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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.internationaljournalofcardiology.com/?rss=yes"><title>International Journal of Cardiology</title><description>International Journal of Cardiology RSS feed: Current Issue. The  International Journal of Cardiology  is devoted to cardiology in the broadest sense. Both basic research and clinical papers 
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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> © 2010 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>139</prism:volume><prism:number>2</prism:number><prism:publicationDate>4 March 2010</prism:publicationDate><prism:copyright> © 2010 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527310000513/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527309008560/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527309008511/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010656/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010668/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS016752730801067X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010681/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010693/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010711/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010723/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010735/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010929/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010930/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308008887/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009005/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009224/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009807/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009844/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009856/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308008759/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009819/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009868/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308011030/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308011170/abstract?rss=yes"/><rdf:li rdf:resource="http://www.internationaljournalofcardiology.com/article/PIIS0167527308011595/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527310000513/abstract?rss=yes"><title>Editorial Board</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527310000513/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0167-5273(10)00051-3</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2010-03-04</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2010-03-04</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</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/PIIS0167527309008560/abstract?rss=yes"><title>Lack of effect of perhexiline in ischaemic heart failure</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527309008560/abstract?rss=yes</link><description>The editor is to be congratulated for publishing the paper in this issue by Bansal et al.  in which they report the results of a clinical trial of perhexiline. In this study patients were recruited if they had reversible ischaemic myocardium and heart failure, but no anginal pain. Heart failure in such patients has been reported to be improved subsequent to revascularisation. It was postulated that improvement of ischaemia by the alternative method of pharmacological metabolic intervention with perhexiline would also improve the heart failure, but no such improvement was obtained. It is very important that such negative results be published in order to avoid the unnecessary repeated retesting of fashionable therapies .</description><dc:title>Lack of effect of perhexiline in ischaemic heart failure</dc:title><dc:creator>Mark I.M. Noble, Angela J. Drake-Holland</dc:creator><dc:identifier>10.1016/j.ijcard.2009.08.004</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2009-09-14</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2009-09-14</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>105</prism:startingPage><prism:endingPage>106</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527309008511/abstract?rss=yes"><title>Effects of perhexiline on myocardial deformation in patients with ischaemic left ventricular dysfunction</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527309008511/abstract?rss=yes</link><description>Abstract: Background: Perhexiline improves functional capacity in heart failure, but the mechanisms are undefined. We sought its effects on myocardial deformation in patients with viable myocardium.Methods: Thirty-six medically-treated patients, stable at least 6 months post-infarction with LV dysfunction and myocardial viability shown by dobutamine echo (DbE) were randomised to receive perhexiline or matching placebo for 1 year. Cardiopulmonary exercise testing and DbE were performed at baseline and follow-up. Peak-systolic strain (S) and strain rate (SR) were measured offline in 111 dysfunctional segments in the placebo and 88 in the treatment group at rest, low-dose (LDD) and peak-dose dobutamine (PDD).Results: The serum perhexiline level was 0.27±0.7 µg/l. There was no difference in the wall motion response to dobutamine at baseline and follow-up. Resting strain and SR were similar in the two groups at baseline and follow-up. However, SR at LDD and PDD increased in the placebo group and worsened during the same period in the perhexiline group. Patients on perhexiline and placebo had a similar rate-pressure product and exercise duration at baseline (7.9±2.7 vs 8.7±3.3 min, p=NS) and follow-up (9.6±4.6 vs 10.1±3.03 min, p=NS).Conclusion: Perhexiline does not improve the deformation of abnormal myocardial segments in patients with ischaemic LV dysfunction.