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(Circulation. 1995;91:1918-1922.)
© 1995 American Heart Association, Inc.
Articles |
Heart Rate Variability During Specific Sleep Stages
A Comparison of Healthy Subjects With Patients After Myocardial Infarction
From the Department of Internal Medicine, Cardiovascular Disease Section, University of Oklahoma, HSC, Oklahoma City, Okla (E.V., P.B.A., R.L.); Centro di Fisiologia Clinica e Ipertensione, Instituto di Clinica Medica II, Università degli Studi di Milano, Milan, Italy (E.V.); Institute for Healthcare Research, Baptist Medical Center, Oklahoma City, Okla (B.-L., W.C.O.); Fondazione Clinica del Lavoro, Centro Medico di Riabilitazione di Montescano, Montescano, Italy (G.D.P.); and the Department of Physiology, University of Oklahoma, HSC, Oklahoma City, Okla (E.V., P.B.A.).
Correspondence to Philip B. Adamson, MD, MSc, Department of Internal Medicine, Cardiology Section, PO Box 26901, 5SP300, Oklahoma City, OK 73190.
Background Heart rate variability (HRV) is typically higher during nighttime. This evidence supports the concept that overall, sleep is a condition during which vagal activity is dominant. Myocardial infarction (MI) results in a loss in the overall nocturnal HRV increase. However, the characteristics of HRV during specific sleep stages in normal subjects and, more importantly, after MI, are unknown. This study describes HRV during sleep stages in normal subjects and in patients with a recent MI.
Methods and Results HRV was measured from 5 minutes of continuous ECG recording in 8 subjects with no clinical evidence of coronary artery disease (age, 47±4 years) and in 8 patients with a recent MI (age, 51±2 years; NS versus control subjects) in the awake state, non–rapid eye movement (REM), and REM sleep. In normal subjects, the low- to high-frequency ratio (LF/HF) derived from power spectral analysis of HRV decreased significantly from the awake state to non-REM sleep (from 4±1.4 to 1.22±0.33, P<.01). During REM sleep, the LF/HF increased to 3±0.74 (P<.01 versus non-REM, NS versus awake). In post-MI patients, the LF/HF showed an opposite trend toward an increase from 2.4±0.7 to 5.11±1.4 (NS, P<.01 versus the control subjects). REM sleep produced a further increase in the LF/HF up to 8.9±1.6 (P<.01 versus awake and versus REM in control subjects).
Conclusions Myocardial infarction causes a loss in the capability of the vagus to physiologically activate during sleep. This results in a condition of relative sympathetic dominance even in a situation such as sleep, normally described as a condition of vagal dominance and, consequently, low risk for lethal events. The evidence that the sleep-related vagal activation is lost after MI may provide new insights to understanding the nocturnal occurrence of sudden death.
Key Words: heart rate • myocardial infarction • vagus nerve
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