Discussion
Hypoxic pulmonary vasoconstriction was first described in 1947, by Von Euler and Liljestrand. The vasoconstriction appears to be in the pulmonary arteriolar bed. Elevation of pulmonary artery pressure has been demonstrated in OSA patients. It has been ascribed to hypoxemia and has been shown to progress from wakefulness through the various stages of sleep to REM sleep.’ Right ventricular hypertrophy is expected to result from such pulmonary artery hypertension, which is at first intermittent and subsequently sustained. Cor pulmonale has been described in OSA. Recent studies have suggested that the development of cor pulmonale may require daytime hypoxemia in addition to OSA. The early natural history of OSA-induced cardiac abnormalities is unknown, since most studies have focused on the end-stage, right ventricular failure.
In this study, we for the first time have been able to document the prevalence of RVH in OSA patients. Right ventricular hypertrophy is a difficult measure to ascertain on two-dimensional echocardiography. We, therefore, used the methods previously described in the literature and used the services of two board-certified cardiologists. The statistical analysis of correlation showed a linearly related correlation of r = 0.87 between the two cardiologists. This would seem to document that our numbers are reproducible.