</description><dc:title>Effects of perhexiline on myocardial deformation in patients with ischaemic left ventricular dysfunction</dc:title><dc:creator>Manish Bansal, Jonathan Chan, Rodel Leano, Peter Pillans, John Horowitz, Thomas H. Marwick</dc:creator><dc:identifier>10.1016/j.ijcard.2009.08.007</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2009-10-20</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2009-10-20</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>107</prism:startingPage><prism:endingPage>112</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010656/abstract?rss=yes"><title>Molecular mechanisms of irbesartan suppressing atherosclerosis in high cholesterol-diet apolipoprotein E knock-out mice</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308010656/abstract?rss=yes</link><description>Abstract: Objective: Atherosclerosis is a chronic inflammatory disease in which the renin–angiotensin–aldosterone system plays an important role. Evidence indicate that the angiotensin type 1 receptor blockers can suppress atherogenesis, but the exact mechanisms have not been fully elucidated. The study was undertaken to investigate the potential effects and molecular mechanisms of an angiotensin type 1 receptor blocker irbesartan on atherogenesis in high cholesterol-diet apolipoprotein E knock-out mice.Methods and results: Adult male apolipoprotein E knock-out mice were given normal diet or high cholesterol-diet and randomized to receive no treatment or irbesartan 10 mg kg−1 d−1 for 12 weeks. The apolipoprotein E knock-out mice with high cholesterol-diet were associated with a marked increase in atherosclerotic lesion area, plasma lipid and angiotensin II levels, as well as the expressions of angiotensin type 1 receptor in the aorta. High cholesterol-diet feeding increases the activity of NADPH oxidase subunits (p47phox and Rac), extracellular signal-regulated kinase 1/2, janus kinase 2, signal transducer and activator of transcription 3, nuclear factor-κB and the expression of tumor necrosis factor-α, interleukin 6, monocyte chemoattactant protein-1 and vascular cell adhesion molecule-1 in the aortas. These changes were suppressed in mice that were treated with irbesartan 10 mg kg−1 d−1, with no significant change in systolic blood pressure and plasma lipid levels.Conclusions: The results suggest that irbesartan can attenuate atherosclerosis, and this effect is partly related to the inhibition of oxidative stress and inflammatory signal transduction pathways which eventually leads to the decrease in the expression of inflammatory cytokines.</description><dc:title>Molecular mechanisms of irbesartan suppressing atherosclerosis in high cholesterol-diet apolipoprotein E knock-out mice</dc:title><dc:creator>Rui Yao, Xiang Cheng, Yong Chen, Jiang-Jiao Xie, Xian Yu, Meng-Yang Liao, Ying-Jun Ding, Ting-Ting Tang, Yu-Hua Liao</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.013</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-11-25</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-11-25</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>113</prism:startingPage><prism:endingPage>122</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010668/abstract?rss=yes"><title>Obesity in patients with non-ST-segment elevation acute coronary syndromes: Results from the SYNERGY trial</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308010668/abstract?rss=yes</link><description>Abstract: Background: Obese patients are at increased risk of acute coronary syndromes (ACS). We evaluated the prevalence of obesity in a large ACS population, as well as the relationship between body mass index (BMI) and the use of cardiac medications and procedures, clinical outcomes, and treatment effects between enoxaparin and unfractionated heparin (UFH).Methods: Using the database of the SYNERGY trial, we identified 9978 patients in 12 countries who were randomly assigned to receive enoxaparin or UFH. Patient weight at baseline and 30-day follow-up was recorded. BMI information was available on 9837 patients. BMI was analyzed in clinically meaningful categories (&lt;20, 20–25, 30–35, ≥35 kg/m2) and as a continuous variable.Results: Thirty-two percent of patients were obese (BMI≥30), with a greater proportion of patients with obesity from North America (36%) compared with other regions. Enoxaparin was dosed as 1 mg/kg regardless of body weight without maximum. The first dose of enoxaparin was underdosed in 15% of patients assigned enoxaparin, and obese patients were more likely to be underdosed than non-obese patients. Obese patients were younger, less often white, had more diabetes, hypertension, hyperlipidemia, family history of coronary artery disease, and congestive heart failure but fewer strokes, less peripheral vascular disease, and less often smoked. After adjustment, increased BMI was not an independent predictor of bleeding outcomes or 30-day death/myocardial infarction (MI), but increased BMI was predictive of lower 1-year mortality in the subgroup of patients with BMI at baseline below approximately 30 kg/m2. No statistical interaction term was observed between obesity and randomized therapy for the outcomes of death/MI at 30 days and 6 months; death at 30 days, 6 months, and 1 year; and GUSTO or TIMI bleeding.Conclusions: Nearly one third of patients in SYNERGY were obese. Despite multiple comorbidities, obese patients had better unadjusted short- and long-term outcomes. After adjustment, higher BMI was not an independent predictor of in-hospital bleeding events or 30-day death/MI, but increased BMI was an independent predictor of 1-year mortality in patients with lower BMI but not in heavier patients. No interaction between the randomized treatment and obesity for efficacy and safety outcomes was observed across the range of BMI in this dataset. Standard dosing of enoxaparin should be used in patients without extreme obesity due to limited outcome data in these patients.</description><dc:title>Obesity in patients with non-ST-segment elevation acute coronary syndromes: Results from the SYNERGY trial</dc:title><dc:creator>Kenneth W. Mahaffey, Simon T. Tonev, Sarah A. Spinler, Glenn N. Levine, Richard Gallo, John Ducas, Shaun G. Goodman, Elliott M. Antman, Richard C. Becker, Anatoly Langer, Harvey D. White, Philip E. Aylward, Jacques J. Col, James J. Ferguson, Robert M. Califf, on behalf of the SYNERGY Trial Investigators</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.008</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-11-17</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-11-17</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>123</prism:startingPage><prism:endingPage>133</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS016752730801067X/abstract?rss=yes"><title>Paracrine effects of CD34 progenitor cells on angiogenic endothelial sprouting</title><link>http://www.internationaljournalofcardiology.com/article/PIIS016752730801067X/abstract?rss=yes</link><description>Abstract: Background: Progenitor cells contribute to repair of ischemia-associated disturbances of microcirculations, but detailed mechanisms of paracrine angiogenic activation of endothelium by progenitor cells are unclear. The present study was designed to test whether progenitor cells maintain their activation pattern of cytokine secretion and capillary-like endothelial sprout attraction under conditions of hypoxia induced