Cardiovascular Consequences of Sleep Apnea

Richard J. Castriotta, MD, FCCP

Professor
Director of the Division of Pulmonary, Critical Care, and Sleep Medicine
Baylor College of Medicine
Houston, Texas

The relationship between obstructive sleep apnea (OSA) and systemic hypertension is thought to be causal, but conclusive proof remains elusive because of the number of confounding elements, most notably obesity. The pathogenesis of hypertension in OSA may include intermittent hypoxemia with reoxygenation and increased sympathetic nervous system activity that persists into wakefulness, eventually translating into systemic hypertension. The Wisconsin Sleep Cohort study1 published a longitudinal prospective study of more than 700 patients that found a significant risk for systemic hypertension in a cohort of patients with an apnea-hypopnea index (AHI) >15/hr who were followed for more than 4 years; a lesser risk was found in those with AHI between 5-15/hr. This risk was maintained after adjusting for obesity, alcohol and tobacco use, and demographic groups. However, the Sleep Heart Health longitudinal study2 of an older cohort of OSA patients found a causal relationship in thinner patients, but in the more obese cohort the confidence interval fell below 1. Thus, after adjusting for BMI, the AHI score was not a significant predictor of future hypertension. One reason for these divergent findings may be masked hypertension. Some studies rely on one in-office measurement and others rely on continuous or ambulatory blood pressure readings. Indeed, a very important finding is nocturnal blood pressure, which is often overlooked. Many OSA patients do not show a reduction in blood pressure at night, so-called non-dippers; it is postulated that these patients have an increase in markers for hypertension. Another possible reason for these divergent study findings may be the triangular relationship among OSA, hypertension, and obesity. Other studies have found that patients who are obese desaturate more despite the same degree of hypopnea and are much more likely to have hypertension and OSA. Similarly, patients who have OSA are much more likely to be obese; among the metabolic consequences of sleep apnea is a decrease in leptin, generating an increase in appetite and greater likelihood for developing the metabolic syndrome. All of these interrelationships make it more difficult to prove conclusively the causal relationship between hypertension and OSA. Studies have been able to ascertain, however, that snoring itself does not contribute to the development of hypertension. Clinicians should be aware that, although the relationship between OSA and hypertension has not been definitively found to be causal, there is nonetheless substantial evidence in support of the interrelationship between OSA, hypertension, and obesity. Clinicians should be attentive to this relationship when assessing and managing these patients.

References

Peppard PE, Young T, Palta M, et al. Prospective study of the association between sleep-disordered breathing and hypertension. New Engl J Med 2000;342:1378-1384.
O'Connor GT, Caffo B, Newman AB, Quan SF, Rapoport DM, Redline S, Resnick HE, Samet J, Shahar E. Prospective Study of Sleep-disordered Breathing and Hypertension: The Sleep Heart Health Study. Am J Respir Crit Care Med 2009; 179:1159-1164.

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