Regression of left ventricular hypertrophy: do antihypertensive classes differ?

Left ventricular hypertrophy (LVH) is now recognized as a major risk factor for cardiac morbidity and mortality, a component of which is independent of associated coronary heart disease. The mechanisms that underlie this risk are increasingly understood and include disturbances in cardiac electrophysiology, coronary perfusion and myocardial contractile function. Recognition that regression of LVH confers prognostic benefit has focused attention on developing optimal treatments to achieve this. Early studies suggested that regression is achievable using a variety of antihypertensive classes. Many of these early studies were either poorly controlled or of inadequate size to provide reliable comparisons between different agents. Subsequently a number of meta-analyses, based on selections of these early studies, have been published. More recently, a number of well-designed prospective clinical trials have been published or are under way. In summary of these results: (1) the extent of regression seen in early studies appears to be greater than that reported in recent large, well-designed trials, possibly due to regression to the mean in small studies with high coefficients of variation for echocardiographically measured left ventricular (LV) mass index; (2) meta-analyses based on these early studies tend to suggest that angiotensin-converting enzyme (ACE) inhibitors may be most effective in regressing LVH; (3) recent larger trials [Treatment Of Mild Hypertension Study (TOMHS), the Veterans Administration (VA) study, and Left ventricular hypertrophy: Indapamide Versus Enalapril (LIVE)] indicate that angiotensin-converting enzyme inhibitors and diuretics maintain a strong place in achieving regression of LVH. Long-term studies currently under way should help clarify the prognostic benefit associated with regression of LVH using antihypertensive therapy. Future work will focus on whether regression of LV mass is associated with reversal of the underlying pathophysiology of hypertrophy and, ultimately, whether prevention of LVH should be the optimal goal.