Antidepressant Paroxetine may attenuate myocardial fibrosis in post MI setting: JAMA

In this double-blind, placebo-controlled randomized clinical trial patients with acute anterior ST-segment elevation myocardial infarction with left ventricular ejection fraction (LVEF) of 45% or less were randomly allocated to 2 study arms. Patients in the experimental arm received 20 mg of paroxetine daily; patients in the control group received a placebo daily. Both treatments were provided for 12 weeks.

The primary end point was the difference in patient-level improvement of LVEF between baseline and 12 weeks as assessed by cardiac magnetic resonance tomography. Secondary end points were changes in left ventricular dimensions and late gadolinium enhancement between baseline and follow-up.

At the end of trial period, the extent of LVEF recovery was comparable in patients treated with paroxetine or placebo. There were no significant differences in changes of left ventricular dimensions and volumes. In contrast, patients treated with paroxetine had greater reduction in late gadolinium enhancement (by approximately 9%), indicating attenuation of myocardial fibrosis and scar formation after myocardial infarction.

In contrast with the mouse model, in which treatment was started 2 weeks after inducing acute myocardial infarction, patients in this study were included 48 to 96 hours after primary percutaneous coronary revascularization and paroxetine was started on top of guideline-directed optimal medical therapy less than 7 days after percutaneous coronary revascularization.

In conclusion, in this randomized clinical trial, a 3-month course of paroxetine treatment following acute myocardial infarction did not lead to an improvement in left ventricular ejection fraction compared with placebo but a beneficial effect on late gadolinium enhancement paves way for future research in this arena.

Source: JAMA Cardiology: doi:10.1001/jamacardio.2021.2247