Why the study?
Does severe obstructive sleep apnea increase surrogate markers of cardiovascular disease (such as left ventricular mass and abnormal blood pressure profiles) in newly diagnosed patients without known cardiovascular disease compared to less severe OSA?
Does severe obstructive sleep apnea increase surrogate markers of cardiovascular disease (such as left ventricular mass and abnormal blood pressure profiles) in newly diagnosed patients without known cardiovascular disease compared to less severe OSA?
Severe obstructive sleep apnea is associated with early cardiovascular abnormalities, including increased left ventricular mass and abnormal blood pressure dipping, even in patients without clinically recognized cardiovascular disease.
Severe OSA may warrant closer BP and echo monitoring in newly diagnosed patients; leaves open whether treatment alters LV mass or dipping.
Obstructive sleep apnea (OSA) is associated with high cardiovascular morbidity and mortality. Recent studies have shown that it is associated with atherosclerosis and left ventricular dysfunction markers. The aim of this study was to assess the cardiovascular effects of OSA depending on its severity, in patients without clinically diagnosed cardiovascular disease. One hundred thirty newly diagnosed, nondiabetic OSA patients (mean age 49 +/- 10 years), without vasoactive treatment were included. They underwent clinical and ambulatory blood pressure measurements, echocardiography, carotid ultrasound examination, and a carotid-femoral pulse wave velocity (PWV) measurement. Seventy-five percent of the subjects were hypertensive according to the clinical or ambulatory measurement. More patients with the most severe forms (respiratory disturbance index >37/hour) had a nondipper profile (52% vs 34%; P = 0.025) and their left ventricular mass was higher (40 +/- 7 vs 36 +/- 8 g/m, p = 0.014). This last parameter was independently and inversely associated with mean nocturnal oxygen saturation (P = 0.004). PWV and carotid intima-media thickness did not differ between one OSA severity group to another, but the prevalence of carotid hypertrophy was higher when mean SaO(2) was below 93.5% (29.5 vs 16%; P = 0.05). Our study shows that in OSA patients without clinically diagnosed cardiovascular disease, there is a significant left ventricular and arterial effect, which is even more marked when OSA is severe.
No takes yet. Share an insight, caveat, or question.
Jean-Philippe Baguet (2009) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: