© 2003 American Thoracic Society
Continuous positive airway pressure normalizes pulmonary artery pressures in subjects with obstructive sleep apnea and pulmonary hypertensionTo the Editor:I am writing to point out that Dr. Sajkov and colleagues understate the significance of their finding that effective treatment of obstructive sleep apnea (OSA) normalizes pulmonary artery pressures in patients with OSA and pulmonary hypertension (PH) (1). Their study showed that continuous positive airway pressure (CPAP) reduces pulmonary artery pressures in patients with OSA, most of whom had normal pulmonary artery pressures at the outset. Of the five subjects who had PH and OSA, all five experienced normalization of their pulmonary artery pressures after CPAP treatment. Five out of five is statistically significant (p = 0.03). The authors have demonstrated that OSA can cause PH. In recent years, this has been an issue of considerable contention. Until now, most of the research literature has favored the premise that OSA is not a cause of PH (2), although Dr. Sajkov and his colleagues have argued otherwise (3, 4). The majority of prior research has found that day time hypoxemia and abnormal lung functioning correlates better with PH than does the severity of the OSA correlate with PH. Accordingly, many investigators have concluded that OSA does not cause PH, but rather, abnormal pulmonary functioning with resultant day time hypoxemia is more likely the cause of PH in these individuals. That OSA can cause PH has enormous implications for patients with pulmonary hypertension, especially those diagnosed with primary PH (PPH). If OSA causes PH, then a proper diagnostic evaluation to identify the etiology of PH should include a polysomnogram. Likewise, a diagnosis of PPH cannot be accurately made unless a sleep study has been performed. Many publications regarding the etiology of PH have not included polysomnograms in the evaluation of the research subjects. Of particular note, some research linking appetite suppressants and PPH did not include sleep evaluations (5). Since obese individuals use appetite suppressants, and since obesity can cause OSA, research demonstrating a relationship between appetite suppressants and PPH that fails to evaluate subjects for sleep-disordered breathing may not be worth the paper, or cyberspace, on which it is printed. If the results of Sajkov and colleagues (1) are verified by other researchers, then the field of PPH will be dramatically altered, for much of what has been "learned" in recent years may no longer be applicable or correct.
Berea Health Center Berea, Ohio REFERENCES
From the Authors:We read with interest Dr. Blankfield's letter, in which he speculates that the causal link between obstructive sleep apnea and pulmonary hypertension, as demonstrated in our previous studies (1–3) is relevant to patients with primary pulmonary hypertension. He further argues that in order to diagnose primary pulmonary hypertension, obstructive sleep apnea should be excluded by polysomnography, and criticizes the study (4) linking appetite-suppressants and primary pulmonary hypertension for failing to exclude obesity-related obstructive sleep apnea as a cause of pulmonary hypertension.As published in our previous papers (1–3), pulmonary hypertension in patients with obstructive sleep apnea, without coexisting heart or lung disease, is only of mild severity (mean pulmonary artery pressure, range 20–31 mm Hg, average 23.6 + 1.1 mm Hg). This contrasts with patients with primary pulmonary hypertension, in which pulmonary hypertension is moderate to severe (4). Further, the majority of patients with obstructive sleep apnea, as in our studies, are men, whereas in Abenhaim and colleagues' study (4) 66% of patients with primary pulmonary hypertension were women. Therefore, not disputing that obstructive sleep apnea should be excluded as a contributing factor before a diagnosis of primary pulmonary hypertension is established, we believe that obstructive sleep apnea alone is unlikely to explain the degree of pulmonary hypertension commonly found in patients with primary pulmonary hypertension.
a The Queen Elizabeth Hospital Adelaide, Australia REFERENCES
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