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Psychosocial factors in acute myocardial infarction

Author
Geoffrey H Tofler, MD
Section Editor
Jonathan M Silver, MD
Deputy Editor
David Solomon, MD

INTRODUCTION

Although acute and chronic stress have long been suspected as risk factors for myocardial infarction (MI) and sudden cardiac death, the presence of a causal link has been viewed with skepticism. However, an increasing body of evidence supports a link even though the mechanisms remain uncertain. Recent observations have opened the broad field of acute risk to study and have highlighted the potential role of psychosocial factors in acute disease onset and prognosis after MI. As an example, ST elevation (Q-wave) MI is now recognized to be preceded by coronary thrombosis, which is in turn associated with plaque fissuring [1,2]. Plaque disruption and thrombosis frequently occurs at the site of a previously mild stenosis, suggesting that the transformation from a stable to unstable plaque occurs acutely (algorithm 1) [3]. (See "The role of the vulnerable plaque in acute coronary syndromes".)

CIRCADIAN VARIATION

The circadian variation in frequency of MI, sudden cardiac death, and myocardial ischemia is characterized by a morning peak. A meta-analysis of 66,635 patients with an acute MI and 19,390 patients with sudden death reported an excess of MIs (relative risk 1.38) and sudden deaths (relative risk 1.29) between the hours of 6 am and noon compared to the rest of the day (figure 1A-B) [4].

The circadian variation in event frequency suggests that cardiac events may be triggered by external activities, particularly those activating the sympathetic nervous system [5]. Support for this comes from one study of 1225 patients which reported an absence of a circadian variation in diabetics, particularly those with evidence of cardiac autonomic neuropathy who have absent heart rate variability [6], and those taking beta blockers or aspirin at the time of admission for an MI [7]. (See "Diabetic autonomic neuropathy".)

A circadian variability in fibrinolytic capacity may be another factor contributing to the morning increase in MI. Among patients with stable coronary heart disease, plasminogen activator inhibitor-1 activity peaks in the early morning while tissue plasminogen activator activity is at its nadir; treatment with a beta blocker ameliorated this relatively prothrombotic state [8]. (See "Fibrinolytic markers and cardiovascular risk".)

TRIGGERING OF ACUTE MI

Data from the Multicenter Investigation of the Limitation of Infarct Size (MILIS) indicated that among 849 patients with acute MI, 48 percent described one or more possible triggers, the most common of which was emotional upset (14 percent) [9]. Other studies have identified possible triggers in up to 10 percent of patients [10-12].

                    

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Literature review current through: Nov 2016. | This topic last updated: Wed Nov 25 00:00:00 GMT+00:00 2015.
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