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The relevance of sympathetic activity in the pharmacological treatment of chronic stable angina.

A large body of evidence suggests that persistently high heart rate may be associated with a significant increase in sudden death, myocardial infarction and total mortality. Such deleterious effects may be mediated via neurohumoral activation. Conversely, interventions, such as beta-blockers, that consistently reduce heart rate may reduce sudden death and prolong survival, especially in patients who survive myocardial infarction. Thus, the deleterious effect of antianginal compounds, which may increase heart rate, is especially important in chronic myocardial syndromes as well as in chronic stable angina. In this setting, the evidence is consistent with the belief that antianginal agents that increase heart rate significantly, irrespective of their other properties, may also increase the incidence of myocardial infarction or death, in contrast to agents that induce little or no tachycardic effect or those that produce frankly bradycardic responses. Data discussed in this paper indicate that long acting calcium channel blockers of the dihydropyridine type do not increase heart rate significantly. Their slower onset and offset of action may reflect a lack of neurohumoral activation, recently confirmed in the case of nifedipine gastrointestinal therapeutic system (GITS). Data from the Nifedipine gastrointestinal therapeutic system Circadian Antiischemic Program (N-CAP) study, summarized herein, confirmed that the GITS formulation produces a minimal increase in heart rate over a period of 24 h. When the compound was given alone or with a beta-blocker, it was highly effective in suppressing symptomatic and asymptomatic episodes of myocardial ischemia in patients with chronic stable angina. These findings have important implications for the treatment of ischemia in patients with chronic stable angina.