Elsevier

Sleep Medicine Reviews

Volume 12, Issue 1, February 2008, Pages 19-31
Sleep Medicine Reviews

CLINICAL REVIEW
Obstructive sleep apnea and coronary artery disease

https://doi.org/10.1016/j.smrv.2007.08.002Get rights and content

Summary

In the recent years intensive research has revealed numerous negative consequences of obstructive sleep apnea (OSA) for the cardiovascular system. The pathophysiological interaction between OSA and coronary artery disease is complex and comprises neural, humoral, mechanical and haemodynamic components. One of the most important effects of OSA is an increase of sympathetic nerve traffic, which persists during the day and is thought to play a key role in the association of OSA and elevated systemic blood pressure. Nowadays, OSA is accepted as an independent risk factor for arterial hypertension. Several investigations support an association of OSA with ischemic ST-segment changes, ventricular arrhythmias, and sudden cardiac death. In line with this, a growing body of evidence strongly supports OSA having prognostic implications for cardiovascular morbidity and mortality. Continuous positive airway pressure (CPAP) has been shown to have several beneficial effects on the cardiovascular system. Uncontrolled studies indicate that it reduces cardiovascular risk in patients with severe OSA and increased risk or manifest coronary artery disease. However, ongoing studies still have to confirm this.

Introduction

Coronary artery disease (CAD) is a chronic, life-threatening disease. Progressive arteriosclerosis in the coronary arteries may lead to intimal thickening and eventual stenosis of the coronary arteries, with flow limitation and a subsequent imbalance of myocardial oxygen supply and demand, causing stable angina pectoris or its equivalents. Atherosclerotic plaque rupture with associated platelet adhesion and thrombus formation form the basis of acute coronary syndromes ranging from unstable angina to non-Q-wave and Q-wave myocardial infarction.1

Although mortality due to CAD has slightly decreased in the past decade, CAD remains the most common cause of death, with an incidence of 380 myocardial infarctions per 100 000 persons aged between 36 and 64 years per year.2 In the Physicians’ Health Study, the incidence was even higher, with 440 myocardial infarctions per 100 000 physicians per year.3 Risk factors, lifestyle and socio-economic circumstances probably account for the large regional variation.2

Obstructive sleep apnea (OSA) is characterized by repetitive collapse of the upper airway, thereby inducing apnea and hypopnea episodes despite persistent thoracic and abdominal respiratory effort. The disease has a high prevalence in the general population. It is estimated that in the middle-aged population about 4% of men and 2% of women suffer from manifest OSA.4 Numerous deleterious effects result from obstructive apnea and hypopnea with large negative intrathoracic pressure changes and blood gas deterioration. It has long been known that OSA causes substantial sleep fragmentation with excessive daytime sleepiness.5 Moreover, intensive research in recent years has also revealed negative consequences for the cardiovascular system, such as pulmonary hypertension, congestive heart failure, stroke, atrial fibrillation, and left ventricular diastolic dysfunction.6, 7, 8, 9, 10 This review focuses on the association of OSA and coronary artery disease (CAD), including ischemia, ventricular arrhythmias and arterial hypertension, and its prognostic implications.

Section snippets

Pathophysiology

The pathophysiological interaction between OSA and coronary artery disease is complex and comprises neural, humoral, mechanical and hemodynamic components (Figure 1).

Myocardial ischemia

As mentioned above, myocardial ischemia occurs as a result of reduced oxygen supply or increased oxygen demand. OSA may reduce myocardial blood flow and/or increase demand by acute changes in heart rate on the one hand and increase in afterload on the other hand. This occurs in the setting of reduced oxygen supply caused by apnea-associated hypoxemia. These factors may predispose to myocardial ischemia. Indeed, asymptomatic ST-segment depressions during sleep were evident in patients with OSA

Effect of CPAP treatment

General therapeutic options for OSA comprise first of all reduction of body weight, which may reduce the severity of OSA,132 but also abstinence from alcohol and sedatives, positional therapy or treatment of nasal obstruction. More specific therapeutic options for OSA involve oral appliances or in selected patients surgical approaches.133, 134 Recently, atrial overdrive pacing has been suggested as new alternative therapy for OSA, however subsequent studies could not confirm the beneficial

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