(Circulation. 2000;101:e213.)
© 2000 American Heart Association, Inc.
Circulation Electronic Pages |
Mental Versus Physical Stress, QT Prolongation, and the Autonomic Nervous System
From the Division of Cardiology, Department of Medicine, Cedars-Sinai Research Institute, Cedars-Sinai Medical Center, and the Department of Medicine, University of California at Los Angeles School of Medicine, Los Angeles, Calif; and the Department of Cardiology, Sapir Medical Center, Meir Hospital, Kfar Saba, Israel.
Correspondence to C. Noel Bairey Merz, MD, 444 S San Vicente Blvd, Suite 901, Los Angeles, CA 90048. E-mail merz{at}cshs.org
 |
Introduction |
|---|
 Top Introduction References |
|---|
A 56-year-old male physician with essential hypertension, elevated blood cholesterol, and irritable bowel syndrome underwent exercise radionuclide perfusion imaging and 24-hour Holter monitor because of palpitations at rest. The exercise perfusion test was within normal limits. During the Holter monitoring period, the subject was taking enalapril, simvastatin, and clonipine. The Holter study demonstrated no clinically significant arrhythmias. During the monitoring, the patient was awakened from sleep at 4:40 AM and told that his brother-in-law had suddenly died. The Holter ECG tracing at that time is shown in the Figure
, panel A,
demonstrating a sinus tachycardia heart rate elevation to
147 bpm and marked QT prolongation (400 ms), obliterating the p
wave (arrow). Later the same morning, while still wearing the Holter
monitor, the patient performed his usual morning aerobic exercise at
8:15 AM. The Holter ECG tracing during that time period is
shown in the Figure, B. Notably, during exercise, the heart rate is
again elevated to a sinus tachycardia at 150 bpm; however,
the QT interval has shortened (220 ms), and clear demarcation between
the T and p waves is evident (arrow). Neither strip demonstrates
evidence of ST-segment depression or T-wave inversion, and the patient
did not report any symptoms during either tachycardiac
episode. Time duration, heart rate, and QT and QTc intervals before and
after mental stress and physical exercise are shown in the Figure, C
and D. Notably, mental stress triggered an abrupt heart rate elevation
over 30 seconds that was not accompanied by any significant QT-interval
shortening and that showed actual QTc lengthening, in contrast to the
exercise-induced gradual heart rate elevation over 30 minutes, which
was accompanied by a 40% QT-interval shortening and actual QTc
shortening.
|
Sudden arousal has previously been demonstrated to lengthen the QT interval in the setting of congenital long-QT syndrome,1 in established heart disease patients,2 and in healthy physicians during emergency call awakenings.3 This arousal has also been demonstrated to produce lethal ventricular arrhythmias in diseased subjects.1 2 Mental stress–triggered electrophysiological effects may represent a particularly dangerous electrical substrate for sudden cardiac death, which may explain the infrequent but nevertheless described cases of sudden cardiac death in the absence of underlying heart disease.4
|
Acknowledgments |
|---|
This work was supported in part by grants from the Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center; the John D. and Catherine T. MacArthur Foundation; and the National Institutes of Health (HL-47337). Dr Pardo was supported in part by the Save A Heart Foundation and the Kurian Family Foundation Fellowship, Los Angeles, Calif.
|
Footnotes |
|---|
The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.
Circulation encourages readers to submit cardiovascular images to Dr Hugh A. McAllister, Jr, St Luke’s Episcopal Hospital and Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.
|
References |
|---|
|
TopIntroductionReferences |
|---|
1. Schwartz PJ. Idiopathic long QT syndrome: progress and questions. Am Heart J. 1985;109:399–411.[Medline] [Order article via Infotrieve]
2.
Schwartz PJ, Wolf S. QT interval prolongation as
predictor of sudden death in patients with myocardial infarction.
Circulation. 1978;57:1074–1077.
3. Toivonen L, Helenius K, Viitasalo M. Electrocardiographic repolarization during stress from awakening on alarm call. J Am Coll Cardiol. 1997;30:774–779.[Abstract]
4. Lown B, Temte JV, Reich P. Basis for recurring ventricular fibrillation in the absence of coronary heart disease and its management. N Engl J Med. 1976;294:623–629.[Abstract]
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||