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Heart Rate Variability During the Week of September 11, 2001
To the Editor: Catastrophes such as war or earthquake are known to result in increased incidence of sudden cardiac death among survivors, but the physiological mechanisms remain unknown.1-2 The events of September 11, 2001, produced psychological distress among large numbers of people who were not physically affected by them. We hypothesized that such stress may lead to autonomic dysfunction, which may be reflected in changes in heart rate variability (HRV). Diminished HRV is associated with an increased incidence of cardiovascular and sudden death in patients both with and without coronary artery disease (CAD).3-4
Methods
We measured HRV in 12 patients at the Yale-New Haven Hospital who wore 24-hour ambulatory heart monitors during the week of September 11, as well as 12 in control patients who had worn monitors in the preceding 2 months. Control patients were matched for age (within 10 years), sex, presence of CAD or congestive heart failure, and diabetes. Two patients in each group were using  -blockers. Indications for monitoring included palpitations (4 cases, 4 controls), history of or risk for arrhythmia (6 cases, 5 controls), and syncope (2 cases, 3 controls). All patients had been scheduled for heart monitoring prior to September 11. This study was approved by the Yale Human Investigation Committee.
Frequency domain indices of HRV were analyzed using standard power spectrum analysis methods. After editing the R-R interval file to remove ectopic beats and noise, gaps were estimated by interpolated linear splines (recordings with >20% interpolation excluded). The heart rate power spectrum was computed through Fast Fourier Transform and integrated over 5 discrete frequency bands, with high frequency defined as 0.15 to 0.40 Hz.3 Indices of HRV were log-normalized and compared by paired t test.
Results
The logarithm of high-frequency power (a measure of parasympathetic tone) was lower in the subjects monitored after September 11 than in controls (5.54 vs 6.23, P = .047). High-frequency power was lower in 9 of the 12 cases compared with their controls (P = .045). Mean heart rate did not differ between groups (R-R interval: 857 milliseconds [cases] vs 829 milliseconds [controls], P = .64).
Comment
We found a decrease in parasympathetic tone during the week of September 11, 2001, which may represent a physiological perturbation among individuals exposed to large-scale psychological stress. Unlike previous studies in which subjects were directly affected by war or natural disaster,1-2 the stress experienced by subjects in our study was purely psychological. It is not yet known whether there was increased cardiac mortality or morbidity as a result of the September 11 attacks. Mental stress can induce coronary ischemia2 and can facilitate lethal arrhythmias.5 These changes in cardiac blood flow and rhythm may in turn be caused by alterations in autonomic nervous system function.6 Our data demonstrate that the September 11 attacks may have produced similarly decreased parasympathetic output, which may increase susceptibility to lethal arrhythmias.7
Rachel Lampert, MD;
Suzanne J. Baron, BA;
Craig A. McPherson, MD;
Forrester A. Lee, MD
Department of Internal Medicine
Yale University School of Medicine
New Haven, Conn
1. Leor J, Poole WK, Kloner RA. Sudden cardiac death triggered by an earthquake. N Engl J Med. 1996;334:413-419.
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2. Rozanski A, Blumenthal J, Kaplan J. Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation. 1999;99:2192-2217.
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3. Bigger J, Fleiss J, Steinman R, Rolnitsky L, Kleiger R, Rottman J. Frequency domain measures of heart period variability and mortality after myocardial infarction. Circulation. 1992;85:164-171.
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4. Liao D, Cai J, Rosamond JC, et al. Cardiac autonomic function and incident coronary heart disease: a population-based case-cohort study. Am J Epidemiol. 1997;145:696-706.
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5. Lampert R, Jain D, Burg M, Batsford W, McPherson C. Destabilizing effects of mental stress on ventricular arrhythmias in patients with implantable cardioverter-defibrillators. Circulation. 2000;101:158-164.
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6. Pagani M, Mazzuero G, Ferrare A, et al. Sympathovagal interaction during mental stress: a study using spectral analysis of heart rate variability in healthy control subjects and patients with a prior myocardial infarction. Circulation. 1991;83(suppl 4):II43-II51.
7. Cerati D, Schwartz PJ. Single cardiac vagal fiber activity, acute myocardial ischemia, and risk for sudden death. Circ Res. 1991;69:1389-1401.
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Letters Section Editor: Stephen J. Lurie, MD, PhD, Senior Editor.
JAMA. 2002;288:575.
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