angiogenic activation.Methods: CD34 progenitor cells were kept separated together with spheroids of human umbilical vein endothelial cells (HUVEC) sharing a common medium supernatant to generate a paracrine diffusion gradient from CD34 cells to the endothelial cell spheroids. The expression of 27 cytokines was analyzed in the supernatant. The length and the direction of the capillary like sprouts were analyzed under 20% and 1% oxygen concentration.Results: Co-culture with CD34 cells increased sprout length of HUVEC spheroids by 18%, while reduction of oxygen concentration from 20% to 1% increased sprout length by 52%. Analysis of the direction of the sprout growth revealed a directed growth toward CD34 cells under normoxic as well as under hypoxic conditions. Paracrine induction of cytokine secretion by co-culture was similar in normoxia and in hypoxia with IL-8 (60–80-fold induction) &gt;IL-6 and MIP-1β (10–20-fold) &gt;MIP-1α and MCP-1 (3–10-fold).Conclusions: These data indicate that CD34 cell induced paracrine activation of cytokine secretion pattern and attraction of endothelial sprouting are well maintained under conditions of hypoxia induced endothelial cell sprout growth. This is a prerequisite for paracrine effectiveness of trapped progenitor cells in hypoperfused and hypooxygenated tissue areas.</description><dc:title>Paracrine effects of CD34 progenitor cells on angiogenic endothelial sprouting</dc:title><dc:creator>Robert J. Scheubel, Juergen Holtz, Ivar Friedrich, Jochen Borgermann, Simone Kahrstedt, Alexander Navarrete Santos, Rolf-Edgar Silber, Andreas Simm</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.009</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-11-13</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-11-13</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>134</prism:startingPage><prism:endingPage>141</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010681/abstract?rss=yes"><title>Bone regulatory factors NFATc1 and Osterix in human calcific aortic valves</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308010681/abstract?rss=yes</link><description>Abstract: Background: Emerging evidence suggests that calcific aortic valve stenosis constitutes an active process sharing common features with atherosclerosis and bone formation. To further support this hypothesis, we investigated the expression of bone regulatory factors in calcified aortic valves.Methods–results: Formalin-fixed, paraffin-embedded tissue samples of human aortic tricuspid valves (n=54) were used from patients undergoing valve replacement for calcific, non-rheumatic aortic stenosis. As controls, fourteen aortic tricuspid valves (n=14) were obtained at autopsy from patients without clinical and morphological aortic valve lesions. Sections from both stenotic and normal aortic valve leaflets were studied immunohistochemically. Interstitial cells in stenotic valves showed intense expression of Sox9, Runx2 and Osterix (Osx) whereas NFATc1 was expressed in interstitial and inflammatory cells. In addition, NFATc1 expression correlated significantly with Osx (r=0.458, p&lt;0.001) and Runx2 (r=0.387, p&lt;0.001). Finally, there was accumulation of activated interstitial cells, T lymphocytes and macrophages as well as intense neoangiogenesis in pathological leaflets.Conclusions: The presence of NFATc1 and Osx in our material lends further support to the hypothesis that during the process of aortic valve calcification there is expression of osteoblastic phenotypes by valvular cells.</description><dc:title>Bone regulatory factors NFATc1 and Osterix in human calcific aortic valves</dc:title><dc:creator>Alexandros Alexopoulos, Vasiliki Bravou, Stavros Peroukides, Loukas Kaklamanis, John Varakis, Dimitrios Alexopoulos, Helen Papadaki</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.014</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-11-19</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-11-19</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>142</prism:startingPage><prism:endingPage>149</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010693/abstract?rss=yes"><title>Selective serotonin re-uptake inhibitors decrease the cytokine-induced endothelial adhesion molecule expression, the endothelial adhesiveness to monocytes and the circulating levels of vascular adhesion molecules</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308010693/abstract?rss=yes</link><description>Abstract: Background: Selective serotonin reuptake inhibitors (SSRIs) exert cardioprotective effects. We examined whether SSRIs a) modulate endothelial cell expression of vascular cell adhesion molecule (VCAM-1), intracellular adhesion molecule (ICAM-1) and adhesiveness to U937 monocytes, b) reduce the circulating levels of these adhesion molecules in vivo.Methods: We assessed the effect of SSRIs, (citalopram, fluvoxamine and fluoxetine), on TNF-alpha-induced expression of VCAM-1 and ICAM-1 in human aorta endothelial cells and adhesiveness to U937 monocytes. Cells were incubated with TNF-alpha in the absence and in the presence of SSRIs concentrations from 10−7 M to10−4 M and the VCAM-1 and ICAM-1 expression was quantified by cell-ELISA. The TNF-alpha-stimulated adhesiveness to U937 monocytes was also assessed. Twenty five patients with chronic heart failure and depression were randomized to receive sertaline 50 mg, p.o., o.d. (n=13) or placebo. At baseline and 3-months after treatment, we measured VCAM-1and ICAM-1 plasma levels.Results: SSRIs decreased the TNF-alpha-induced endothelial expression of VCAM-1 at concentration range 10−7 M to 10−4 M (p&lt;0.05). ICAM-1 expression was decreased in the presence of fluvoxamine and fluoxetine at concentrations from10−7 M to 10−4 M (p&lt;0.05) and in the presence of citalopram at concentrations from 10−7 M to 10−5 M (p&lt;0.05). All SSRIs inhibited the TNF-alpha-stimulated adhesiveness to U937 cells at 10−5 M and 10−4 M (p&lt;0.05). Compared to baseline, there was a greater reduction in ICAM-1 and VCAM-1 levels post-sertaline than post placebo in heart failure patients (p&lt;0.05).Conclusion: SSRIs may exhibit an anti-inflammatory activity on endothelial cells and reduce circulating VCAM-1 and ICAM-1 in vivo, a mechanism which may partly mediate their cardioprotective effects.