Abstract
We investigated the effects of intermittent hypoxia (IH), such as that encountered in severe obstructive sleep apnea (OSA) patients, on the development and severity of myocardial ischemia-related ventricular arrhythmias. Rats were exposed to 14 days of IH (30 s at 5%O2 and 30 s at 21%O2, 8 h·day−1) or normoxia (N, similar air-air cycles) and submitted to a 30-min coronary ligature. Arterial blood pressure (BP) and ECG were recorded for power spectral analysis, ECG interval measurement and arrhythmia quantification. Left ventricular monophasic action potential duration (APD) and expression of L-type calcium (LTCC) and transient receptor potential (TRPC) channels were assessed in adjacent epicardial and endocardial sites. Chronic IH enhanced the incidence of ischemic arrhythmias, in particular ventricular fibrillation (66.7% vs. 33.3% in N rats, p < 0.05). IH also increased BP and plasma norepinephine levels along with increased low-frequency (LF), decreased high-frequency (HF) and increased LF/HF ratio of heart rate and BP variability. IH prolonged QTc and Tpeak-to-Tend intervals, increased the ventricular APD gradient and upregulated endocardial but not epicardial LTCC, TRPC1 and TRPC6 (p < 0.05). Chronic IH, is a major risk factor for sudden cardiac death upon myocardial ischemia through sympathoactivation and alterations in ventricular repolarization, transmural APD gradient and endocardial calcium channel expression.
Highlights
Obstructive sleep apnea (OSA) syndrome is a common sleep-related breathing disorder and represents a substantial public health problem as it affects at least 10% of the general population and is recognized as an important and independent risk factor for cardiovascular disease
Myocardial ischemia (MI) is a leading cause of sudden cardiac death (SCD), in particular through lethal ventricular arrhythmias such as sustained and irreversible ventricular tachycardia and/or fibrillation (VF)[5]. In accordance with their increased rate of nocturnal SCD4, apneic patients exhibit a high prevalence of myocardial ischemia during the night[6] and ventricular arrhythmias are prominent during sleeping hours[7]
Systolic and mean arterial blood pressures values were significantly increased in rats exposed to intermittent hypoxia (IH) compared to N, whereas heart rate and pulse pressure values were not different
Summary
Obstructive sleep apnea (OSA) syndrome is a common sleep-related breathing disorder and represents a substantial public health problem as it affects at least 10% of the general population and is recognized as an important and independent risk factor for cardiovascular disease. Accumulating evidence indicates that sleep apnea is associated with hypertension, left ventricular dysfunction, coronary artery disease and cardiac rhythm disorders[1]. Myocardial ischemia (MI) is a leading cause of SCD, in particular through lethal ventricular arrhythmias such as sustained and irreversible ventricular tachycardia and/or fibrillation (VF)[5] In accordance with their increased rate of nocturnal SCD4, apneic patients exhibit a high prevalence of myocardial ischemia during the night[6] and ventricular arrhythmias are prominent during sleeping hours[7]. The aims of the present study were to investigate the effects of chronic exposure to intermittent hypoxia on the incidence of MI-related ventricular arrhythmias and to identify the potential mechanisms involved with particular emphasis on sympathoactivation, alterations in ventricular electrophysiological properties and cardiac ion channel expression
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