Impact of obstructive sleep apnea on the right ventricle.

BACKGROUND: Right ventricular (RV) involvement in obstructive sleep apnea syndrome (OAS) is controversial. The aim of this study was to determine a correlation between echocardiographic parameters of RV function and severity of OSA assessed by the apnea- hypopnea index (AHI). METHODS: Sixty patients with suspected OSA were enrolled. All patients had overnight polygraphy and an echocardiographic assessment of RV structure and function. Patients were divided into three groups: a control group (n=20) with an AHI<5/h, a group of mild to moderate OSA (n=18) with an AHI=5-30/h and a group of severe OSA (n=22) with AHI≥30/h. RESULTS: There were no differences of age, body mass index and sex among the three groups. There was no difference in systolic pulmonary pressure. RV free wall thickness, end-diastolic surface and right atrium surface were statistically higher in OSA patients compared with controls. The peak systolic myocardial velocity at tricuspid lateral annulus S' were significantly lower in patients compared with controls (14.5±3 vs 12.2±2 cm / s, p<0.001; respectively). This decrease was greater in patients with severe OSA compared with mild to moderate OSA (11.4±3 vs 13.0±1 cm/s, p=0.05, respectively). Right ventricular myocardial performance index (MPI) was significantly higher in OSA compared with controls (0.55±0.12 vs 0.46±0.14, p=0.024, respectively) but it was not correlated with the severity of IAH. CONCLUSIONS: In OSA patients, there was a significant RV dysfunction independently of pulmonary pressure, although the correlation with the severity of IAH was moderate.

Impact of obstructive sleep apnea on the right ventricle.

BACKGROUND: Right ventricular (RV) involvement in obstructive sleep apnea syndrome (OAS) is controversial. The aim of this study was to determine a correlation between echocardiographic parameters of RV function and severity of OSA assessed by the apnea- hypopnea index (AHI). METHODS: Sixty patients with suspected OSA were enrolled. All patients had overnight polygraphy and an echocardiographic assessment of RV structure and function. Patients were divided into three groups: a control group (n=20) with an AHI<5/h, a group of mild to moderate OSA (n=18) with an AHI=5-30/h and a group of severe OSA (n=22) with AHI≥30/h. RESULTS: There were no differences of age, body mass index and sex among the three groups. There was no difference in systolic pulmonary pressure. RV free wall thickness, end-diastolic surface and right atrium surface were statistically higher in OSA patients compared with controls. The peak systolic myocardial velocity at tricuspid lateral annulus S' were significantly lower in patients compared with controls (14.5±3 vs 12.2±2 cm / s, p<0.001; respectively). This decrease was greater in patients with severe OSA compared with mild to moderate OSA (11.4±3 vs 13.0±1 cm/s, p=0.05, respectively). Right ventricular myocardial performance index (MPI) was significantly higher in OSA compared with controls (0.55±0.12 vs 0.46±0.14, p=0.024, respectively) but it was not correlated with the severity of IAH. CONCLUSIONS: In OSA patients, there was a significant RV dysfunction independently of pulmonary pressure, although the correlation with the severity of IAH was moderate.

Recurrent native and prosthetic mitral valve thrombosis in idiopathic hypereosinophilic syndrome.

Hypereosinophilic syndrome (HES) is defined as a prolonged, unexplained peripheral eosinophilia. Endomyocardial fibrosis and mural thrombus formation are common occurrences such that patients are exposed to lethal thromboembolic complications. The valvular damage described is mainly related to iterative valve thromboses that are amenable to surgery. Here, the case is reported of a 39-year-old woman suffering from HES with mitral valve thrombosis and mechanical prosthetic mitral valve replacement, in whom a new thrombosis of the inserted prosthesis occurred one month postoperatively, concomitant with severe hypereosinophilia and despite adequate anticoagulation. The patient had received a new bioprosthetic mitral valve replacement, and her eosinophil count had been normalized after treatment with corticosteroids. Oral anticoagulation with warfarin was maintained. Subsequently, no recurrent thromboembolic events were reported, and echocardiography performed at the one-year follow up showed the bioprosthesis to have a normal hemodynamic profile.