</description><dc:title>Selective serotonin re-uptake inhibitors decrease the cytokine-induced endothelial adhesion molecule expression, the endothelial adhesiveness to monocytes and the circulating levels of vascular adhesion molecules</dc:title><dc:creator>John Lekakis, Ignatios Ikonomidis, Zoi Papoutsi, Paraskevi Moutsatsou, Maria Nikolaou, John Parissis, Dimitrios Th. Kremastinos</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.010</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-11-12</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-11-12</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>150</prism:startingPage><prism:endingPage>158</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010711/abstract?rss=yes"><title>The metabolic syndrome increased risk of cardiovascular events in Chinese—A community based study</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308010711/abstract?rss=yes</link><description>Abstract: Background: Whether metabolic syndrome (MetS) could serve as a valid indicator for cardiovascular disease (CVD) is in controversy. The aim of the study was to prospectively evaluate the predictive value of the MetS for CVD events in Chinese population by different MetS definitions.Methods: This was a community-based cohort study. MetS was defined according to the World Health Organization (WHO), the International Diabetes Federation (IDF), the National Cholesterol Education Program Adult Treatment Panel III (NCEPIII) and Joint Committee for Developing Chinese Guidelines on Prevention and Treatment of Dyslipidemia in Adults (JCDCG), respectively. 2788 subjects were included. The incidence of CVD events was monitored during a 5.5-year period.Results: The proportion of MetS defined by the WHO, IDF, NCEPIII and JCDCG criteria was 25.9%, 15.4%, 22.0% and 26.1%, respectively in men, and 24.5%, 28.0%, 31.1% and 23.0%, respectively in women. After adjusting for age, all four definitions were associated with increased risk of CVD events in women, but not in men. The corresponding hazard ratios (HRs) [95% confidence intervals (CIs)] in women were 2.13 (1.44–3.16), 1.49 (1.01–2.19), 1.50 (1.02–2.21) and 2.10 (1.41–3.11). The HRs remained significant with WHO and JCDCG definitions, not with the IDF and NCEPIII definitions, when factors of LDL cholesterol, and smoking were adjusted.Conclusion: The MetS by the WHO and JCDCG definition was associated with increased risk of CVD events in Chinese women after adjustment for age, total cholesterol, LDL cholesterol, and smoking.</description><dc:title>The metabolic syndrome increased risk of cardiovascular events in Chinese—A community based study</dc:title><dc:creator>Chen Wang, Xuhong Hou, Yuqian Bao, Jiemin Pan, Yuhua Zuo, Wenhong Zhong, Weiping Jia, Kunsan Xiang</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.012</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-12-01</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-12-01</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>159</prism:startingPage><prism:endingPage>165</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010723/abstract?rss=yes"><title>Improvement of cardiac function and remodeling by transplanting adipose tissue-derived stromal cells into a mouse model of acute myocardial infarction</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308010723/abstract?rss=yes</link><description>Abstract: Background: We investigated the effect of adipose tissue-derived stromal cells (ADSC) therapy on cardiac contractility and remodeling in the C57BL/6 mouse model of acute myocardial infarction (AMI).Methods: 30 adult male C57BL/6 mice were randomized into 2 groups, namely, AMI+media (control, n=15) and AMI+ADSC (n=15). AMI was produced by left anterior descending coronary artery ligation. After AMI induction, 1×106 ADSC or media were intramyocardially injected and the results compared. Echocardiographic and histological analyses of surviving mice (n=20) were conducted. Echocardiography was performed before cell implantation and 2 weeks after transplantation.Results: LVEF and FS improved in the ADSC group compared to the control (P&lt;0.01). LVEDD in the ADSC group decreased slightly from 4.65±0.63 mm to 4.14±0.53 mm compared to the control, but there was no statistical difference (P=0.072). LVESD decreased significantly in the ADSC group (P&lt;0.05). A significant difference in scar formation and infarct size was observed between the ADSC and control group 2 weeks after AMI (P&lt;0.05). ADSC were observed to migrate into injured sites and integrate into scar areas and increased vascular density in the infarct site compared to control group (P&lt;0.05). Additionally, some transplanted ADSC expressed the endothelial marker.Conclusions: Echocardiography and histological analysis revealed that improvement in cardiac function and ventricular remodeling was better in the ADSC group than in the control. This suggests that ADSC is a good candidate for cell therapy in cardiovascular disease.</description><dc:title>Improvement of cardiac function and remodeling by transplanting adipose tissue-derived stromal cells into a mouse model of acute myocardial infarction</dc:title><dc:creator>Long Hao Yu, Moo Hyun Kim, Tae Ho Park, Kwang Soo Cha, Young Dae Kim, Mei Lian Quan, Mi Sook Rho, Su Yeoung Seo, Jin Sup Jung</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.024</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-12-01</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-12-01</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>166</prism:startingPage><prism:endingPage>172</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010735/abstract?rss=yes"><title>Atrial fibrillation prevalence, incidence and risk of stroke and all-cause death among Chinese</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308010735/abstract?rss=yes</link><description>Abstract: Background: We investigated atrial fibrillation (AF) prevalence, incidence and the risk of stroke and all-cause death because little is known about AF risk among ethnic Chinese.Methods: We conducted a community-based prospective cohort study among 3560 participants. Prevalent and incident AF was documented by using the 12-lead ECG in baseline and serial follow-ups, and the stroke and all-cause death events were ascertained.Results: Overall prevalence rates of AF in the cohort were 1.4% in men and 0.7% in women. Incidence rates of AF were 1.68 per 1000 person-years for men and 0.76 per 1000 person-years for women. During a median 13.8 years' follow-up, we documented 208 cases of stroke and 776 deaths. As compared with those without AF, participants with AF had nearly 4 times the age, gender-adjusted risk of stroke (relative risk [RR], 3.87, 95% confidence interval [CI], 2.12–7.15), and twice the risk of death associated with all causes (RR, 2.23, 95% CI, 1.52–3.27). Further adjustment for body mass index, lifestyle factors, socioeconomic status and clinical diseases slightly attenuated these risks. In addition, after adjusting for echocardiographic measures, the following risks remained significant: the multivariate RRs were 2.90 (95% CI, 1.28–6.59) for risk of stroke and 2.05 (95% CI, 1.27–3.32) for risk of all-cause death among participants with AF.Conclusion: Our data demonstrate that AF is a significant risk factor for stroke and all-cause death for the Chinese.