(Circulation. 1999;100:1250-1252.)
© 1999 American Heart Association, Inc.
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Worried to Death?
Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC
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To the Editor:
We were interested to read the report of the 70-year-old woman who developed ST-segment changes, elevated cardiac enzymes, and ventricular akinesis on hearing of her husband's death.1 Bereavement or other significant life stressors have been associated with life-threatening arrhythmias and increased mortality. Although clinical laboratory studies have demonstrated that acute psychological stress produces ischemia in patients with coronary artery disease,2 rarely has an acute ischemic response to real-life psychological stress been clinically documented in an otherwise healthy individual.
Prospective studies, however, have demonstrated that otherwise healthy individuals with chronically elevated anxiety are at greater risk of sudden cardiac death (SCD).3 Anxiety increases the risk of SCD, with even low-to-moderate levels of anxiety being sufficient to produce some elevation in risk.3 Recently, we reported a dose-dependent relationship between anxiety level and impaired vagal reflex control of heart rate in young healthy volunteers,4 suggesting that low vagal cardiac control may mediate the relationship between anxiety and SCD. Reduced vagal cardiac control, as measured by low heart rate variability, clearly predicts cardiac risk. In addition, low levels of vagal control of heart rate have been found in survivors of SCD with no evidence of coronary disease.5
Acute increases in stress may evoke acute myocardial ischemia, life-threatening arrhythmias, and death in some individuals. Understanding the mechanisms by which stress triggers these events may allow us to identify individuals who are susceptible to stress-induced cardiac responses and may ultimately help us develop effective preventive strategies. Although the significance of the sympathetic nervous system in the production of stress-induced arrhythmias is well known, recently vagal cardiac control has also been shown to be important in the prediction of fatal arrhythmias. The data from our laboratory and others suggest that individuals with low vagal control may represent a group with increased susceptibility to stress.
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1. Brandspiegel HZ, Marinchak RA, Rials SJ, Kowey PR. A broken heart. Circulation. 1998;98:1349.
2.
Blumenthal JA, Jiang JW, Waugh RA, Frid DJ, Morris JJ,
Coleman RE, Hanson M, Babyak M, Thyrum ET, Krantz DS. Mental
stress-induced ischemia in the laboratory and ambulatory
ischemia during daily life: association and
hemodynamic features. Circulation. 1995;92:2102–2108.
3.
Kawachi I, Sparrow D, Vokonas PS, Weiss ST. Symptoms
of anxiety and risk of coronary heart disease: the Normative
Aging Study. Circulation. 1994;90:2225–2229.
4.
Watkins LL, Grossman P, Krishnan R, Sherwood A.
Anxiety and vagal control of heart rate. Psychosom Med. 1998;60:498–502.
5.
Fei L, Anderson MH, Katritsis D, Sneddon J, Statters
DJ, Malik M, Camm JA. Decreased heart rate variability in survivors of
sudden cardiac death not associated with coronary artery
disease. Br Heart J. 1994;71:16–21.
Response
Division of Cardiovascular Diseases, Lankenau Hospital and, Medical Research Center, Wynnewood, Pa, Department of Medicine Jefferson Medical College, Philadelphia, Pa
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We agree that a demonstration of a relationship between psychological stress (in particular, grief) and a transient compromise of coronary perfusion is rare, which is why we were pleased to present our case to the physician public. The mechanism by which a stressor such as intense bereavement leads to a severe reduction of coronary blood flow is not clear and may be multifactorial. Clearly, autonomic imbalance, as pointed out by Watkins and Blumenthal, is of paramount importance. A sympathetic discharge, evident in this case during our patient's acute emotional response, can cause marked changes in coronary vascular tone and rheology by effects on such diverse factors as coagulability, platelet adhesion, and endothelial function.1 2 Patients with low vagal tone may be particularly susceptible to these phenomena, because we know they are particularly susceptible to the electrical instability that is the substrate for sudden cardiac death.3 Whether our patient was so disposed is unknowable. We did not discern any signals of dysautonomia in her case, such as ventricular arrhythmia, or marked alterations in heart rate, and her blood pressure remained steadily normal after her acute trauma. We did not perform any formal measurements of autonomic tone, nor did we assess her vascular response to autonomic manipulation.
We sincerely appreciate the comments made by Drs Watkins and Blumenthal. They underscore the need for a deeper understanding of the interaction between grief reactions and major cardiac events, a phenomenon that needs to be expected and recognized by all clinicians.4 5
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1. Simons M, Downing SE. Coronary vasoconstriction and catecholamine cardiomyopathy. Am Heart J. 1985;109:297–304.[Medline] [Order article via Infotrieve]
2. Haft JI. Role of platelets in coronary artery disease. Am J Cardiol. 1979;43:1197–1206.[Medline] [Order article via Infotrieve]
3. de Silva RA, Verrier RL, Lown B. Protective effect of the vagotonic effect of morphine sulphate on vulnerability to ventricular fibrillation. Cardiovasc Res. 1978;12:161–172.
4. Helsing KJ, Szklo M. Mortality after bereavement. Am J Epidemiol. 1981;113:41–52.
5.
Kapiro J, Koskenvuo M, Rita H. Mortality after
bereavement: a prospective study of 95,647 widowed persons.
Am J Public Health. 1987;77:283–287.
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