Cardiovascular complications of sleep apnoea

Abstract

The strong associations of cardiovascular diseases (CVD) with obstruc-tive as well as central sleep apnea have been well documented. Retro-spective case controlled studies suggest that subjects with CVD and OSAmay be more at risk of sudden cardiac death during sleeping hourscompared to those without OSA or in the general population.Apart from comorbidity of CVD and obstructive sleep apnea (OSA)due to the common link of obesity, various pathophysiologic mecha-nisms in OSA may contribute to cardiovascular pathogenesis. Repetitiveepisodes of hypoxemia-reperfusion, hypercarbia, sympathetic activa-tion, and intrathoracic pressure swings may trigger cellular and bio-chemical processes which predispose to atherosclerosis, the underlyingpathology to many CVD such as hypertension, ischemic heart andrelated diseases and stroke. Several biochemical or functional markers ofendothelial dysfunction, which precedes or indicates early atheroscle-rosis, and carotid artery atherosclerosis, have been reported to be inde-pendently associated with OSA. OSA may also be causally related todysfunction in insulin/glucose or lipid metabolism which are risk factorsfor atherosclerotic CVD.A strong association of OSA and hypertension has long beenobserved. Epidemiologic and randomized controlled studies haveshown that increase in apnea-hypopnea index or oxygen desaturation are independently related to increase in blood pressure, and CPAPtreatment of OSA can decrease blood pressure in both normotensive andhypertensive subjects. Recent reports suggest that daytime sleepinessmay be a phenotypic marker for blood pressure lowering response toCPAP and requires further exploration.Other than contributing to atherosclerosis and thus ischemic heartdisease and related disorders such as heart failure and arrhythmias, OSAexerts acute effects on oxygenation and hemodynamics that may pre-dispose to myocardial ischemia or heart failure. Nocturnal ECG changesof ischemia during post-apneic periods have been demonstrated inpatients with coronary artery disease, and myocardial infarct patientswith OSA appeared to have worse prognosis. Both systolic and diastolicdysfunction, independent of hypertension, have been described in OSA,and treatment of OSA has been shown to improve ventricular functionin left heart failure.Central sleep apnea (CSA) occurs commonly in ventricular dysfunc-tion and heart failure, Presence of CSA is reported to be a poor prog-nostic factor of the outcome of heart failure. It is not yet clear if CPAPtreatment alters heart function, although some studies have suggestedthat use of nocturnal CPAP could improve cardiac function and reduceCSA (8).ReferencesIp M et al. Circulating nitric oxide is suppressed in obstructive sleepapnoea and is reversed by nCPAP. Am J Respir Crit Care Med 2000.Ip M et al. Endothelial function in obstructive sleep apnea and responseto treatment. Am J Respir Crit Care Med 2004.Somers VK et al. Day-night pattern of sudden death in OSA. NEJM2005.Robinson GV et al. Obstructive sleep apnoea/hypopnoea syndrome andhypertension. Thorax 2004.Bradley TD et al. Sleep apnea and heart failure Part I: Obstructive sleepapnea. Circulation 2003.Ip M et al. OSA is independently associated with insulin resistance. AmJ Respir Crit Care Med 2000.Tan K et al. HDL-dysfunction in obstructive sleep apnea. Atherosclerosis2005.Bradley TD et al. Sleep apnea and heart failure Part II: Central sleepapnea. Circulation 2003.