Glassman A H, Preud'homme X A
Department of Clinical Psychopharmacology, New York State Psychiatric Institute, NY 10032.
J Clin Psychiatry. 1993 Feb;54 Suppl:16-22.
We review the effects of heterocyclic antidepressant compounds on the cardiovascular system. It has been shown that tricyclic antidepressants (TCAs) slow intraventricular conduction, and this can be seen on a standard ECG as the increased QRS, PR, and QTc intervals. This prolonged conduction is dangerous to patients in two conditions. In overdose, delayed conduction may lead to a complete heart block or ventricular reentry arrhythmias. Either of these complications, or a combination of both, may lead to death. When treated with TCAs at therapeutic plasma levels, depressed patients with preexisting conduction disease, particularly bundle-branch block, are at higher risk to develop symptomatic A-V block than depressed patients free of conduction disorders. Clinically, the effects of TCAs on conduction does not differ significantly within the family of drugs. Who gets complications is much more a function of severity of the patient's preexisting cardiac condition. The most common cardiovascular effect of TCAs is orthostatic hypotension. Postural hypotension is more dangerous in elderly patients because it may lead to falls that cause serious physical injuries. Severe orthostatic hypotension is more likely to develop in depressed patients with left ventricular impairment and/or in patients taking other drugs like diuretics or vasodilators. Nortriptyline has been shown to cause significantly less serious postural blood pressure drops, an important difference between this drug and other TCAs. Another cardiovascular effect of TCAs is that they reduce ventricular arrhythmias. They share this property with Type 1A antiarrhythmic compounds, and a variety of Type 1 antiarrhythmics have recently been shown to increase mortality in postmyocardial infarction patients.(ABSTRACT TRUNCATED AT 250 WORDS)
我们综述了杂环类抗抑郁化合物对心血管系统的影响。研究表明,三环类抗抑郁药(TCAs)会减慢心室内传导,在标准心电图上可表现为QRS、PR和QTc间期延长。这种传导延长在两种情况下对患者是危险的。在过量用药时,传导延迟可能导致完全性心脏传导阻滞或室性折返性心律失常。这些并发症中的任何一种,或两者的组合,都可能导致死亡。当以治疗性血浆水平使用TCAs治疗时,患有既往传导疾病(尤其是束支传导阻滞)的抑郁症患者比没有传导障碍的抑郁症患者发生有症状房室传导阻滞的风险更高。临床上,TCAs家族内药物对传导的影响没有显著差异。谁会出现并发症更多地取决于患者既往心脏疾病的严重程度。TCAs最常见的心血管效应是体位性低血压。体位性低血压在老年患者中更危险,因为它可能导致跌倒并造成严重身体损伤。严重的体位性低血压更可能在患有左心室功能损害的抑郁症患者和/或正在服用利尿剂或血管扩张剂等其他药物的患者中发生。已证明去甲替林引起的体位性血压下降明显较轻,这是该药物与其他TCAs之间的一个重要区别。TCAs的另一个心血管效应是它们能减少室性心律失常。它们与1A类抗心律失常化合物具有这一特性,最近还表明,多种1类抗心律失常药物会增加心肌梗死后患者的死亡率。(摘要截选至250词)