</description><dc:title>Atrial fibrillation prevalence, incidence and risk of stroke and all-cause death among Chinese</dc:title><dc:creator>Kuo-Liong Chien, Ta-Chen Su, Hsiu-Ching Hsu, Wei-Tien Chang, Pei-Chung Chen, Ming-Fong Chen, Yuan-Teh Lee</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.045</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-12-01</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-12-01</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>173</prism:startingPage><prism:endingPage>180</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010929/abstract?rss=yes"><title>Influence of atenolol on coronary artery spasm after acute myocardial infarction in a Japanese population</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308010929/abstract?rss=yes</link><description>Abstract: Background: Japanese patients with acute myocardial infarction (MI) have a greater incidence of coronary artery spasm than Caucasians. Some beta-blockers have been reported to aggravate coronary spasm. This study sought to assess the effects of beta-adrenoceptor blockade on coronary vasospasm in Japanese patients with acute MI who had been treated with primary angioplasty.Methods: In 69 patients we analyzed the effect of atenolol 50 mg/day initiated the day after emergency primary angioplasty on the results of intracoronary ergonovine provocation test performed 4 weeks after onset.Results: Among 35 patients in the atenolol group, the drug was discontinued in 9 (26%) due to hemodynamic compromise. The remaining 26 in the atenolol group and 34 in the control group underwent the spasm provocation test. Atenolol did not significantly increase the incidence of coronary vasospasm (31% vs. 15% in the atenolol and control groups, respectively, p= 0.135). Multivariate analysis revealed that only the pre-provocation diameter of the distal segment of the infarct-related artery predicted coronary spasm whereas atenolol did not.Conclusions: This study showed that atenolol 50 mg/day did not increase coronary spasm in Japanese acute MI patients. It is suggested that beta-blockers can be safely used soon after coronary intervention for acute MI without the risk of increasing coronary spasm; however, attention should be paid to hemodynamic change in the acute phase.</description><dc:title>Influence of atenolol on coronary artery spasm after acute myocardial infarction in a Japanese population</dc:title><dc:creator>Manabu Shirotani, Ryoji Yokota, Ichiro Kouchi, Taku Hirai, Noritsugu Uemori, Kazunao Haba, Ryuichi Hattori</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.017</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-11-19</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-11-19</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>181</prism:startingPage><prism:endingPage>186</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308010930/abstract?rss=yes"><title>Myeloperoxidase may contribute to the no-reflow phenomenon in patients with acute myocardial infarction</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308010930/abstract?rss=yes</link><description>Abstract: Background: The no-reflow phenomenon is a deteriorating factor for prognosis of acute myocardial infarction (AMI). Leukocyte enzymes may be involved in developing the no-reflow phenomenon. The aim of this study was to clarify the association of myeloperoxidase, a leukocyte enzyme, with the no-reflow phenomenon in patients with AMI after percutaneous coronary inetervention (PCI).Methods: We enrolled 50 patients with AMI whose infarct-related coronary arteries were rescued by thrombectomy devices. Blood samples were collected from peripheral vein (PV), ostium and culprit lesion of infarct-related coronary artery. Myeloperoxidase, elastase and interleukin (IL)-8 were measured by ELISA. Antegrade blood flow in the infarct-related coronary artery and myocardial perfusion were evaluated according to the corrected TIMI frame counts (cTFC) and the myocardial blush grade (MBG).Results: Plasma myeloperoxidase and IL-8 levels at the ostium and the culprit lesion of infarct-related coronary artery were significantly greater than those in PV. No-reflow was found in 10 patients (20%). Plasma levels of myeloperoxidase at the culprit lesion of infarct-related coronary artery were significantly greater in the patients with no-reflow than those without no-reflow. Plasma myeloperoxidase levels at the culprit lesion of infarct-related coronary artery positively correlated with the cTFC. Also, plasma myeloperoxidase levels were significantly higher in the patients with MBG 0–1 than those with MBG 2–3.Conclusions: The present findings indicate that local myeloperoxidase levels in the culprit coronary artery may contribute to the no-reflow phenomenon in the patients with AMI.</description><dc:title>Myeloperoxidase may contribute to the no-reflow phenomenon in patients with acute myocardial infarction</dc:title><dc:creator>Hiroshi Funayama, San-e Ishikawa, Yoshitaka Sugawara, Norifumi Kubo, Shin-ichi Momomura, Masanobu Kawakami</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.018</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2009-01-12</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2009-01-12</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>187</prism:startingPage><prism:endingPage>192</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308008887/abstract?rss=yes"><title>Chronic total occlusion of the left main coronary artery with normal left ventricular motion: The occluded site confirmed by three-dimensional computed tomography</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308008887/abstract?rss=yes</link><description>Abstract: Total occlusion of the left main trunk (LMT) frequently results in sudden cardiac death. As a result, it is rarely observed on coronary arteriogram. There are only a few reports on chronic total occlusion of the LMT. Most patients present with recent, severe angina, but it is not easy to distinguish chronic total occlusion of the LMT from other types of severe coronary heart diseases.Here, we report a very rare case of chronic total occlusion of the LMT. The patient is a 38-year-old female with a history of three normal deliveries. Chronic total occlusion of the LMT was suspected on coronary arteriogram 2years previously in the other hospital; however, she continued working as a part-time employee at a supermarket. She was referred to our hospital because of slightly increased effort angina and shortness of breath.The final diagnosis and the site of occlusion were determined by three-dimensional computed tomography (3-D CT). The patient underwent coronary artery bypass graft (CABG) surgery, and ischemic symptoms completely disappeared.