplanted and pathology of her explanted heart was consistent with LVNC. The patient's infant underwent an echocardiogram that also demonstrated LVNC. At 12months post-transplant, both our patient and her child are doing well.</description><dc:title>Left ventricular noncompaction presenting as peripartum cardiomyopathy</dc:title><dc:creator>Brian Lea, Alison L. Bailey, Matthew E. Wiisanen, Anil Attili, Navin Rajagopalan</dc:creator><dc:identifier>10.1016/j.ijcard.2011.06.073</dc:identifier><dc:source>International Journal of Cardiology 154, 3 (2012)</dc:source><dc:date>2011-07-08</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2011-07-08</prism:publicationDate><prism:volume>154</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S0167-5273(11)X0029-3</prism:issueIdentifier><prism:section>Online Letters to the Editor</prism:section><prism:startingPage>e65</prism:startingPage><prism:endingPage>e66</prism:endingPage></item></rdf:RDF>
