OBJECTIVE: Our objectives were to study anger as a trigger of acute myocardial infarction (MI) and to explore potential effect modification by usual behavioral patterns related to hostility. METHODS: This study was a case-crossover study within the Stockholm Heart Epidemiology Program. Exposure in the period immediately preceding MI was compared with exposure during a control period for each case. From April 1993 to December 1994, 699 patients admitted to coronary care units in Stockholm County were interviewed. RESULTS: During a period of 1 hour after an episode of anger, with an intensity of at least "very angry," the relative risk of MI was 9.0 (95% CI, 4.4-18.2). In patients with premonitory symptoms, the time of disease initiation may be misclassified. When restricting the analyses to those without such symptoms, the trigger risk was 15.7 (95% CI, 7.6-32.4). The possibility of examining effect modification was limited by a lack of statistical power (eight exposed cases). Results of the analyses suggested, however, an increased trigger effect among subjects reporting nonhostile usual behavior patterns, nonovert strategies of coping with aggressive situations (not protesting when being treated unfairly), and nonuse of beta-blockers. CONCLUSIONS: The hypothesis that anger may trigger MI is further supported, with an increased risk lasting for approximately 1 hour after an outburst of anger. It is suggested that the trigger risk may be modified by personal behavior patterns.
OBJECTIVE: Our objectives were to study anger as a trigger of acute myocardial infarction (MI) and to explore potential effect modification by usual behavioral patterns related to hostility. METHODS: This study was a case-crossover study within the Stockholm Heart Epidemiology Program. Exposure in the period immediately preceding MI was compared with exposure during a control period for each case. From April 1993 to December 1994, 699 patients admitted to coronary care units in Stockholm County were interviewed. RESULTS: During a period of 1 hour after an episode of anger, with an intensity of at least "very angry," the relative risk of MI was 9.0 (95% CI, 4.4-18.2). In patients with premonitory symptoms, the time of disease initiation may be misclassified. When restricting the analyses to those without such symptoms, the trigger risk was 15.7 (95% CI, 7.6-32.4). The possibility of examining effect modification was limited by a lack of statistical power (eight exposed cases). Results of the analyses suggested, however, an increased trigger effect among subjects reporting nonhostile usual behavior patterns, nonovert strategies of coping with aggressive situations (not protesting when being treated unfairly), and nonuse of beta-blockers. CONCLUSIONS: The hypothesis that anger may trigger MI is further supported, with an increased risk lasting for approximately 1 hour after an outburst of anger. It is suggested that the trigger risk may be modified by personal behavior patterns.
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