Awareness of the ability of sudden emotional stress to provoke arrhythmia has been present throughout recorded history. When Jacob is told that his long-lost son Joseph is alive, "his heart fainted for he believed them not" (Genesis 45, verse 26). Despite numerous studies, however, the relationship of psychosocial factors to cardiovascular disease, and in particular sudden cardiac death, has been difficult to quantify. This has been due to several reasons:
- It is difficult to objectively quantify emotional stress
- Research has until recently been more focused on the chronic factors leading to the development of coronary artery disease rather than on the precipitation of acute coronary syndromes once such disease is present
- The division between the social science and medical science investigators have impeded dialogue
- There are inherent difficulties in accurately assessing the triggers of sudden death.
Despite these limitations, the weight of evidence for a role for psychosocial factors in sudden cardiac death has become compelling and in one review of 96 published studies on this topic, a positive association was observed in 92 percent . New studies are therefore warranted to determine whether behavioral and pharmacologic interventions will lower cardiovascular risk .
Since acute myocardial infarction is an important precipitant of ventricular fibrillation and sudden death, many of the advances in understanding the pathophysiology of acute myocardial infarction are applicable for sudden death. (See "Psychosocial and other social factors in acute myocardial infarction".) In addition, emotional stress may lower the threshold for arrhythmia both directly and secondary to the provocation of transient myocardial ischemia.
The task of accurately determining the time of occurrence of sudden cardiac death is often difficult for two main reasons: a possible inability to ascertain if a sudden cardiac event is actually the cause of death; and the occurrence of unwitnessed deaths, often at night, for which time of death is uncertain. Despite these limitations, a circadian variation has been found for sudden cardiac death that parallels that of myocardial infarction, with a peak in the morning. It has been suggested that a primary arrhythmic event is more likely to occur in the morning because increased adrenergic activity at this time may increase electrical instability or induce myocardial ischemia without infarction.