</description><dc:title>Chronic total occlusion of the left main coronary artery with normal left ventricular motion: The occluded site confirmed by three-dimensional computed tomography</dc:title><dc:creator>Kuniyuki Shirasawa, Myung-Woo Hwanga, Yoshio Sasaki, Hidefumi Oya, Shinichi Takeda, Katsura Inenaga-Kitaura, Tetsuya Doi, Rei Takeoka, Yasushi Kitaura, Yoshihide Sawada, Chuichi Kawai</dc:creator><dc:identifier>10.1016/j.ijcard.2008.07.001</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-08-26</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-08-26</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Letters to the Editors</prism:section><prism:startingPage>193</prism:startingPage><prism:endingPage>195</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009005/abstract?rss=yes"><title>Use of landiolol hydrochloride, a new β-blocker, in coronary computed tomography angiography</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308009005/abstract?rss=yes</link><description>Abstract: We investigated the usefulness of landiolol hydrochloride, an ultrashort-acting β1-selective agent, for coronary computed tomography angiography (CTA). Intravenous landiolol was administered to 133 patients before coronary CTA. Hemodynamic changes, adverse effects, image quality, and diagnostic accuracy for detection of coronary stenoses were evaluated. HR was significantly reduced during injection, but quickly recovered after cessation of landiolol. Neither significant changes in BP nor adverse effects were seen. The sensitivity, specificity, and positive and negative predictive values of coronary CTA for detection of significant stenoses were excellent, compared with invasive angiography. Therefore, our results show that intravenous landiolol administration gives a favorable image quality and facilitates diagnostic accuracy without causing adverse effects, indicating that landiolol is a useful premedication for coronary CTA.</description><dc:title>Use of landiolol hydrochloride, a new β-blocker, in coronary computed tomography angiography</dc:title><dc:creator>Satoshi Isobe, Kimihide Sato, Kaichiro Sugiura, Takeo Mimura, Mikiko Kobayashi, Chizuka Meno, Makoto Kato, Hideki Ishii, Toyoaki Murohara</dc:creator><dc:identifier>10.1016/j.ijcard.2008.06.088</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-08-15</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-08-15</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Letters to the Editors</prism:section><prism:startingPage>196</prism:startingPage><prism:endingPage>198</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009224/abstract?rss=yes"><title>Postinfarction left ventricular pseudoaneurysm with left-to-right shunt: Case report and review of the literature</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308009224/abstract?rss=yes</link><description>Abstract: Postinfarction left ventricular pseudoaneurysms are rarely detected because the clinical manifestations are heterogeneous. Pseudoaneurysms are especially difficult to detect and manage in patients whose ischemic heart disease is concomitant with other conditions. Here we report a unique case of postinfarction pseudoaneurysm with left-to-right shunt in a patient with the triple vessel disease who also had end-stage renal failure and was treated with long-term hemodialysis. We discuss the clinical course, diagnosis and treatment of pseudoaneurysms and the association of this condition with left-to-right shunts.</description><dc:title>Postinfarction left ventricular pseudoaneurysm with left-to-right shunt: Case report and review of the literature</dc:title><dc:creator>Leszek Bryniarski, Aleksandra Kubinyi, Marta Ekiert-Kubinyi, Kalina Kawecka-Jaszcz</dc:creator><dc:identifier>10.1016/j.ijcard.2008.07.002</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-09-09</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-09-09</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Letters to the Editors</prism:section><prism:startingPage>199</prism:startingPage><prism:endingPage>201</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009807/abstract?rss=yes"><title>Dyslipidemia and abdominal aortic aneurysm: Another piece of the puzzle?</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308009807/abstract?rss=yes</link><description>Abstract: The underlying cause of aneurysmal aortic dilation is uncertain in most patients. It is unclear whether atherosclerosis causes aneurysmal disease or vice versa, while familial clusters are suggestive of a possible genetic predisposition. The data obtained from well-designed molecular and clinical studies support a multifactorial, systemic, nonatherosclerotic causal hypothesis, such as a defect in vascular structural proteins, with atherosclerosis occurring as a secondary process.</description><dc:title>Dyslipidemia and abdominal aortic aneurysm: Another piece of the puzzle?</dc:title><dc:creator>Turgay Celik, Atila Iyisoy, Murat Celik, Yalcin Tan</dc:creator><dc:identifier>10.1016/j.ijcard.2008.08.021</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-09-19</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-09-19</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Letters to the Editors</prism:section><prism:startingPage>202</prism:startingPage><prism:endingPage>203</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009844/abstract?rss=yes"><title>A brief office educational intervention improved referral rates for hypertension control in women</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308009844/abstract?rss=yes</link><description>Abstract: As part of an initiative to increase physician awareness about hypertension and cardiovascular disease (CVD); we studied the effects of a pilot intervention on the rates of referral for uncontrolled hypertension in an Ob-Gyn office. Physicians in an Ob-Gyn practice completed an educational session regarding hypertension and used a 1-page tracking form in their medical records for 3 months. Trained personnel reviewed medical records to compare baseline rates of hypertension control to those at the end of the intervention. Rates of counseling about lifestyle modification to control hypertension were also documented. The rate of referral for hypertension was significantly increased after 3 months (p&lt;0.001). The rates of counseling about CVD risk factors approached 100%. In this study, hypertension was commonly under-treated, despite being a major risk factor for CVD. As primary care physicians, obstetrician-gynecologists are in an excellent position to facilitate evaluation and treatment of hypertension in women. Education about the importance of hypertension control along with a simple tracking form can assist Ob-Gyn physicians in complying with JNC 7 guidelines.