Is hypertensive left ventricular hypertrophy a cause of sustained ventricular arrhythmias in humans?

R Nadarajah1, P A Patel1, M H Tayebjee2

  • 1Department of Cardiology, Leeds General Infirmary, Leeds, UK.

Insights

Left ventricular hypertrophy (LVH) from hypertension may increase non-sustained ventricular arrhythmias (VAs). However, LVH alone is unlikely to cause sustained VAs or sudden cardiac death (SCD).

Area of Science:

  • Cardiology
  • Electrophysiology
  • Hypertension Research

Background:

  • Sudden cardiac death (SCD) is primarily caused by sustained ventricular arrhythmias (VAs).
  • Left ventricular hypertrophy (LVH) is a common consequence of systemic hypertension.
  • The role of hypertensive LVH as an independent risk factor for life-threatening arrhythmias remains unclear.

Purpose of the Study:

  • To review the evidence evaluating left ventricular hypertrophy (LVH) secondary to systemic hypertension as an isolated risk factor for ventricular arrhythmogenesis.
  • To determine if hypertensive LVH directly contributes to sustained ventricular arrhythmias (VAs) and sudden cardiac death (SCD).

Main Methods:

  • Literature review of animal models and clinical data concerning hypertensive LVH and ventricular arrhythmias.
  • Analysis of studies examining ion channel function, gap junction distribution, and fibrosis in hypertensive LVH.
  • Evaluation of clinical trial data on the progression from non-sustained to sustained VAs and SCD in patients with hypertensive LVH.

Main Results:

  • Animal models of hypertensive LVH show structural and electrical remodeling, including ion channel and gap junction alterations, and fibrosis.
  • Clinical data indicate an increased prevalence and complexity of non-sustained VAs in patients with hypertensive LVH.
  • Limited evidence directly links hypertensive LVH to sustained VAs or SCD, often confounded by co-existing coronary artery disease (CAD) or other factors.

Conclusions:

  • Hypertensive LVH is associated with non-sustained ventricular arrhythmias but may not be an independent risk factor for sustained VAs or SCD.
  • Pathophysiological changes in hypertensive LVH might be more homogenous than in conditions like hypertrophic cardiomyopathy (HCM) or myocardial infarction.
  • Sustained VAs in the context of hypertensive LVH are likely precipitated by other conditions such as CAD or electrolyte disturbances.

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