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Sleep‐Induced Hypotension Causes Akinesis in Presence of Coronary Stenosis: Potential Mechanism for Adverse Cardiac Events
Author(s) -
Moss Brian Neal,
Kohl Sharat,
Crystal George J.,
Kim SongJung
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1154-a
Subject(s) - medicine , cardiology , myocardial infarction , coronary artery disease , stenosis , heart rate , blood pressure , sudden cardiac death , anesthesia
Epidemiological studies have shown a high rate of occurrence of nocturnal adverse cardiac events including acute myocardial infarction and sudden cardiac death in patients with coronary artery disease. Most researchers assume that these events are exclusively due to the sympathetic surges accompanying rapid eye movement (REM) sleep. The contribution of non‐REM sleep, which comprises 80% of total sleep duration, to adverse cardiac events has been neglected. Eight domestic pigs were chronically instrumented to measure contractile function [wall thickening (WT)] and coronary blood flow (CBF) in the left anterior coronary artery bed, as well as mean arterial pressure and heart rate. While in the awake condition, a coronary stenosis was produced to cause a 30% reduction in baseline CBF (from 40±4 to 27±3ml/min) resulting in a decrease in WT (from 23.3±3.4 to 15.7±2.0%). Mean arterial pressure and heart rate were not altered. With the stenosis in place, the onset of non‐REM sleep caused parallel 20% decreases in mean arterial pressure and CBF, and a 14% increase in HR. These changes were associated with a loss of regional contractile activity (WT, 0.2±12.8%), indicative of severe myocardial ischemia. The present findings demonstrate how hypotensive episodes during non‐REM sleep may precipitate severe myocardial ischemia in a region supplied by a flow‐limiting stenosis. This phenomenon, when repeated over the sleep cycle, could result in progressive myocardial injury and potentially set the stage for a major adverse cardiac event during the sympathetic activation accompanying REM sleep or early morning mental or physical activity.