Objective: To investigate the cross-sectional association between serum adipocyte fatty acid–binding protein (A-FABP) level and diagnosis or severity of obstructive sleep apnea syndrome (OSAS) and some echocardiographic indices related with cardiac dysfunction. Methods: In this study, plasma A-FABP and high-sensitivity C-reactive protein concentrations were measured, and echocardiography was performed in subjects without any cardiac or pulmonary disease who were referred for evaluation of OSAS. According to the apnea-hypopnea index (AHI), subjects were classified into 3 groups: control group (AHI AHI ≥ 5; n = 30), and severe OSAS (AHI ≥ 30; n = 31). Results: Levels of A-FABP were significantly different between the groups ( P < 0.001). After post hoc analyses, all 3 groups were also significantly different from each other. The levels of A-FABP were significantly higher in the patients with severe OSAS (36.4 ± 13.0 ng/mL) than in the control subjects (9.3 ± 4.6 ng/mL; P < 0.0001) or in patients with mild-moderate OSAS (24.5 ± 10.5 ng/mL; P < 0.001). Patients with myocardial performance index (MPI) greater than 0.47 had higher serum A-FABP levels than those with MPI of less than 0.47 (31.8 ± 13.2 ng/mL vs 10.9 ± 6.3 ng/mL; P = 0.001). Multivariable regression analyses revealed that increased serum A-FABP concentrations were independently associated with increased left ventricular mass index (β = 0.195; P = 0.033) and increased MPI (β = 0.165; P = 0.015). Conclusions: Increased A-FABP levels were found in the patients with OSAS, which were correlated significantly with left ventricular mass index and MPI. Further prospective studies are needed to clarify whether increased serum A-FABP level is a marker or a potential mechanism for left ventricular involvement in patients with OSAS.

To investigate an association between left atrial (LA) structural and P wave dispersion (PWD) during sinus rhythm, and electrical remodeling in cryptogenic stroke (CS) patients. Forty CS patients and 40 age- and sex-matched healthy controls were enrolled. P wave calculations were based on 12-lead electrocardiography (ECG) at a 50-mm/s-paper speed with an amplitude of 10 mm/mV. Difference between the maximum and minimum P wave duration was the P wave dispersion (PWD=Pmax-Pmin). LA deformation was evaluated by speckle tracking echocardiography within 3 days of the acute event. PWD was 30.1±7.0 ms and 27.4±3.5 ms in CS and control group (P=0.02), whereas LA maximum volume index [LAVImax] was 20.4±4.5 mL/m(2) and 19.9±2.4 mL/m(2) in CS and control group, respectively (P = 0.04). While global peak LA strain was [pLA-S] (LA reservoir function) 41.4 ± 6.3% and 44.5 ± 7.1% in CS and control group, (P = 0.04), global peak late diastolic strain rate values [pLA-SRa] (LA pump function) were 2.5 ± 0.4% and 2.9 ± 0.5% in CS and control group, respectively (P = 0.001). A mild and a strong negative correlation between global pLA-S and LAVImax (r=-0.49; P<0.01), and between PWD and global pLA-S (r = -0.52; P < 0.01), respectively, was observed in CS. Increased PWD is associated with impaired LA mechanical functions and enlargement, and involved in the pathophysiology of AF or an AF-like physiology in CS.