Cardiac Hypertrophy in Obstructive Sleep Apnea Syndrome

医学 心脏病学 左心室肥大 内科学 多导睡眠图 血压 阻塞性睡眠呼吸暂停 体质指数 睡眠呼吸暂停 呼吸暂停 原发性高血压
作者
Akiko Noda,Tamotsu Okada,Fumihiko Yasuma,Naoki Nakashima,Mitsuhiro Yokota
出处
期刊:Chest [Elsevier]
卷期号:107 (6): 1538-1544 被引量:144
标识
DOI:10.1378/chest.107.6.1538
摘要

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. 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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