Circulation. 1999;100:1250-1252
(Circulation. 1999;100:1250-1252.)
© 1999 American Heart Association, Inc.
Worried to Death?
Lana L. Watkins, PhD;
James A. Blumenthal, PhD
Department of Psychiatry and Behavioral Sciences,
Duke University Medical Center,
Durham, NC
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Introduction
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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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References
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Brandspiegel HZ, Marinchak RA, Rials SJ, Kowey PR.
A broken heart. Circulation. 1998;98:1349.[Free Full Text]
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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.[Abstract/Free Full Text]
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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.[Abstract/Free Full Text]
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Watkins LL, Grossman P, Krishnan R, Sherwood A.
Anxiety and vagal control of heart rate. Psychosom Med. 1998;60:498–502.[Abstract/Free Full Text]
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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.[Abstract/Free Full Text]
Response
Peter R. Kowey, MD;
Haim Z. Brandspiegel, MD;
Roger A. Marinchak, MD;
Seth J. Rials, MD, PhD
Division of Cardiovascular Diseases,
Lankenau Hospital and,
Medical Research Center,
Wynnewood, Pa,
Department of Medicine Jefferson Medical College,
Philadelphia, Pa
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Introduction
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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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References
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Simons M, Downing SE. Coronary
vasoconstriction and catecholamine
cardiomyopathy. Am Heart J. 1985;109:297–304.[Medline]
[Order article via Infotrieve]
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Haft JI. Role of platelets in coronary
artery disease. Am J Cardiol. 1979;43:1197–1206.[Medline]
[Order article via Infotrieve]
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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.
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Helsing KJ, Szklo M. Mortality after bereavement.
Am J Epidemiol. 1981;113:41–52.
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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.[Abstract/Free Full Text]
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Introduction
References