title: Review of the cardiovascular effects of heterocyclic antidepressants.
abstract: 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)
authors.affiliation: Department of Clinical Psychopharmacology, New York State Psychiatric Institute, NY 10032.
authors.forename: A H
authors.initials: AH
authors.lastname: Glassman
authors.forename: X A
authors.initials: XA
authors.lastname: Preud'homme
mesh_terms: D000657:Amoxapine / Q000009:adverse effects; D000928:Antidepressive Agents / Q000009:adverse effects*; D000929:Antidepressive Agents, Tricyclic / Q000009:adverse effects; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000150:complications; D016642:Bupropion / Q000009:adverse effects; D002318:Cardiovascular Diseases / Q000139:chemically induced* / Q000150:complications; D002320:Cardiovascular Physiological Phenomena; D002319:Cardiovascular System / Q000187:drug effects*; D003866:Depressive Disorder / Q000150:complications / Q000188:drug therapy; D006321:Heart / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007024:Hypotension, Orthostatic / Q000139:chemically induced; D008376:Maprotiline / Q000009:adverse effects; D017367:Selective Serotonin Reuptake Inhibitors / Q000009:adverse effects; D014196:Trazodone / Q000009:adverse effects
chemical_list: D000657:Amoxapine; D000928:Antidepressive Agents; D000929:Antidepressive Agents, Tricyclic; D016642:Bupropion; D008376:Maprotiline; D017367:Selective Serotonin Reuptake Inhibitors; D014196:Trazodone