Echocardiography findings in a sleep apnea pacients with morbid obesity

Abstract

Morbidly obese subjects have a high risk of left ventricular (LV) hypertrophy. Whether obstructive sleep apnea (OSA) contributes to LV hypertrophy is controversial. We performed a pilot descriptive study of echocardiographic parameters in a cohort of morbidly obese patients with OSA. We included retrospectively all patients form a bariatric surgery cohort assessed preoperatively with either polisomnography or respiratory polygraphy and transthoracic echocardiography. 2D imatges, M-mode and Doppler recording were obtained (General Electric Vivid 7). The following parameters were analyzed: LV diastolic diameter, LV systolic diameter, LV systolic diameter corrected by body surface area, % ejection fraction by Teichholz method, left ventricular mass index, septal thickness, posterior wall thickness and pulmonary hypertension. We included 59 patients with a mean age of 59 ± 9 years, 34% of males, BMI 46 ± 8 kg/m 2 . 59% had hypertension. All of them presented OSA with mean apnea hypopnea index (AHI) of 52 ± 30 events/h, median of cumulative time under 90% of SpO2 was 11(4–27). We split the population by the median AHI. Patients with more than 41events/h had wider aortic root (29,33 ± 4; 32,11 ± 4, p = 0,009), higher posterior wall thickness (9,8 ± 1; 10,6 ± 1, p = 0,03), and tendency to have higher LV Mass that was no longer significant when it was adjusted by body surface. Patients with more than 41events/h had higher rates of hypertension (30% vs 70%). There was a positive correlation between AHI and diastolic diameter ( r = 0.268, p = 0.043), aortic root ( r = 0.275, p = 0.03), LV Mass ( r = 0.352, p = 0.008) but it was lost when was corrected by body surface ( r = 0.275, p = 0.065). There was also a positive correlation between pulmonary arterial pressure and AIH but it was available in 20 patients. Only 17 (37%) patients presented a LV abnormal hypertrophy pattern (8 concentric remodeling, 1 eccentric hypertrophy, 8 concentric hypertrophy). Despite the high prevalence and severity of OSA in the studied population of morbidly obese patients, a low percentage of echocardiographic abnormalities were found. Although more sever OSA patients presented higher LV Mass, it could be related to higher hypertension frequency and to obesity itself. Further prospective studies are necessary to elucidate if OSA has an additive effect to obesity on LV hypertrophy. Web thank the whole team of sleep laboratory (Maria Calvo, Carme Rodriguez, Tomas Brinquis and Neus Marti) for the help to recruit the pacients and also the endocrinologist Theodora Michalopoulou.