Affiliations: Jackson, MS
Dr. Collop is Professor of Pulmonary and Critical Care Medicine, University of Mississippi Medical Center and the C.V. “Sonny” Montgomery VA Medical Center.
Correspondence to: Nancy Collop, MD, FCCP, Division of Pulmonary/Critical Care, University of Mississippi Medical Center, 2500 N State St, Jackson, MS 39216; e-mail: email@example.com
In 1996, I wrote an editorial discussing the relationship between obstructive sleep apnea (OSA) and hypertension.1In that issue of CHEST, Coy et al2 presented data supporting the link between these two common disorders. They examined patients with OSA to determine if the severity of OSA as defined by the apnea-hypopnea index (AHI) was correlated with the presence of hypertension. Indeed, AHI was correlated with an elevated diastolic BP, independent of body mass index and age.
New information has subsequently become available to further define this relationship. Two large epidemiologic studies showed increasing odds ratios for the presence of hypertension related to the severity of OSA as defined by the AHI.3–4 In both articles, this relationship persisted even after adjusting for a variety of confounding variables often noted in the patient populations with these disorders (age, gender, body mass index, tobacco use, etc). These again showed OSA and hypertension are clearly linked, without conferring causality.
One approach to establishing causation would be to demonstrate that treatment of OSA mitigates hypertension. Although several studies have used this approach,5–9 the study in this issue of CHEST (see page 1125) is the only one to use a hypertensive, nonapneic control group and treat them with nasal continuous positive airway pressure (CPAP). The experimental design, therefore, examined the possibility that CPAP itself may alter BP unassociated with any effects it may have on eliminating OSA. Another unique aspect of this study was that the recruited study population was hypertensive patients rather than patients with OSA, and was reportedly “asymptomatic” with regards to the presence of hypersomnia and/or sleep fragmentation.
The study participants wore nasal CPAP for 3 weeks, during which time the authors noted a significant change in nocturnal BP in the OSA group with a similar trend of decreasing daytime BP. The control group had no significant change in BP with CPAP, suggesting the CPAP itself does not alter BP independent of its effect on OSA.
There are some notable limitations of this study. Nasal CPAP is an onerous therapy, particularly if the person wearing it receives no benefit from its use. As would be expected, the control group was not as compliant with CPAP as the OSA group, raising the possibility that hypertension was not improved in the control population because they did not wear their CPAP as frequently. The difference in CPAP adherence between the groups could also suggest that symptoms were less “occult” than suggested, as they used their CPAP much more than the control subjects (5.7 ± 1.7 hours per night vs 3.5 ± 2.2 hours per night). Unfortunately, no measurements of subjective or objective sleepiness were reported.
As we inch inexorably closer to confirming that OSA can cause diurnal hypertension, additional questions arise. Does OSA-induced hypertension have the same cardiovascular consequences as hypertension from other causes? Should hypertensive patients with milder forms of OSA be treated more aggressively with regard to their OSA than nonhypertensive OSA patients? What is the mechanism explaining why some OSA patients acquire hypertension and others do not? The outcome data, as are being collected in the Sleep Heart Health Study and Wisconsin Cohort Study, should help answer some of these questions.
It appears that OSA is a contributing risk factor for cardiovascular disease. Physicians treating patients with hypertension should now consider OSA in their differential diagnosis of all patients with hypertension.
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