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Cardiac Hypertrophy in Obstructive Sleep Apnea Syndrome FREE TO VIEW

Akiko Noda; Tamotsu Okada; Fumihiko Yasuma; Nobuo Nakashima; Mitsuhiro Yokota
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From the Department of Clinical Laboratory Medicine, Nagoya University College of Medical Technology, Nagoya University Hospital, Nagoya, Japan


1995 by the American College of Chest Physicians


Chest. 1995;107(6):1538-1544. doi:10.1378/chest.107.6.1538
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Abstract

Fifty-one middle-aged male patients with obstructive sleep apnea syndrome (OSAS) were evaluated using two-dimensional echocardiography, 24-h blood pressure measurements, polysomnography, and plasma norepinephrine (NE) measurements. Among these patients, left ventricular hypertrophy (LVH) (left ventricular posterior wall thickness [LVPWT] or interventricular septal thickness [IVST]≥12 mm) and right ventricular hypertrophy (RVH) (right ventricular wall thickness [RVT]≥5 mm) were present in 41.2% (21/51) and 11.8% (6/51). LVH was present in 50.0% of group 2 patients (apnea index≥20) and in 30.5% of group 1 patients (apnea index <20). All patients with LVH had hypertension. RVH was present in 21.4% of group 2 patients and none of the group 1 patients. IVST, LVPWT, LV mass, LV mass/body surface area (BSA), and obesity index were significantly greater in group 2 than in group 1. Apnea index and the duration in which nocturnal oxygen saturation was decreased under 90% (duration of SaO2 <90%), were significantly correlated with LV mass/BSA and 24-h mean blood pressure. Apnea index, number of apneas, duration of nocturnal oxygen saturation less than 90%, weight, and obesity index were significantly greater in patients with both LVH and RVH than in patients without LVH and RVH, or those with only LVH. Plasma NE after waking significantly increased compared with that before sleep (p<0.05). The ratio of plasma NE levels after waking to those before sleep was significantly correlated with the duration of SaO2 <90% (r=0.83, p<0.05), but not with apnea index. These results suggest that frequent episodes of oxygen desaturation and/or arousal responses caused by apnea may contribute to the complication of LVH and RVH in the long term, and apnea-induced cyclical increases in blood pressure and the resulting sustained elevation in blood pressure associated with the increase in afterload and sympathetic activity may play a role in the development of LVH.


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