The effect of obstructive sleep apnea-hypopnea syndrome on acute myocardial infarction

Abstract

Background and objectives: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is the most clinically common type of sleep-related breathing disorders. In this study, the effect of OSAHS on ST segment elevation myocardial infarction (STEMI) was investigated. Methods: Seventy-fi ve patients with STEMI were included in this study. The patients were divided into two groups: STEMI accompanied by OSAHS (O + ) group (33 patients) and STEMI without OSAHS (O -) group (42 patients). The differences of the clinical characteristics between the two groups were compared. The relationship between oxyhemoglobin desaturation index (ODI) and Gensini Score, and the relationships between OSAHS and clinical parameters were analyzed by a regression analysis. Results: AMI mainly occurred from 10 pm to 6 am in the O + group (45.5 %) and from 6 am to 2 pm in the O -group (52.3 %). The peak of serous creatine kinase (CK), high-sensitivity C-reactive protein (hs-CRP), N-terminal Pro-brain natriuretic peptide (NT-proBNP), and left ventricle end-diastolic volume index (LVEDVI) were significantly increased in the O + group compared to the O -group, while the left ventricular ejection fraction (LVEF) were signifi cantly decreased. The regression analysis showed that ODI was positively correlated with Gensini Score, while serous CK, hs-CRP, NT-proBNP, and OSAHS were independently associated with left ventricular insuffi ciency (LVI), and the incidence of LVI in O + group was 5.8 times as O -group. Conclusions: In STEMI patients with OSAHS, myocardial infarction mainly occurred from 10 pm to 6 am, and the incidence of LVI was signifi cantly higher than STEMI patients without OSAHS (Tab. 5, Fig. 2 Obstructive sleep apnea-hypopnea syndrome (OSAHS) is the most common type of sleep-related breathing disorders, which was caused by throat obstruction (1, 2). The syndrome associates somnolence and one or two of the following symptoms: severe snoring, nocturnal respiratory arrest, repeated nocturnal awakening, non-recuperative sleep, diurnal fatigue, and altered concentration (3 4). OSAHS may act to cause and promote the progression of hypertension, coronary artery disease (CAD), acute myocardial infarction (AMI) and cerebral vascular disease (1, 5). It is reported that its incidences in adult women is 2 %, and in adult men is 4 % (6). While in China, its incidence is about 3.62 % in people beyond 30 years, which means that there are more than 47 million of patients in China by now (7).Numerous studies showed that OSAHS is closely associated with the development and progression of CAD. The changes of hemodynamics, enhancement of the sympathetic activity, and oxidative stress that are caused by OSAHS can accelerate the process of artherosclerosis (8, 9). Peker et al (10) reported that the incidence of OSAHS is higher in the patients with CAD than in normal people, and OSAHS can raise the mortality of angiocardiopathy, while patients treated by continuous positive airway pressure (CPAP) can reverse this state. The results of Peker et al (10) al...

Effects of Obstructive Sleep Apnea on Cardiac Function and Clinical Outcomes in Chinese Patients with ST-Elevation Myocardial Infarction

“…This data is in accordance with the proportion reported by previous studies [35, 36]. Our study showed that a greater BMI and abdominal circumference were associated with OSA ( P < 0.001, P = 0.046), since the BMI and abdominal obesity were reported as important factors in occurrence of OSA [37–39].…”

Nitric oxide metabolites and erythrocyte deformability in a group of subjects with obstructive sleep apnea syndrome

“…OSAS has been proposed as an independent risk factor for the development of essential hypertension and the isolated increase in diastolic pressure is often the earliest pressure modification in these subjects [24,37]. Some author have described higher incidence of myocardial infarction in OSAS subjects during night-time (from 10 pm to 6 am) [46] suggesting that OSAS could precipitate myocardial ischemia during sleep in patients with coronary disease. Untreated [24].…”

The relationship between apnoea hypopnoea index and Gensini score in patients with acute myocardial infarction undergoing emergency primary percutaneous coronary intervention

“…Some supported our result, such as Ludka's (10) research while the others had the opposite opinion, for example, Kuniyoshi et al (23) reported that there was a different diurnal variation among patients with AMI with or without SAHS. and Zhang et al (2) reported that myocardial infarction mainly occurred between 10 pm and 6 am among patients with OSAHS.…”

“…Sleep apnoea hypopnoea syndrome (SAHS) causes repetitive nocturnal hypoxemia, which could promote the progression of hypertension, arrhythmia, coronary artery disease (CAD) and cerebral vascular disease (1,2). There are many reports regarding the effect of SAHS on high blood pressure (3,4) and arrhythmia (5,6).…”