It has been known anecdotally for thousands of years that acute positive or negative emotions can trigger sudden death. Indeed, there is even a Bible story about a man who died suddenly when confronted with a rebuke from one of Jesus’s disciples: “St. Luke reports that when Ananias was charged by Peter, ‘You have not lied to man but to God,’ Ananias fell down dead (Acts 5:1-2).”1
Other anecdotal accounts have supported the idea that extreme emotional states can result in markedly heightened autonomic nervous system activity that can lead to malignant ventricular arrhythmias followed by ventricular fibrillation. The revered Harvard physiologist, Walter Cannon, wrote about Voodoo death in 1942, ascribing the sudden deaths of individuals who had been “hexed” to massive adrenal gland discharge.2 In 1971, psychiatrist George Engel published a report of 170 sudden deaths that occurred in the setting of acute and severe emotional stress.3 These deaths usually developed in situations involving personal losses such as death of a loved one or situations of potential bodily danger. Occasionally, however, some sudden deaths develop when individuals are confronted with markedly positive emotional events such as great relief, pleasure, or triumphal success. For example, 2 of my colleagues recently suffered acute myocardial infarctions shortly after finishing honor lectures. This could have led to malignant and potentially fatal arrhythmias. Fortunately, however, both of these individuals were rapidly diagnosed and successfully treated with good outcomes. I have also been told of 2 sisters who were reunited after many years of separation, with 1 of the 2 suffering a cardiac arrest at the time of their very emotional reunion. Each of these emotionally charged situations had a number of shared factors: the situation was impossible to ignore or escape, intense emotions were elicited, and the individual involved had no way of controlling the situation.
In his review of emotional sudden death, Dimsdale1 refers to a number of laboratory studies involving experiments with animals in which severely stressful situations were created that resulted in the sudden deaths of a number of the animals. For example, Richter4 exposed rats to potential drowning and observed many sudden deaths that he attributed to powerful vagal activation. Subsequent work in animals and humans has confirmed that stressful events leading to malignant ventricular arrhythmias or sudden death were initiated by powerful activation of the autonomic nervous system, both sympathetic and parasympathetic.1
During my 2 years of Naval service, I was fortunate enough to meet and work with Dr. Richard Rahe, a pioneer stress investigator who was exploring the effects of stress on human health.5, 6 Rahe and his co-workers set out to examine the effects of emotionally charged life events on health. They developed a list of “life changing events,” 42 in number, starting with the most powerful events such as death of a parent or child and descending to events that would be less likely to elicit powerful emotional responses, such as a temporary separation from a loved one. They then correlated a total life change score by summing recent events and compared this number with the number of health-related events that had recently occurred in their population sample. There was a strong correlation between the total score of life-changing events and recent illness. In a subsequent study, Rahe and Romo6 studied a number of individuals in Helsinki, Finland who had died suddenly from myocardial infarction. Spouses or next of kin were extensively interviewed concerning recent life-changing events. In the 2 years prior to the sudden demise of these individuals, Rahe and Romo observed a 143% increase in life-changing events.6These studies and many others have confirmed the strong link between exaggerated emotional responses and illness, including potentially fatal cardiac arrhythmias.1
Less-severe clinical correlates with stress are commonly observed in the clinic, with some patients demonstrating marked elevation in blood pressure that disappears when individuals measure their blood pressure at home, so-called “white coat hypertension.” Moreover, the recently described stress cardiomyopathy (Takotsubo cardiomyopathy) is another pathological state that is usually induced by an emotional event.7, 8 The general consensus among investigators and clinicians who have studied and thought about the connection between emotions and health is that the negative events that are triggered are the result of inappropriately high activation of the autonomic nervous system, sympathetic or parasympathetic.1
In the current issue of The American Journal of Medicine, Lane et al9 studied electocardiogram samples during a variety of emotional states from patients with the long QT syndrome, as well as normal individuals and patients with coronary artery disease. They observed remarkable changes in the QTc intervals of these subjects, dependent on their emotional state at the time of the recordings. In patients with the long QT syndrome, a myocardial channelopathy associated with an increased risk for sudden death, heightened emotional states shortened the QTc interval, while calm and relaxation lengthened this variable. Similar changes in QTc were observed in patients with coronary artery disease. Normal controls did not alter the length of their QTc interval with changing emotions. The authors conclude that electrical instability in arrhythmia-prone patients occurs in response to shifting emotional states of mind. While reading this study, it occurred to me that some form of personal emotional control such as that induced by meditation, yoga, and tai chi might decrease the effect of emotion on the heart. One unfortunate outcome of the study by Lane et al9 was that beta-blockade did not seem to block the changes in QTc intervals that occurred with shifts in emotional arousal. Thus, beta-blockade alone would not seem to be an adequate intervention to control QTc variability. In my mind, this area deserves a lot more investigative attention because sudden cardiac death continues to be a major health problem in the United States and throughout the world.
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-Joseph S. Alpert, MD
This article originally appeared in the May issue of The American Journal of Medicine.
