Heart rate as a target for the prevention of sudden death

In epidemiological studies, baseline heart rate was of prognostic significa nce in apparently healthy subjects. Elevated heart rate predicted increased mortality and, in addition, seemed to reflect increased propensity to sudd en death. A similar, but overall stronger, association between increased he art rate and overall mortality and/or sudden death has been found in patien ts after myocardial infarction. In other types of heart disease, e.g. in he art failure, the importance of heart rate as an indicator of prognosis has been less clear. Although an association between heart rate and overall car diac mortality has been demonstrated, in most studies this relation was not independent of other risk factors. A prognostic value of heart rate for th e 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 c ertain limitations, heart rate can be considered useful in clinical practic e as it may help in the selection of high risk patients for therapy. Reduct ion of elevated heart rate by beta-blockers has been shown to exert benefic ial effects, i.e. a reduction in mortality and sudden cardiac death in post -myocardial infarction patients. Since increased heart rate may be pro-arrh ythmic, it should be reduced during therapy with antiarrhythmic agents that demonstrated use-dependence and slow conduction. To achieve this. concomit ant use of beta-blockers has; been recommended. So far, it has not been conclusively demonstrated that slowing of heart rat e per se has a beneficial effect in patients with normal heart rates. Sever al 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 dise ase substrate as well as potential substrates of arrhythmogenesis, the ques tion whether reduction of normal heart rate per se is beneficial, would req uire large clinical trials with drugs with purely or at least predominantly bradycardic action. How ever. such trials are vet not available.