Abstract
Hypertension (HTN) is the most common cause of hypertensive heart disease, which comprises
of left ventricular hypertrophy (LVH), left atrial enlargement, diastolic dysfunction,
functional mitral regurgitation and neurohormonal changes. All of these lead to significant
arrhythmias such as atrial fibrillation (AF) as well as ventricular arrhythmias, and
are known risk factors for sudden cardiac death (SCD). The association between LVH
and SCD is well established, especially in the presence of myocardial ischemia, fibrosis
and scar tissue, and AF. Inflammation, fibrosis and oxidative stress, as well as ischemia
play a significant role and are the leading pathways to remodeling, arrhythmias, and
SCD. Aggressive HTN control may lead, at least in part, to regression of LVH and thus
lower the risk of AF and SCD. Therefore, LVH is a powerful, independent predictor
of AF, ventricular arrhythmias and SCD, and is significantly underrecognized. Further
investigation of the relationship and management of diastolic dysfunction, LVH and
genetic factors and their association with SCD is certainly warranted.
Abbreviations:
AF (atrial fibrillation), HTN (hypertension), LVH (left ventricular hypertrophy), SCD (sudden cardiac death), VA (ventricular arrhythmia), VF (ventricular fibrillation), VT (ventricular tachycardia)Keywords
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References
- Heart disease and stroke statistics-2016 update: a report from the American Heart Association.Circulation. 2016; 133: e38-e360
- Hypertension. 2017; (Available from:. (http://www.world-heart-federation.org/cardiovascular-health/cardiovascular-disease-risk-factors/hypertension/))
- Hypertensive heart disease.J. Clin. Hypertens. 2005; 7: 231-238
- Incidence and predictors of sudden cardiac death in patients with diastolic heart failure.J. Cardiovasc. Electrophysiol. 2007; 18: 1231-1235
- Left ventricular hypertrophy in hypertension: its arrhythmogenic potential.Heart. 2005; 91: 250-256
- Risk of ventricular arrhythmias in left ventricular hypertrophy: the Framingham heart study.Am. J. Cardiol. 1987; 60: 560-565
- Left ventricular diameter and risk stratification for sudden cardiac death.J. Am. Heart Assoc. 2014; 3e001193
- Meta-analysis of left ventricular hypertrophy and sustained arrhythmias.Am. J. Cardiol. 2014; 114: 1049-1052
- Atrial fibrillation in hypertension: predictors and outcome.Hypertension. 2003; 41: 218-223
- Hypertension and sudden cardiac death.Am. J. Hypertens. 1999; 12: 181S-188S
- Hypertension and Sudden Cardiac Death.in: Andreadis E. Hypertension and Cardiovascular Disease. Springer, 2016
- Causes of death and influencing factors in patients with atrial fibrillation.Am. J. Med. 2016; 129: 1278-1287
- Relationship of sudden cardiac death to new-onset atrial fibrillation in hypertensive patients with left ventricular hypertrophy.Circ. Arrhythm. Electrophysiol. 2013; 6: 243-251
- Left ventricular hypertrophy and arrhythmogenesis.Card. Electrophysiol. Clin. 2015; 7: 207-220
- Assessment of myocardial fibrosis with cardiovascular magnetic resonance.J. Am. Coll. Cardiol. 2011; 57: 891-903
- Fibrosis and Arrhythmogenesis.in: Shenasa M. al. et Cardiac Mapping. Wiley-Blackwell, 2017
- Arrhythmogenic implications of fibroblast-myocyte interactions.Circ. Arrhythm. Electrophysiol. 2012; 5: 442-452
- Role for MicroRNA-21 in atrial profibrillatory fibrotic remodeling associated with experimental postinfarction heart failure.Circ. Arrhythm. Electrophysiol. 2012; 5: 1027-1035
- Fibroblast inward-rectifier potassium current upregulation in profibrillatory atrial remodeling.Circ. Res. 2015; 116: 836-845
- Arrhythmogenic consequences of myofibroblast-myocyte coupling.Cardiovasc. Res. 2012; 93: 242-251
- Electrocardiographic Markers of Sudden Cardiac Death in Different Substrates.in: Shenasa M. Josephson M. Estes M. The ECG Handbook of Contemporary Challenges. Cardiotext Publishing, Minneapolis, Minnesota2015
- Anisotropic conduction and functional dissociation of ischemic tissue during reentrant ventricular tachycardia in canine myocardial infarction.Circulation. 1988; 77: 1162-1176
- Metabolic inhibition of ICa,L and IK differs in feline left ventricular hypertrophy.Am. J. Physiol. Heart Circ. Physiol. 1994; 266: H1121-H1131
- ATP-sensitive K+ channels are altered in hypertrophied ventricular myocytes.Am. J. Physiol. Heart Circ. Physiol. 1988; 255: H1254-H1258
- Cellular basis for triggered ventricular arrhythmias that occur in the setting of compensated hypertrophy and heart failure: considerations for diagnosis and treatment.J. Electrocardiol. 2007; 40: S8-S14
- Genome-wide association study identifies single-nucleotide polymorphism in KCNB1 associated with left ventricular mass in humans: the HyperGEN study.BMC Med. Genet. 2009; 10: 43
- Diffusion Magnetic Resonance Imaging: Tractography of the Heart.in: Shenasa M. al. et Cardiac Mapping. Wiley-Blackwell, 2017
Article info
Publication history
Published online: March 04, 2017
Accepted:
March 1,
2017
Received:
February 22,
2017
Identification
Copyright
© 2017 Elsevier B.V. All rights reserved.