Effect of Diuretics on Cardiac Arrhythmias and Left Ventricular Hypertrophy in Hypertension

Abstract

Ventricular arrhythmias pose a serious risk in patients with high blood pressure. The concept that diuretics predispose to life-threatening arrhythmias, however, was originally based solely on observations made in patients with severe congestive heart failure pretreated with digitalis and not in patients with high blood pressure. In hypertensive patients, some studies have also indicated that diuretic therapy may be associated with an increase in premature ventricular beats, though most have failed to demonstrate a conclusive link between hypokalemia and the precipitation of such cardiac arrhythmias. Prospective studies, however, have demonstrated that diuretic therapy had no effect on the incidence of serious ventricular arrhythmias in hypertensive patients whether they had left ventricular hypertrophy (LVH) or not, and neither at rest nor during or immediately following dynamic exercise. Correction of diuretic-induced hypokalemia similarly had no effect on the incidence of ventricular arrhythmias. In hypertensive patients, LVH is an independent and particularly sinister risk factor for cardiovascular morbidity and mortality, and its regression is now a specific goal of antihypertensive therapy. Diuretics have been shown to be at least as effective in that respect as other antihypertensive agents. The Veterans Administration Cooperative Study Group reported that after 2 years of treatment, only hydrochlorothiazide of 6 antihypertensive regimens resulted in significant reduction of left ventricular mass. In the Treatment of Mild Hypertension Study, all the antihypertensive drugs used resulted in reductions in LVH but the diuretic caused a significantly greater reduction than other non-diuretic agents. In the Systolic Hypertension in the Elderly Study, which primarily used diuretics, there was a significant reduction in LVH at 5 years. It is reasonable to conclude, therefore, that diuretics are safe and effective antihypertensive agents, which can no longer be considered arrhythmogenic and which induce LVH regression as effectively as other drugs.