Ventricular function in snorers and patients with obstructive sleep apnea.
We hypothesized that intermittent hypoxemia and increased ventricular afterload due to obstructive apnea during sleep (OSA) would cause chronic left ventricular dysfunction. Overnight polysomnography, M-mode and two-dimensional echo-Doppler studies while awake were performed on 51 consecutive snorers, 30 with OSA and 21 without apnea. Patients with previous myocardial infarction, awake hypoxemia or hypercapnia, or other causes of nocturnal hypoxemia were excluded. Echo-Doppler measurements included end-diastolic right and left ventricular dimensions and wall thickness, indices of left ventricular systolic performance (fractional shortening, ejection fraction and ejection time and diastolic performance, (isovolumic relaxation time, ratio of peak early [E] to late [A] diastolic transmitral flow and mitral pressure half-time). Both OSA patients and nonapneic snorers were of similar age. Although OSA patients were heavier, had a greater apnea-hypopnea index, and significant nocturnal hypoxemia, their echo-Doppler measurements were within normal limits and were not significantly different from nonapneic snorers. It is concluded that isolated obstructive sleep apnea does not cause chronic left ventricular dysfunction.
Hanly
P
P
Department of Medicine, Wellesley Hospital, Toronto, Ontario, Canada.
Sasson
Z
Z
Zuberi
N
N
Alderson
M
M
D000328:Adult; D002245:Carbon Dioxide / Q000097:blood; D003430:Cross-Sectional Studies; D003971:Diastole; D004452:Echocardiography; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D012891:Sleep Apnea Syndromes / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D012913:Snoring / Q000097:blood / Q000473:pathology / Q000503:physiopathology*; D013599:Systole; D016277:Ventricular Function, Left / Q000502:physiology*
D002245:Carbon Dioxide; D010100:Oxygen