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Wrath.

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S Chapman. Wrath.. https://doi.org/10.1136/bmj.313.7072.1593

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The recognition that the onset of cardiovascular events follows a circadian periodicity and is frequently triggered by physical or mental stresses has created new possibilities for disease prevention. Morning peaks in occurrence are now well-documented for acute myocardial infarction, sudden cardiac death, transient myocardial ischemia, and ischemic stroke. The morning increase in events begins after subjects assume an upright posture and start the day's activities, during a time of sympathetic nervous system activation. Additional triggers of onset include heavy physical exertion, sexual activity, and anger, the risks of which have been quantified in the Determinants of Myocardial Infarction Onset Study. A general hypothesis of the triggering of coronary thrombosis has been proposed. The process begins with the development of a vulnerable atherosclerotic plaque, which may become disrupted by internal forces or by external hemodynamic or vasoconstrictive changes. Once disrupted, the plaque becomes a thrombogenic focus. An occlusive thrombus is more likely to form if other factors come into play to increase coagulability and vasoconstriction. From a clinical standpoint these findings provide theoretical support for the use of long-acting agents to provide adequate anti-ischemic protection during the higher risk morning hours in patients already taking anti-ischemic medications. From a research standpoint this new information on triggering provides clues to a mechanism of onset that might lead to more effective preventive therapy. Because most deaths from coronary artery disease occur before any type of acute therapy can be given, further efforts to explore this new field are warranted.

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Breast cancer, personality and the feminine role.

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Anger

Anger expression and incident stroke: prospective evidence from the Kuopio ischemic heart disease study.

BACKGROUND AND PURPOSE: High levels of anger are associated with an increased risk of coronary heart disease and hypertension, but little is known about the role of anger in stroke risk. METHODS: Anger expression style and risk of incident stroke were examined in 2074 men (mean age, 53.0+/-5.2 years) from a population-based, longitudinal study of risk factors for ischemic heart disease and related outcomes in eastern Finland. Self-reported style of anger expression was assessed by questionnaire at baseline. Linkage to the FINMONICA stroke and national hospital discharge registers identified 64 first strokes (50 ischemic) through 1996. Average follow-up time was 8.3+/-0.9 (mean+/-SD) years. RESULTS: Men who reported the highest level of expressed anger were at twice the risk of stroke (relative hazard, 2.03; 95% CI, 1.05 to 3.94) of men who reported the lowest level of anger, after adjustments for age, resting blood pressure, smoking, alcohol consumption, body mass index, low-density and high-density lipoprotein cholesterol, fibrinogen, socioeconomic status, history of diabetes, and use of antihypertensive medications. Additional analysis showed that these associations were evident only in men with a history of ischemic heart disease (n=481), among whom high levels of outwardly expressed anger (high anger-out) predicted >6-fold increased risk of stroke after risk factor adjustment (relative hazard, 6.87; 95% CI, 1.50 to 31.4). Suppressed anger (anger-in) and controlled anger (anger-control) were not consistently related to stroke risk. CONCLUSIONS: This is the first population-based study to show a significant relationship between high levels of expressed anger and incident stroke. Additional research is necessary to explore the mechanisms that underlie this association.

Anger