The emotional state of anger has been implicated in the precipitation of myocardial ischemia, myocardial infarction and life-threatening ventricular arrhythmias, including sudden cardiac death (8,10-12). In a recent and excellent article, Hemingway et al (13) reviewed evidence from prospective epidemiological and clinical studies, supported by experimental studies, that suggest a link between psychosocial factors such as anger, anxiety, depression, hostility/type A behavior, social supports and work characteristics and ventricular arrhythmias, sudden death and cardiac autonomic function. Overall, 88/96 (92%) of identified published studies investigating psychosocial and social aspects of arrhythmic risk were positive (13). This remarkable consistency across different populations and study designs, lends cautious support to a casual association (13).

Indirect and circumstantial evidence has strongly suggested that psychological stress may be an important factor in the development of malignant ventricular arrhythmias and sudden death (10-13). Sympathetic arousal can trigger arrhythmic events (10). Ventricular tachycardia, like sudden death, occurs more frequently in the morning, at the time of peak of catecholamine level and lowest vagal tone as demonstrated in patients with implantable cardioverter defibrillators (ICDs) (10,14). Ventricular tachycardia occurs more frequently on Monday in working patients with ICDs, suggesting a role for stress (15). In addition, atrial and ventricular ectopy and nonsustained arrhythmias increase during the stress of being in-call in house officers (16) and during exposure to a hostile environment in animals (17). Mittleman et al (8) reported and important association between outbursts of anger and nonfatal myocardial infarction and sudden death. Reich et al (18) determined that anger precede episodes of arrhythmias in 15 % of patients with recurring life-threatening arrhythmias. In a recent article Kovach et al (12) reported that provocation of an intense anger like state in six canines increases the magnitude of T-wave alternans to a greater degree than does a brief period of myocardial ischemia. Superimposition of the anger like response during occlusion-induced myocardial ischemia potentiates the increase in the magnitude of T wave alternans elicited by myocardial ischemia alone, further magnifying the risk of ventricular arrhythmias in this setting (12). The cardioselective beta-1 adrenergic blocker metoprolol blunts the magnitude of this increase in behavioral stress-induced alternans, suggesting that adrenergic factors are, in part, responsible for T-wave alternans during the anger like response (12). However, arousal-induced increases in heart rate are likely to contribute in the setting of myocardial ischemia (12). An alternative explanation is that factors in addition to sympathetic nerve activity contributed to the development of T-wave alternans during the anger state (12). One likely possibility is that aggressive arousal result in a decrease in cardiac vagal tone. This might conduce to the residual sinus tachycardia as well as to T-wave alternans (12).

The population of patients with ICDs provides a unique opportunity to evaluate the effects of mental stress on human arrhythmias. Lampert et al (14) reported that mental stress (anger recall and mental arithmetic) shortens cycle lengths and renders induced ventricular tachycardia more difficult to terminate. These alterations in ventricular tachycardia characteristics were associated with increased norepinephrine levels, which are known to rise during mental stress, but with no evidence of ischemia on ECG or left ventricular ejection fraction (14). In these patients with defined arrhythmic substrate, anger destabilized the circuit, creating a potentially more dangerous arrhythmia. This suggest that psychological stress may facilitate sudden cardiac death by increasing the lethal potential of arrhythmias in susceptible patients (14)

We examined a series of 57 consecutive victims of sudden death. Among them, we found anger as the most frequent trigger mechanism preceding the final event (19)