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Review
. 2009 Aug;2(4):450-9.
doi: 10.1161/CIRCEP.109.867028.

Impact of sleep on arrhythmogenesis

Richard L Verrier  1 , Mark E Josephson
Affiliations
Review

Impact of sleep on arrhythmogenesis

Richard L Verrier et al. Circ Arrhythm Electrophysiol. 2009 Aug.
No abstract available

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Conflict of interest statement

Disclosures

Dr. Richard L. Verrier is co-inventor of a patent for T-wave alternans measurement by the Modified Moving Average method, which was assigned to Beth Israel Deaconess Medical Center and licensed to GE Healthcare. He has received research equipment and honoraria from GE Healthcare and grant support from Medtronic, Inc.

Dr. Mark E. Josephson declares no conflicts of interest related to this subject.

Figures

Fig. 1
Fig. 1
Panel A: Hourly incidence of sudden cardiac death onset between midnight and 5:59 a.m. from 12 studies enrolling 1981 patients. Panel B: Hourly incidence of automatic implantable cardioverter defibrillator (ICD) discharge between midnight and 5:59 a.m. from 7 studies enrolling 1197 patients. The number of discharges observed each hour is indicated above each bar.
Fig. 1
Fig. 1
Panel A: Hourly incidence of sudden cardiac death onset between midnight and 5:59 a.m. from 12 studies enrolling 1981 patients. Panel B: Hourly incidence of automatic implantable cardioverter defibrillator (ICD) discharge between midnight and 5:59 a.m. from 7 studies enrolling 1197 patients. The number of discharges observed each hour is indicated above each bar.
Fig. 2
Fig. 2
Importance of monitoring nocturnal oxygen saturation in patients who have sustained a myocardial infarction. Nonsustained ventricular tachycardia (lower panel) and hypoxemia measured by pulse oximetry (upper panel) occurred simultaneously on the third night after infarction. The patient died on the following day of cardiogenic shock. Reprinted with permission from the British Medical Journal Publishing Group Ltd and the British Cardiovascular Society.
Fig. 3
Fig. 3
Arrhythmia prevalence (%) according to sleep-disordered breathing (SDB) status. Shaded bars, SDB; open bars, non-SDB. AF, atrial fibrillation; CVE, complex ventricular ectopy; NSVT, nonsustained ventricular tachycardia. N = 228 with SDB; N = 338 without SDB. Reprinted with permission from the American Thoracic Society.
Fig. 4
Fig. 4
Recordings of sympathetic nerve activity (SNA), respiration (RESP), and intraarterial blood pressure (BP) in the same subject when awake, with obstructive sleep apnea during rapid eye movement (REM) sleep, and with elimination of obstructive apnea by continuous positive airway pressure (CPAP) therapy during REM sleep. SNA was very high during wakefulness but increased even further secondary to obstructive apnea during REM. BP increased from 130/65 mmHg when awake to 256/110 mmHg at the end of apnea. Elimination of apneas by CPAP resulted in decreased nerve activity and prevented BP surges during REM sleep. Reprinted with permission from The American Society for Clinical Investigation.
Fig. 5
Fig. 5
Survival of heart failure patients with or without central sleep apnea (CSA) after accounting for all other confounders. AHI = apnea-hypopnea index. Reprinted with permission from American College of Cardiology.
Fig. 6
Fig. 6
Freedom from cardiac mortality based on modified moving average analysis of T-wave alternans (TD-TWA) from 24-hour ambulatory ECGs in ischemic (A) and nonischemic (B) study subgroups. Reprinted with permission from Heart Rhythm Society.
Fig. 7
Fig. 7
Representative rhythm strip (left) and QRS-aligned superimposed modified moving average waveforms (right) for the maximum TWA (≥65μV) in lead V3 from a heart failure patient enrolled in the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS). Note the lack of separation between the superimposed beats in the isoelectric PQRS complex, indicating the low level of noise. The ABAB separation is concentrated within the JT segment, as observed experimentally and in other clinical studies. Reprinted from permission from John Wiley & Sons.
Fig. 8
Fig. 8
Heart rate trend from an ambulatory ECG (AECG) recording showing a normal circadian rhythm with a sleep-induced decrease in heart rate (panel A) as compared with a nocturnal increase in heart rate caused by paroxysmal atrial fibrillation at the onset of sleep and a drop in heart rate after awakening due to spontaneous conversion to sinus rhythm (Panel B). The ECG (below) documents atrial fibrillation during the sleep period.
Fig. 9
Fig. 9
Incidence of AF based on presence or absence of OSA. Cumulative frequency curves for incident atrial fibrillation (AF) for subjects <65 years of age with and without obstructive sleep apnea (OSA) during an average 4.7 years of follow-up (P = 0.002). Reprinted with permission from American College of Cardiology.
See this image and copyright information in PMC

References

    1. Verrier RL, Mittleman MA. Sleep-related cardiac risk. In: Kryger MH, Roth T, Dement WC, editors. Principles and Practice of Sleep Medicine. 4. Philadelphia: WB Saunders; 2005. pp. 1161–1170.
    1. Lavery CE, Mittleman MA, Cohen MC, Muller JE, Verrier RL. Nonuniform nighttime distribution of acute cardiac events: A possible effect of sleep states. Circulation. 1997;5:3321–3327. - PubMed
    1. Yamashita T, Murakawa Y, Hayami N, Sezaki K, Inoue M, Fukui E, Omata M. Relation between aging and circadian variation of paroxysmal atrial fibrillation. Am J Cardiol. 1998;82:1364–1367. - PubMed
    1. National Center for Health Statistics: Deaths: Final data for 2001. National Vital Statistics Report. 2003. p. 52. Available at http://www.cdc.gov/nchs/data/nvsr/nvsr52/nvsr52_03.pdf. - PubMed
    1. Bradley TD, Floras JS. Obstructive sleep apnoea and its cardiovascular consequences. Lancet. 2009;373:82–93. - PubMed

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