Determinants of ventricular ectopy in hypertensive cardiac hypertrophy

Abstract

Left ventricular hypertrophy in arterial hypertension has repeatedly been documented to trigger or aggravate ventricular ectopy. To determine cardiovascular mechanisms underlying ventricular ectopy, we examined 53 hypertensive patients with mild to moderate nondilated left ventricular hypertrophy by 24-hour echocardiographic monitoring and two-dimensional (2-D)-guided M-mode echocardiography. Patients with more severe ectopy (Lown's class II to IV) were older and had greater increases in left ventricular mass, ejection fraction, velocity of circumferential fiber shortening, end-diastolic volume index, and left ventricular stroke work than patients with less severe ectopy (Lown's class 0 to I). Left ventricular mass, end-diastolic diameter, stroke volume, stroke work, ejection rate, velocity of circumferential fiber shortening, and fractional fiber shortening were enhanced in a subgroup with complex ventricular ectopy (multiform or paired premature ventricular beats or runs of ventricular tachycardia) when compared with a subgroup matched with respect to age, sex, body surface area, and mean arterial pressure, which had uniform monofocal ventricular beats occurring with a frequency of less than 10/hr only. Our data indicate that the frequency and severity of ventricular ectopy in patients with essential hypertension is determined by age, severity of left ventricular hypertrophy, chamber volume, and indices of contractility and pump function. Whether or not the pattern of ventricular ectopy will identify hypertensive patients with left ventricular hypertrophy who are at increased risk of sudden death remains to be determined.