Emotional and Physical Precipitants of Ventricular Arrhythmia
Abstract & Commentary
Synopsis: Anger and moderate physical activity function as triggers for ventricular arrhythmias.
Source: Lampert R, et al. Circulation. 2002;106: 1800-1805.
Lampert and colleagues performed a study on the psychological factors leading to ventricular arrhythmias in a population of patients with implantable cardioverter defibrillators (ICDs). Two hundred and forty patients were enrolled in the study. Each patient was given a structured diary to record their activities and mood states in the period preceding any arrhythmia treated by their ICDs. The diary included measurements of anxiety, anger, worry, sadness, and happiness and feelings of challenge, interest, and being in control. The diary also included a checklist of specific physical activities, which were classified as a level of 1-5. Patients were instructed to complete the diary for the 15-minute period immediately preceding the shock and for the 15- minute to 2-hour period preceding that. Patients who reported a shock went over their diary with a research nurse who then recontacted 1 week later to record a second diary for the same time of day. In this way, data from each patient could be analyzed using the 2 predefined hazard periods (0-15 minutes preshock and 15 minutes to 2 hours preshock) compared to the same time periods 1 week later.
Sixty-one patients recorded diaries for 187 shock events. However, of these, 80 events were not appropriate shocks for ventricular arrhythmias. Therefore, the data used in the study were obtained from 107 shock events reported by 42 patients. Anger was significantly associated with shock with 3 patients reporting 2 anger-associated shocks, and 11 patients reporting 1 each. Anxiety was also associated with shocks, but anxiety did not remain an independently significant risk factor after adjustment for other variables. There was no difference in the levels of the other mood states between the hazard periods and the control periods. Vigorous activity was rarely reported during either the preshock periods or during the control periods. However, mild-to-moderate physical activity preceded 53% of the shocks and was reported in only 32% of the control periods. Activity during the preshock period was a risk factor independent of emotional factors. Walking slowly and physical activity at work were the two activities most commonly seen in the preshock period as compared to the control period.
Lampert et al conclude that anger and moderate physical activity function as triggers for ventricular arrhythmias. It remains unknown whether therapy directed at influencing the psychological state of patients or their activity pattern will affect the frequency of ventricular arrhythmias.
Comment by John P. DiMarco, MD, PhD
Over the years, it has been recognized that psychological factors can affect the clinical course of patients with cardiac disease. There have been reports of an increased incidence of sudden death or myocardial infarction after earthquakes, during war, or during periods of personal grief. The data presented here agree with those prior observations by documenting a relationship between periods of increased sympathetic tone and ventricular arrhythmias in ICD patients.
In the last several years, beta-adrenergic blockers have been the standard therapy for patients with both ischemic heart disease and congestive heart failure. It is likely that much of the improvement in mortality related to beta blockers may be because of their ability to block increased sympathetic stimulation that comes because of either psychological stress or physical activity. The data presented here support that hypothesis.
It has always been quite puzzling why patients develop arrhythmias at any given point in time. Most arrhythmias are caused by an interaction between substrate and trigger. This paper points out that even with a fixed substrate for arrhythmia, therapy directed at reducing the frequency of triggering events may be beneficial.
Dr. DiMarco is Professor of Medicine, Division of Cardiology University of Virginia, Charlottesville.