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REVIEW ARTICLE
Year : 2022  |  Volume : 6  |  Issue : 4  |  Page : 219-225

Does psychosocial stress lead to spontaneous coronary artery dissection? A review of the evidence


Division of Cardiology, University of British Columbia, Vancouver, Canada

Correspondence Address:
Prof. Simon W Rabkin
University of British Columbia, 9th Floor 2775 Laurel Street, Vancouver, BC, V5Z 1M9
Canada
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/hm.hm_36_22

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Spontaneous coronary artery dissection (SCAD) is the acute development of a false lumen within the coronary artery wall by the spontaneous formation of an intramural hematoma which may compromise coronary (blood) flow by compression of the true lumen. Psychological factors have been implicated in its pathophysiology, but a synthesis of available data has not been previously undertaken. A literature search was conducted with the terms coronary artery dissection or spontaneous coronary artery dissection AND the terms psychological stress, anxiety, or depression. Initial studies in the field reported that psychological stress, anxiety, or depression was associated with SCAD and that acute stress may have a role in producing the SCAD. Recent studies with control groups of either acute coronary syndromes or acute myocardial infarction have produced discordant results. A meta-analysis of these studies, in this review, using a fixed effects model, showed that there was no significant association between SCAD and either moderate-to-high psychological stress or moderate-to-severe depression. However, one study reported that patients with SCAD were two-fold more likely to have experienced an emotional precipitant in the 24 h prior to the event. Assessment of patients with SCAD found long-term psychological consequences, and in some cases similar to posttraumatic stress disorder. In conclusion, chronic psychological stress, anxiety, or depression is not associated with the development of SCAD, however acute emotional stress may be a factor precipitating SCAD in some patients. Further research is necessary to examine the biological basis for SCAD and how acute stress might play a role in its pathogenesis.


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