Clinical Studies of Drug Reversal of Hypertensive Left Ventricular Hypertrophy

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Abstract
Because left ventricular hypertrophy (LVH) is a strong risk factor for cardiac morbidity and mortality considerable interest has been generated concerning the possible effects of modifying LVH in hypertensive patients. In animal models disproportionate regression of left ventricular (LV) mass in relation to blood pressure may produce adverse effects on coronary blood flow reserve or LV systolic function. Clinical studies of modulation of LVH with antihypertensive drug therapy have been of two types: (1) large scale community comparison trials in which the prevalence of LVH and its regression were evaluated serially by electrocardiography (ECG) with stepped care drug therapy and (2) relatively short term (less than 2 years) studies with echocardiographic (ECHO) determination of LVH. The development of anatomically validated measurement of LV muscle mass by ECHO has demonstrated ECHO to be much more sensitive than ECG to assessment of LVH. Community comparison trials of stepped care therapy such as the Multiple Risk Factor Intervention Trial (MRFIT) and Hypertension Detection and Followup Study (HDFP) have not had the statistical power to demonstrate significant effects on risk reduction despite evidence for significant decrease in ECG-LVH despite participant numbers in the range of 8,000 to 10,000 followed serially for 5 to 6 years. Analysis of over 60 studies of hypertensive treatment using ECHO for assessment of LVH mass changes, averaging 10 to 15 subjects/study, indicates that correlation of reduction of LV mass with decrease in blood pressure has been weak (r = 0.255, P < .025). Drug monotherapy studies have shown that use of calcium channel blockers and angiotensin converting enzyme inhibitors predominantly decrease LV mass. /?-Blockers reduce LV mass in approximately 50% of studies with this class of agent, and diuretics and peripheral vasodilators decrease LV mass in far fewer than 50% of studies with these drug classes. Decreased LV mass has not been found to produce adverse effects on LV systolic function, but most study participants were included without evidence of underlying heart disease at entry. Improvement in LV diastolic filling has been found with or without substantial decrease in LV mass. Unfortunately, clinical trials assessing LV mass regression have rarely included the patients most vulnerable to possible adverse effects, that is those with established cardiac disease. The demonstration of a possible benefit or adverse effects of LVH in hypertension on morbidity and mortality must await the results of future clinical trials of large numbers of patients with prolonged serial followup. Am J Hypertens 1990;3:512-517

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