</description><dc:title>A brief office educational intervention improved referral rates for hypertension control in women</dc:title><dc:creator>Vivian Lewis, Janice Barnhart, Jan L. Houghton, Pamela Charney</dc:creator><dc:identifier>10.1016/j.ijcard.2008.08.024</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-09-17</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-09-17</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Letters to the Editors</prism:section><prism:startingPage>204</prism:startingPage><prism:endingPage>206</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009856/abstract?rss=yes"><title>Kounis syndrome: A manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308009856/abstract?rss=yes</link><description>Abstract: Stent components acting as potential antigens and promoting intracoronary mast cell activation can lead to catastrophic intrastent thrombosis. Patients with drug-eluting stent (DES) implantation are prone to hypersensitivity reactions from five potential antigens namely, nickel strut, polymer coating, eluted drug, as well as, concomitant drugs clopidogrel and aspirin. These events may be more common than suspected because it is hard to document them, unless they become systemic, in which case they manifest themselves as the Kounis syndrome characterized by the concurrence of acute coronary events with hypersensitivity reactions. This report concerns of a patient with implanted DES who developed an acute myocardial infarction in the stent area following an allergic reaction to contrast material.</description><dc:title>Kounis syndrome: A manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material</dc:title><dc:creator>John S. Kogias, Emmanouil X. Papadakis, Constantinos G. Tsatiris, George Hahalis, George N. Kounis, Andreas Mazarakis, Maria Batsolaki, Georgia V. Gouvelou-Deligianni, Nicholas G. Kounis</dc:creator><dc:identifier>10.1016/j.ijcard.2008.08.026</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-09-22</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-09-22</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Letters to the Editors</prism:section><prism:startingPage>206</prism:startingPage><prism:endingPage>209</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308008759/abstract?rss=yes"><title>Inverted Takotsubo contractile pattern caused by pheochromocytoma with tall upright T-waves, but not typical deep T-wave inversion</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308008759/abstract?rss=yes</link><description>Abstract: We describe a 36-year-old woman with inverted Takotsubo cardiomyopathy caused by pheochromocytoma crisis. In the acute phase, her electrocardiogram showed ST segment depression in lead II, III, aVF and V2 through V5. On day 14, tall upright T-waves were observed in leads V2 through V5 despite heart failure and basal to midventricular ballooning improved on day 4, and all electrocardiographic abnormalities finally normalized after surgical removal of the pheochromocytomas. This is the first report of electrocardiographic course of inverted Takotsubo cardiomyopathy, and these findings seem as if the inverted electrocardiographic findings are contrary to those of apical ballooning.</description><dc:title>Inverted Takotsubo contractile pattern caused by pheochromocytoma with tall upright T-waves, but not typical deep T-wave inversion</dc:title><dc:creator>Shinpei Kimura, Wataru Mitsuma, Masahiro Ito, Hiromi Suzuki, Yukio Hosaka, Satoshi Hirayama, Osamu Hanyu, Satoru Hirono, Makoto Kodama, Yoshifusa Aizawa</dc:creator><dc:identifier>10.1016/j.ijcard.2008.06.073</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-08-22</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-08-22</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Online Letters to the Editors</prism:section><prism:startingPage>e15</prism:startingPage><prism:endingPage>e17</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009819/abstract?rss=yes"><title>Left ventricular hypertrabeculation/noncompaction in a patient with peripartum cardiomyopathy</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308009819/abstract?rss=yes</link><description>Abstract: Left ventricular hypertrabeculation/noncompaction (LVHT) is characterized by prominent apical or mid-ventricular lateral and inferior trabeculations that are separated by deep recesses perfused from the left ventricular cavity. Affected myocardium is often thickened with a distinct two-layer appearance of both spongy or noncompacted elements and “normal” or compacted myocardium. This uncommon condition is considered by the World Health Organization to be an unclassified cardiomyopathy. Both congenital and acquired cases have been reported and the condition is genetically heterogeneous. Differing diagnostic criteria for the condition have been proposed. We report a case in which a 25-year-old woman presented with cardiac arrest and dilated cardiomyopathy 8 weeks after delivering her second child. Intraoperative transesophageal echocardiography performed during emergent placement of a left ventricular assist device revealed the typical changes of LVHT in the apex. To our knowledge, this is the first case in which findings consistent with LVHT have been found in a patient with dilated cardiomyopathy in the peripartum period. The patient we present would thus meet existing diagnostic criteria for both LVHT and peripartum cardiomyopathy.