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Exercise testing may be used to assess symptoms occurring on effort, to search for and evaluate arrhythmias or conduction defects, antiarrhythmic drugs, pacemakers or implantable cardioverter defibrillators. Interpretation of exercise testing is difficult because of the complexity of the factors in play. Exercise itself induces changes in myocardial metabolism and the autonomic nervous system, the nature and importance of which are influenced by the underlying cardiac disease and the presence of cardiac failure or myocardial ischaemia. This is particularly true when studying the behaviour of arrhythmias on effort, which depends on many parameters, in that they may appear or disappear during exercise, irrespective of their relationship to autonomic nervous system activation. The main problem lies in the interpretation of changes in the heart rate before the onset of an arrhythmia. The sinus rhythm is both a passive indicator of the vago-sympathetic equilibrium and one of the determining factor of the arrhythmia (relationship to the rate), but it is, itself, dependent on the presence of myocardial dysfunction, a source of arrhythmias, and its changes then become difficult to interpret. These reasons explain why exercise testing is certainly a valuable tool in assessing arrhythmias but the poor reproducibility, especially in the evaluation of ventricular arrhythmias, advises prudence in the interpretation of results.

The efficacy of beta-blockers in preventing sudden death after myocardial infarction would seem to be greater in patients with cardiac failure and proportional to the reduction in heart rate induced by these drugs. In addition, a reduction in heart rate variability measured by the standard deviation from the average cardiac cycle over 24 hours has been reported to be an independent bad prognostic factor after myocardial infarction. This study compares the heart rates and the standard deviations from the mean cardiac cycle over 24 hours in 41 patients divided into 3 groups of comparable age (group I: normal subjects, n = 15; group II: hypertrophic cardiomyopathy without cardiac failure, n = 13; group III: cardiac failure, n = 13) before and after administration of acebutolol (10 mg/kg). The average 24 hour heart rates, the maximum 8-hour diurnal and minimum average 4-hour nocturnal heart rates, day-night ratio and standard deviations from the average 24 hour heart rate and at the hours of maximum and minimum average heart rates were measured by Holter monitoring with an ATREC II system. The 24 hour heart rates were slower in groups II (-18.1 p. 100) and III (-19.1 p. 100) than in group I (-9.5 p. 100), p less than 0.01, the basal heart rates being comparable and the heart rates after acebutolol being significantly lower in groups II and III. The degree of change was comparable during the diurnal and nocturnal periods.(ABSTRACT TRUNCATED AT 250 WORDS)