Obstructive sleep apnea, cardiovascular disease, and pulmonary hypertension

Abstract

With the growing epidemic of obesity in an aging population, obstructive sleep apnea (OSA) is increasingly encountered in clinical practice. Given the acute cardiopulmonary stressors consequent to repetitive upper airway collapse, as well as evidence for cardiovascular homeostatic dysregulation in subjects with sleep apnea, there is ample biologic plausibility that OSA imparts increased cardiovascular risk, independent of comorbid disease. Indeed, observational studies have suggested strong associations with multiple disorders, such as systemic hypertension, heart failure, cardiac arrhythmias, and pulmonary hypertension. Further data in the form of longitudinal cohort studies and randomized controlled trials are accruing to add to the body of evidence. This review examines pathophysiologic mechanisms and explores current concepts regarding the impact of OSA and its treatment on selected clinical disease states.

Figure 1.

Changes in mean arterial blood pressure (MAP) over 20 hours after treatment with (A) therapeutic continuous positive airway pressure (CPAP) and (B, lower) subtherapeutic CPAP. Reprinted by permission from Reference . nCPAP = nasal CPAP.

Figure 2.

Cumulative percentage of men who had (A) fatal and (B) nonfatal cardiovascular events over more than 10 years of follow-up. The upper tracing in each graph represents men who had severe obstructive sleep apnea–hypopnea and were noncompliant with continuous positive airway pressure (CPAP) therapy. CVS = cardiovascular system; OSAH = obstructive sleep apnea–hypopnea. Reprinted by permission from Reference .

Figure 3.

Pulmonary artery systolic pressure (PASP) after sham and therapeutic continuous positive airway pressure (CPAP). Reprinted by permission from Reference .