Singh B N
Division of Cardiology, VAMC of West Los Angeles, Department of Medicine, UCLA School of Medicine, Los Angeles, CA, USA.
Can J Cardiol. 1999 Mar;15 Suppl A:15A-21A.
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.
大量证据表明，持续的高心率可能与猝死、心肌梗死及总死亡率的显著增加有关。这种有害影响可能是通过神经体液激活介导的。相反，诸如β受体阻滞剂等持续降低心率的干预措施可能会降低猝死率并延长生存期，尤其是在心肌梗死存活患者中。因此，可能会增加心率的抗心绞痛化合物的有害作用在慢性心肌综合征以及慢性稳定性心绞痛中尤为重要。在这种情况下，证据支持这样一种观点，即与几乎不产生或不产生心动过速效应的药物或产生明显心动过缓反应的药物相比，无论其其他特性如何，显著增加心率的抗心绞痛药物也可能增加心肌梗死或死亡的发生率。本文讨论的数据表明，二氢吡啶类长效钙通道阻滞剂不会显著增加心率。它们较慢的起效和作用消失可能反映出缺乏神经体液激活，硝苯地平胃肠道治疗系统（GITS）的情况最近已得到证实。本文总结的硝苯地平胃肠道治疗系统昼夜抗缺血项目（N-CAP）研究的数据证实，GITS制剂在24小时内使心率的增加最小。当该化合物单独使用或与β受体阻滞剂合用时，在抑制慢性稳定性心绞痛患者有症状和无症状的心肌缺血发作方面非常有效。这些发现对慢性稳定性心绞痛患者的缺血治疗具有重要意义。
