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Educational Attainment, Anger, and the Risk of Triggering Myocardial Infarction Onset

Murray A. Mittleman, MDCM, DrPH; Malcolm Maclure, ScD; Manesh Nachnani; Jane B. Sherwood, RN; James E. Muller, MD
Arch Intern Med. 1997;157(7):769-775. doi:10.1001/archinte.1997.00440280091008.
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Background:  While it has recently been shown that anger may trigger the onset of acute myocardial infarction, there has been no study of the role of socioeconomic factors in such triggering. Socioeconomic factors, such as educational attainment, may modulate the risk of triggering because of their influence on individual reactivity to external stressors and on the prevalence of traditional cardiac risk factors.

Objective:  To evaluate the influence of educational attainment on the relative risk of myocardial infarction onset following episodes of anger.

Methods:  We interviewed 1623 patients (501 women) an average of 4 days following a myocardial infarction. Data were collected on standard demographic variables as well as risk factors for coronary artery disease. Educational attainment was categorized into 3 levels: less than high school, completed high school, and at least some college. Anger was assessed by the Onset Anger Scale, a single-item, 7-level, self-report scale. Occurrence of anger in the 2 hours preceding the onset of myocardial infarction was compared with its expected frequency using self-matched control data based on the casecrossover study design.

Results:  The risk of having a myocardial infarction triggered by isolated episodes of anger declined consistently and significantly with increasing levels of educational attainment (P=.03). The relative risk was twice as high among those with less than high school education (relative risk, 3.3; 95% confidence interval, 2.0-5.4) compared with patients with at least some college education (relative risk, 1.6; 95% confidence interval, 0.9-2.9).

Conclusions:  These findings indicate that socioeconomic factors are potent modulators of the risk of triggering acute cardiovascular disease onset. A better understanding of the physiological mechanisms underlying this association may lead to novel approaches to prevent acute cardiovascular events.Arch Intern Med. 1997;157:769-775


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