Cardiac rhythm in hypertension assessed through 24 hour ambulatory electrocardiographic monitoring. Effects of load manipulation with atenolol, verapamil, and nifedipine.

Abstract

summARY In systemic hypertension left ventricular wall stress (afterload) is reduced and function enhanced, compared with normal, in the presence of concentric hypertrophy; the opposite occurs when hypertrophy is combined with dilatation. In this study we tested the hypothesis that cardiac rhythm may be related, in part, to the interacting variables: left ventricular structure, afterload, and function.Eighty-five primary hypertensives were divided into three groups: group 1 (24 cases with normal sized heart), group 2 (33 cases with concentric hypertrophy), and group 3 (28 cases with hypertrophy and dilatation). Cardiac rhythm, through 24-hour ambulatory electrocardiographic monitoring, and end-systolic left ventricular circumferential wall stress were investigated before and after seven days of treatment with atenolol, verapamil, and nifedipine in groups 1 and 2, and with the two calcium antagonists in group 3.Atrial and ventricular extrasystoles were recorded in 75 to 100% of the subjects in the control group (13 normotensives) and in the hypertensive groups. Average 24 hour atrial ventricular extrasystoles in group 1, and ventricular extrasystoles in group 2, were similar to normal before treatment and were not affected by drugs; changes in circumferential wall stress with treatment were comparable. In group 2 the number of atrial extrasystoles in 24 hours was significantly higher than in all the other groups. They were not influenced by changes in wall stress, and were interpreted as related to the atrial "booster pump" action in the presence of concentric hypertrophy. In group 3 a great number of ventricular extrasystoles was associated with the highest baseline left ventricular afterload; circumferential wall stress and ventricular extrasystoles were poorly affected by verapamil, while the remarkable circumferential wall stress reduction caused by nifedipine was paralleled by an obvious decrease in ventricular extrasystoles.These data support the possibility that in systemic hypertension a relation exists between cardiac structure, load, and rhythm, and that ventricular arrhythmias may benefit from effective left ventricular unloading.Although the pathophysiology of the hypertensiveIn the natural history of high blood pressure the heart and the influence of therapy have been investi-condition of the heart is not static, but is subject to a gted extensively over the years, cardiac rhythm in progression of interrelated anatomical and functional high blood pressure has remained almost entirely neg-changes.'-3 Schematically, three successive structural lected.steps may be outlined: normal heart, concentric hypertrophy, and hypertrophy associated with left Accepted for publication 12 April 1983 ventricular cavity enlargement. Because of the differ-118 on 7 June 2019 by guest. Protected by copyright.

Prevalence of circadian variations and spontaneous variability of cardiac disorders and ECG changes suggestive of myocardial ischemia in systemic arterial hypertension.

“…[6][7][8][9] In the presence of left ventricular (LV) hypertrophy, ventricular arrhythmias (VA) are common in treated or temporarily untreated patients.267 Recently, James et a19 described a 26% prevalence of repetitive arrhythmias in untreated hypertensives; in that study, hypokalemia instead of LV hypertrophy was predictive for the presence of VA. This finding had also been discussed in the Multiple Risk Factor Intervention Trial (MRFIT) study10 and enhanced the debate on (drug-induced) hypokalemia as an important arrhythmogenic cofactor in hypertensive patients.1112 Data on prevalence, spontaneous variability, and prognostic relevance of VA in untreated normokalemic hypertensives are missing.…”

Prognostic value of ventricular arrhythmias and transient st‐t changes after myocardial infarction: A two‐year follow‐up with ambulatory ECG recording

“…In this study a strict correlation has been found between multiform VPBs and echocardiographic patterns of cardiomyopathy. The presence of multiform VPBs is also common in other pathologic conditions characterized by diffuse myocardial damage such as idiopathic (Huang et al, 1983), hypertensive (Loaldi et al, 1983), or sclerodermic (Clements et al, 198 1) cardiomyopathy. In cases of ischemic cardiomyopathy, multiform VPBs suggest an involvement of myocardium beyond the area of necrosis.…”

Atrial fibrillation in essential hypertension

“…Antihypertensive therapy with b-blockers or calcium antagonists resulted in a decreased frequency of premature atrial contractions. 22 Moreover, essential hypertension has changes of sympathovagal balance. Sympathetic activity increases focal autorhythmicity, easily resulting in trigger activity.…”