Regression of left ventricular hypertrophy; what are appropriate therapeutic objectives?

Abstract

Cardiac hypertrophy is a morphological adaptive increase in myocardial mass in response to chronic work overload and is a common clinical finding affecting 23% of men and 33% of women over the age of 59 years [1]. Pressure or volume overload on the myocardium results in an increase in myocardial wall stress and hypertrophy may be seen as an attempt to normalise wall stress and oxygen demand. Although initially protective, the increased myocardial mass requires an increase in coronary blood flow to maintain function; indeed, ventricular hypertrophy may be associated with myocardial ischaemia even with angiographically normal coronary arteries [2–4]. Left ventricular hypertrophy (LVH) significantly increases the risk of myocardial infarction, congestive heart failure and sudden cardiac death [5–7]. It is also associated with a greater prevalence of cardiac arrhythmias [8] and is an important risk factor for cardiac morbidity and mortality [9–10]. Understanding the potential mechanisms for these adverse effects has been the focus of much interest in recent years.