Background-Observational studies have suggested that psychological stress increases the incidence of sudden cardiac death. Whether emotional or physical stressors can trigger spontaneous ventricular arrhythmias in patients at risk has not been systematically evaluated. Methods and Results-Patients with implantable cardioverter-defibrillators (ICDs) were given diaries to record levels of defined mood states and physical activity, using a 5-point intensity scale, during 2 periods preceding spontaneously occurring ICD shocks (0 to 15 minutes and 15 minutes to 2 hours) and during control periods 1 week later. ICD-stored electrograms confirmed the rhythm at the time of shock. A total of 107 confirmed ventricular arrhythmias requiring shock were reported by 42 patients (33 men; mean age, 65 years; 78% had coronary artery disease) between August 1996 and September 1999. In the 15 minutes preceding shock, an anger level Ն3 preceded 15% of events compared with 3% of control periods (PϽ0.04; odds ratio, 1.83; 95% confidence intervals, 1.04 to 3.16) Other mood states (anxiety, worry, sadness, happiness, challenge, feeling in control, or interest) did not differ. Patients were more physically active preceding shock than in control periods. Anger and physical activity were independently associated with the preshock period. Conclusions-Anger and physical activity can trigger ventricular arrhythmias in patients with ICDs. Future investigations of therapies aimed at blocking a response to these stressors may decrease ventricular arrhythmias and shocks in these

The frequency of cardiovascular abnormalities was evaluated in 71 consecutive patients with acute injury to the spinal cord. Persistent bradycardia was universal in all 31 patients with severe cervical cord injury and less common in milder cervical injury (6 of 17) or thoracolumbar injury (3 of 23) (p less than 0.00001). Marked sinus slowing (71 versus 12 versus 4%, respectively, p less than 0.00001), hypotension (68 versus 0 versus 0%, p less than 0.00001), supraventricular arrhythmias (19 versus 6 versus 0%, p = 0.05) and primary cardiac arrest (16 versus 0 versus 0%, p less than 0.05) were significantly more frequent in the severe cervical injury group. The frequency of bradyarrhythmias peaked on day 4 after injury and gradually declined thereafter. All observed abnormalities resolved spontaneously within 2 to 6 weeks. The primary mechanism underlying these observations appears to involve the acute autonomic imbalance created by the disruption of sympathetic pathways located in the cervical cord. Acute severe injury to the cervical spinal cord is regularly accompanied by arrhythmias and hemodynamic abnormalities not found with thoracolumbar cord trauma. These abnormalities are limited to the first 14 days after injury, a period in which life-threatening disturbances must be anticipated.

Mental stress alters VT cycle length and termination without evidence of ischemia. This suggests that mental stress may lead to sudden death through the facilitation of lethal ventricular arrhythmias.