Heart rate as a target for the prevention of sudden death

In epidemiological studies, baseline heart rate was of prognostic significance in apparently healthy subjects. Elevated heart rate predicted increased mortality and, in addition, seemed to reflect increased propensity to sudden death. A similar, but overall stronger, association between increased heart rate and overall mortality and/or sudden death has been found in patients after myocardial infarction. In other types of heart disease, e.g. in heart failure, the importance of heart rate as an indicator of prognosis has been less clear. Although an association between heart rate and overall cardiac mortality has been demonstrated, in most studies this relation was not independent of other risk factors. A prognostic value of heart rate for the prediction of sudden death in the setting of chronic heart failure has so far not been reported. Although the use of heart rate as a parameter for risk stratification has certain limitations, heart rate can be considered useful in clinical practice as it may help in the selection of high risk patients for therapy. Reduction of elevated heart rate by beta-blockers has been shown to exert beneficial effects, i.e. a reduction in mortality and sudden cardiac death in post-myocardial infarction patients. Since increased heart rate may be pro-arrhythmic, it should be reduced during therapy with antiarrhythmic agents that demonstrated use-dependence and slow conduction. To achieve this. concomitant use of beta-blockers has; been recommended. So far, it has not been conclusively demonstrated that slowing of heart rate per se has a beneficial effect in patients with normal heart rates. Several studies suggest that normal heart rate seems to indicate a low risk for fatal events. It seems conceivable that such low-risk patients do not need drugs which further slow their heart rate. Since most drugs that slow heart rate have additional pharmacological effects which interfere with the disease substrate as well as potential substrates of arrhythmogenesis, the question whether reduction of normal heart rate per se is beneficial, would require large clinical trials with drugs with purely or at least predominantly bradycardic action. How ever. such trials are vet not available.