</description><dc:title>Left ventricular hypertrabeculation/noncompaction in a patient with peripartum cardiomyopathy</dc:title><dc:creator>Kent H. Rehfeldt, Juan N. Pulido, William J. Mauermann, Roger L. Click</dc:creator><dc:identifier>10.1016/j.ijcard.2008.08.025</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-09-15</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-09-15</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Online Letters to the Editors</prism:section><prism:startingPage>e18</prism:startingPage><prism:endingPage>e20</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308009868/abstract?rss=yes"><title>Myocardial perforation by a guidewire crossing a stenotic aortic valve during cardiac catheterization</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308009868/abstract?rss=yes</link><description>Abstract: Myocardial perforation by a guidewire after retrograde crossing of a stenotic aortic valve during cardiac catheterization is rare. We present a patient with calcific aortic stenosis who suffered this potentially life-threatening complication and in whom conservative treatment was successful. Early recognition of this complication is important for the operator performing cardiac catheterizations in patients with calcific aortic stenosis.</description><dc:title>Myocardial perforation by a guidewire crossing a stenotic aortic valve during cardiac catheterization</dc:title><dc:creator>Ben M. Swinkels, Tim J.F. ten Cate, Nico A. Haenen, Benno J.W.M. Rensing, Jo J.A.M. Defauw, Wybren Jaarsma</dc:creator><dc:identifier>10.1016/j.ijcard.2008.08.027</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-09-17</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-09-17</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Online Letters to the Editors</prism:section><prism:startingPage>e21</prism:startingPage><prism:endingPage>e23</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308011030/abstract?rss=yes"><title>Deficiency of complement factor MBL in a patient required cardiac surgery after an acute myocardial infarction with underlining chronic lymphocytic leukemia</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308011030/abstract?rss=yes</link><description>Abstract: Increasing evidence suggests that Mannan-binding lectin (MBL), the initial factor of the lectin pathway of complement, plays a role in cardiovascular diseases, i.e. inversely associated with risk of myocardial infarction (MI). In the present case, a patient with MBL deficiency underwent coronary artery bypass grafting (CABG) after an acute MI with underlining chronic lymphocytic leukemia (CLL). Post-operatively, the patient had a cerebral vascular accident and eventually expired. Analysis of his blood samples from pre-, intra-, and post-operative periods showed that MBL levels abruptly increased post-operatively. We hypothesize that the post-operative increase of MBL in the patient with pre-existing MBL deficiency may contribute to systemic inflammation, causing a detrimental effect after cardiac surgery.</description><dc:title>Deficiency of complement factor MBL in a patient required cardiac surgery after an acute myocardial infarction with underlining chronic lymphocytic leukemia</dc:title><dc:creator>Lawrence T. Lai, Daniel C. Lee, Wilson Ko, Ketan Shevde, Ming Zhang</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.023</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-11-27</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-11-27</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Online Letters to the Editors</prism:section><prism:startingPage>e24</prism:startingPage><prism:endingPage>e26</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308011170/abstract?rss=yes"><title>Anomalous origin of the right coronary artery from the pulmonary artery (ARCAPA)</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308011170/abstract?rss=yes</link><description>Abstract: Anomalous origin of the right coronary artery from the pulmonary artery (ARCAPA) is a very rare congenital abnormality. Echocardiographic findings are specific but may be easily misinterpreted. We therefore present the case of a 5-year old boy with emphasis on the echocardiographic findings.</description><dc:title>Anomalous origin of the right coronary artery from the pulmonary artery (ARCAPA)</dc:title><dc:creator>Andreas Kühn, Jelena Kasnar-Samprec, Christian Schreiber, Manfred Vogt</dc:creator><dc:identifier>10.1016/j.ijcard.2008.10.036</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-12-22</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-12-22</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Online Letters to the Editors</prism:section><prism:startingPage>e27</prism:startingPage><prism:endingPage>e28</prism:endingPage></item><item rdf:about="http://www.internationaljournalofcardiology.com/article/PIIS0167527308011595/abstract?rss=yes"><title>Atypical cardiac manifestation of hypereosinophilic syndrome and reversible cardiotoxicity to imatinib</title><link>http://www.internationaljournalofcardiology.com/article/PIIS0167527308011595/abstract?rss=yes</link><description>Abstract: Hypereosinophilic syndrome (HES) is a rare disorder characterized by persistent marked eosinophilia combined with eosinophil-mediated organ damage. Myeloproliferative variants are associated with a high prevalence of cardiac involvement, which is very unusual in lymphocytic variants. Imatinib mesylate (Gleevec®) is a small molecule with tyrosine kinase activity that has shown marked effects in some individuals with HES. In this case report, we present a patient with a hypereosinophilic syndrome (lymphocytic variant) that first manifested as hypereosinophilia and heart failure secondary mainly to right ventricle systolic dysfunction. A week after imatinib therapy instauration the eosinophil count was within normal range but the patient suffered a severely left ventricular dysfunction that was restablished after early drug withdrawal. Surgical removal of a new onset mass in right atrium was required because of progressively growth despite anticoagulant therapy. Clinicians should be aware of the variable heart manifestations in patients with HES and the potential cardiotoxicity of imatinib.</description><dc:title>Atypical cardiac manifestation of hypereosinophilic syndrome and reversible cardiotoxicity to imatinib</dc:title><dc:creator>Ana Garcia-Alvarez, Marta Sitges, Xabier Garcia-Albeniz, Alessandro Sionis, Pablo Loma-Osorio, Xavier Bosch</dc:creator><dc:identifier>10.1016/j.ijcard.2008.11.018</dc:identifier><dc:source>International Journal of Cardiology 139, 2 (2010)</dc:source><dc:date>2008-12-08</dc:date><prism:publicationName>International Journal of Cardiology</prism:publicationName><prism:publicationDate>2008-12-08</prism:publicationDate><prism:volume>139</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S0167-5273(10)X0004-3</prism:issueIdentifier><prism:section>Online Letters to the Editors</prism:section><prism:startingPage>e29</prism:startingPage><prism:endingPage>e31</prism:endingPage></item></rdf:RDF>