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January 1, 1993Nordic Journal of Psychiatry21 citations

Cardiovascular effects of antidepressant drugs

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AGAlexander H. GlassmanSRSteven P. RooseSRSarah K. Rivelli

Key Result

Tricyclic antidepressants can cause orthostatic hypotension and delay conduction, whereas newer antidepressants like bupropion and SSRIs appear safer in patients with conduction disease.

Structured PICO

What are the cardiovascular safety profiles and effects of various antidepressant drugs in depressed patients?

P
Population
Depressed patients, including those with and without preexisting cardiac disease (such as conduction disease or post-myocardial infarction)
E
Exposure
Antidepressant drugs (tricyclic antidepressants [TCAs], bupropion, trazodone, SSRIs)
O
Outcome
Cardiovascular effects (orthostatic hypotension, conduction delay, arrhythmias)safety

While tricyclic antidepressants pose significant conduction risks in patients with preexisting cardiac disease, newer antidepressants like SSRIs and bupropion appear to have a safer cardiovascular profile but require further rigorous testing in high-risk patients.

Limitations

  • The SSRIs have not been systematically tested in patients presenting with arrhythmia and/or heart failure.
  • Newer drugs must be more extensively and rigorously tested in patients at risk.
  • Newer drugs have not been systematically tested in patients presenting with arrhythmia and/or heart failure
  • Implications of TCA treatment in post-myocardial infarction patients need further study

Abstract

AbstractThis article reviews data on the cardiovascular effects of tricyclic antidepressants. While cardiotoxic in overdose, at therapeutic doses tricyclics exhibit relatively benign cardiovascular effects in depressed patients without preexisting cardiac disease, with the exception of orthostatic hypotension. They have been shown to delay conduction, manifested by prolonged PR, QRS and QT intervals on the standard ECG. Depressed patients with conduction disease, particularly bundle branch block, when treated with TCAs at therapeutic plasma levels, are at a higher risk of developing symptomatic A-V block than patients free of conduction disorders. Tricyclic antidepressants have been found to reduce ventricular arrhythmias, a property shared with type 1A antiarrhythmic compounds. Recently, a variety of type 1 antiarrhythmics has been shown to increase mortality in post-MI patients. The implications this may have for the TCA treatment of post-myocardial infarction depressed patients needs further study. The newer non-tricyclic antidepressant compounds exhibit different cardiovascular effects from the standard TCAs. Bupropion, trazodone and SSRIs do not prolong conduction and appear safe in patients with conduction disease. Bupropion seems to have fewer cardiovascular side effects than TCAs, including a low rate of orthostatic hypotension and some antiarrhythmic properties. Trazodone, on the other hand, is suspected of being arrhythmogenic. The SSRIs have not been systematically tested in patients presenting with arrhythmia and/or heart failure but do not appear to cause orthostatic hypotension or seriously delay conduction. While these newer drugs do not present the same risk for cardiovascular complications as TCAs, they must be more extensively and rigorously tested in patients at risk.Key Words: AntidepressantArrhythmiaCardiovascularConduction-disorderOrthostatic-hypotension.

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Cite This Study

Glassman et al. (1993) conducted a review in Depression. Antidepressant drugs was evaluated. Tricyclic antidepressants can cause orthostatic hypotension and delay conduction, whereas newer antidepressants like bupropion and SSRIs appear safer in patients with conduction disease.

synapsesocial.com/papers/6a65933c1a73af1ea1b6a4eahttps://doi.org/10.3109/08039489309104124
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