Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction.
Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction.
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DOI：
10.1056/nejm198908103210629
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发表时间：
1989
期刊：
影响因子：
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通讯作者：
W. Rogers;A. Epstein;J. Arciniegas;S. M. Dailey;G. Kay;R. Little;W. Maclean;S. Papapietro
中科院分区：
文献类型：
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作者：
W. Rogers;A. Epstein;J. Arciniegas;S. M. Dailey;G. Kay;R. Little;W. Maclean;S. Papapietro
心肌梗死幸存者发生室性期前除极是随后猝死的危险因素，但抗心律失常治疗是否能降低风险尚不清楚。心律失常抑制试验（CAST）正在评估抗心律失常治疗（恩卡尼、氟卡尼或莫雷西嗪）对心肌梗死后无症状或轻度症状室性心律失常（每小时6次或以上室性早搏）患者的影响。截至1989年3月30日，共有2309名患者被纳入研究的初始药物滴定阶段：1727名（75%）患者通过使用三种研究药物之一来抑制了心律失常（通过霍尔特记录评估），并被随机分配接受活性药物或安慰剂。在平均10个月的随访中，接受活性药物治疗的患者心律失常死亡率高于接受安慰剂治疗的患者。恩卡尼和氟卡尼是心律失常和非致命性心脏骤停死亡的原因（730名服用恩卡尼或氟卡尼的患者中有33名[4.5%]; 725名服用安慰剂的患者中有9名[1.2%];相对风险为3.6; 95%置信区间为1.7至8.5）。他们也解释了较高的总死亡率（730人中有56人[7.7%]，725人中有22人[3.0%];相对风险为2.5; 95%置信区间为1.6至4.5）。由于这些结果，涉及恩卡尼和氟卡尼的试验部分已经停止。我们的结论是，恩卡尼或氟卡尼不应用于治疗心肌梗死后无症状或症状轻微的室性心律失常患者，即使这些药物可能是有效的最初抑制室性心律失常。这些结果是否适用于其他可能接受抗肿瘤治疗的患者尚不清楚。
The occurrence of ventricular premature depolarizations in survivors of myocardial infarction is a risk factor for subsequent sudden death, but whether antiarrhythmic therapy reduces the risk is not known. The Cardiac Arrhythmia Suppression Trial (CAST) is evaluating the effect of antiarrhythmic therapy (encainide, flecainide, or moricizine) in patients with asymptomatic or mildly symptomatic ventricular arrhythmia (six or more ventricular premature beats per hour) after myocardial infarction. As of March 30, 1989, 2309 patients had been recruited for the initial drug-titration phase of the study: 1727 (75 percent) had initial suppression of their arrhythmia (as assessed by Holter recording) through the use of one of the three study drugs and had been randomly assigned to receive active drug or placebo. During an average of 10 months of follow-up, the patients treated with active drug had a higher rate of death from arrhythmia than the patients assigned to placebo. Encainide and flecainide accounted for the excess of deaths from arrhythmia and nonfatal cardiac arrests (33 of 730 patients taking encainide or flecainide [4.5 percent]; 9 of 725 taking placebo [1.2 percent]; relative risk, 3.6; 95 percent confidence interval, 1.7 to 8.5). They also accounted for the higher total mortality (56 of 730 [7.7 percent] and 22 of 725 [3.0 percent], respectively; relative risk, 2.5; 95 percent confidence interval, 1.6 to 4.5). Because of these results, the part of the trial involving encainide and flecainide has been discontinued. We conclude that neither encainide nor flecainide should be used in the treatment of patients with asymptomatic or minimally symptomatic ventricular arrhythmia after myocardial infarction, even though these drugs may be effective initially in suppressing ventricular arrhythmia. Whether these results apply to other patients who might be candidates for antiarrhythmic therapy is unknown.