Effects of sympathetic activation on ventricular ectopic beats in subjects with and without evidence of organic heart disease

F. Lombardi, G. Malfatto, A. Belloni, M. Garimoldi

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In a selected group of 10 apparently healthy subjects and 22 patients with organic heart disease, all with frequent ventricular ectopic heart beats on Holter monitoring, we assessed the influence of sympathetic activation by comparing the arrhythmogenic effects of a symptom-limited bicycle exercise stress test and 90° head up tilt. Tilting reduced ventricular arrhythmias in the normal subjects (-48 ± 18% from 9 ± 2 beats min-1, P <0.05). Exercise stress testing caused small and insignificant changes in arrhythmias during the early (50-75 W) phases and an almost complete suppression of ventricular ectopic beats in the final stages (-99 ± 1%, P <0.01). In six of the 10 subjects, ventricular arrhythmias reappeared in the early recovery phase. In the 22 patients with organic heart disease, tilting increased ventricular ectopic beats (43 ± 17% from 9 ± 3 beats min-1, P <0.05); augmented repetitive forms in 12 patients (179 ± 88% from 1.4 ± 0.6 per 3 min) and produced repetitive forms in six of the 10 remaining patients who did not show repetitive forms during control conditions. Exercise stress testing caused a marked marked increase in ectopic activity in the early phase (84 ± 35%) while the response during the maximal phase of exercise as well as during recovery was related to the effort capabilities. Arrhythmias were increased in 12 patients with limited exercise duration and were reduced in 10 patients with good exercise tolerance. These data indicate that sympathetic activation has different effects on ventricular arrhythmias depending on the clinical setting and that tilting is a useful manoevre to evaluate the arrhythmogenic effects of increased sympathetic activity.

Original languageEnglish
Pages (from-to)1065-1074
Number of pages10
JournalEuropean Heart Journal
Issue number10
Publication statusPublished - 1987

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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