Ventricular arrhythmias in hypertensive heart disease with and without heart failure

Forty-two patients with hypertensive heart disease but without coronary macroangiopathy were examined for ventricular arrhythmias by means of 24-h, long-term electrocardiograms (ECG). They were divided into two groups according to specific criteria. Group 1 was composed of 30 patients with left ventricular hypertrophy but normal ventricular volumes, as determined by ventriculography. Group 2 comprised 12 patients with left ventricular hypertrophy and dilated left ventricles. By means of two 24-h, long-term ECGs, the mean absolute number of ventricular extrasystoles was ascertained and severity was determined according to the classification of Ryan et al. On average, patients in group 2 showed 7.830 +/- 6.579 extrasystoles, a significantly higher (p less than 0.001) number than in patients in group 1 who had 1.132 +/- 2.639 extrasystoles/24 h. Moreover, 67% of patients in group 2 had Ryan's class 4a ventricular arrhythmias (couplets) or 4b disorders (ventricular tachycardia). However, corresponding rhythm disorders could be found in only 7% of the patients in group 1. A comparison of hemodynamic parameters and ventricular arrhythmias showed that a decreasing left ventricular ejection fraction (EF, expressed in %), a decreasing mass/volume ratio (LVMM/EDV), and an increasing systolic wall stress of the left ventricle (Tsyst) are accompanied by a nearly linear increase in ventricular extrasystoles and in the severity of the ventricular arrhythmias. During long-term ECGs, nine of 10 patients with systolic wall stress of greater than or equal to 300 dyn x 10(3)/m2 showed Ryan's class 4a or 4b ventricular arrhythmias or ventricular tachycardia during programmed ventricular stimulation. However, 12 patients with normal systolic wall stress (less than or equal to 200 dyn x 10(3)/m2) showed no or only Ryan's class 1 ventricular arrhythmias. Our investigations have shown that cardiac ventricular rhythm disorders frequently occur during decompensated hypertensive heart disease, but to a lesser extent in left ventricular hypertrophy without dilation. Further investigations are needed to demonstrate whether regression of left ventricular hypertrophy is accompanied by a reduction in the incidence of ventricular arrhythmias.