Treatment of left ventricular hypertrophy in hypertensive patients.

Left ventricular hypertrophy (LVH), as detected by electrocardiography or echocardiography, constitutes a powerful risk factor for cardiovascular morbidity and mortality. Antihypertensive drugs that modulate the sympathetic or renin-angiotensin-aldosterone systems or the intracellular free Ca concentration (i.e. beta-blockers, postsynaptic alpha 1-blockers, centrally acting adrenergic drugs, calcium channel blockers and angiotensin converting enzyme (ACE) inhibitors) can prevent or cause regression of LV mass after short-term therapy, this effect being more pronounced with ACE inhibitors. Diuretics and arterial vasodilators also cause regression of LVH provided that they are used for long enough to effect long-term control of arterial pressure. However, clinical studies also indicate that despite their equipotent blood-pressure lowering effects, there are marked differences not only in the ability of the different types of antihypertensive drugs to prevent or reverse LV mass but also within the same class of pharmacological drugs. Decreased LV mass in hypertensive patients may be associated with an improvement in diastolic function and has not been found to produce adverse effects on LV systolic performance.