Nonalcoholic fatty liver disease (NAFLD) is linked to the metabolic syndrome. The aim of the present study is to determine the effect of the metabolic syndrome on left ventricular (LV) geometry and function using as a model patients with NAFLD. Thirty-eight patients with NAFLD, less than 55 years of age and with a normal exercise test, were compared with an age and sex-matched control group. Patients with diabetes mellitus, hypertension, and body mass index>40 were excluded. A complete echocardiographic study including tissue Doppler imaging (TDI) was performed. The following parameters were assessed by echo Doppler: peak velocities of early (E) and late (A) diastolic filling, E/A ratio, flow propagation velocity (Vp). Using TDI early diastolic velocity (E'), and systolic velocity (S') of mitral annulus were obtained. The patients with NAFLD had a significantly higher body mass index (31.4+/-5 vs. 26.4+/-4 kg/m, P=0.01), higher glucose (100.6+/-13 vs. 83.0+/-10 mg/dL, P=0.01), and triglyceride levels (126.5+/-44 vs. 206.5+/-67 mg/dL, P<0.001). Increased thickness of the intraventricular septum, posterior wall (11.03+/-2.2 vs. 8.9+/-2.9 mm, P=0.001; 8.5+/-1.7 vs. 9.7+/-2.3 mm, P=0.04), and larger LV mass and LV mass/height (160.7+/-58.7 vs.115.3+/-35.4 g, P=0.001 and 92.6+/-29.5 vs. 69.2+/-19.8 g/m, P=0.001, respectively) were found in NAFLD group. LV systolic function was similar in both groups. Patients with NAFLD had a lower E (73.6+/-11.0 vs. 86.4+/-20.0 cm/s, P<0.006) and E/A ratio (1.0+/-0.3 vs. 1.76+/-0.8 P<0.0001). Moreover, the Vp and the E' on TDI were significantly lower compared with the control group (49.0+/-9.7 vs. 74.7+/-18.4 cm/s, P<0.0001 and 10.3+/-2.0 vs. 13.8+/-1.7 cm/s, P<0.0001, respectively). On multivariate analysis the E' on TDI was the only independent parameter associated with NAFLD. In conclusion, patients with NAFLD in the absence of morbid obesity, hypertension, and diabetes have mildly altered LV geometry and early features of left ventricular diastolic dysfunction. Early diastolic velocity on TDI was found to be the only index that could identify the patients with NAFLD and metabolic syndrome.

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Objective: Toevaluate the effects of bosentan on echo-derived hemodynamic measurements, and clinical variables in symptomatic heart failure (HF) patients. Method: Multi- center, double-blind, randomized (2:1), placebo-controlled study comparing bosentan (8–125 mg b.i.d.) to placebo in patients with New York Heart Association class IIIb–IV HF, left ventricular ejection fraction <35% and systolic pulmonary artery pressure (SPAP) >40 mm Hg. Primary and secondary endpoints were change from baseline to 20 weeks in SPAP and cardiac index, respectively. Safety endpoints were treatment emergent adverse events (AEs), change in body weight, hemoglobin, hematocrit, systolic blood pressure and diuretic use. Results: Ninety-four patients enrolled: 60 to bosentan, 34 to placebo. There was no significant difference between the 2 arms in SPAP change (0.1 ± 11.5 mm Hg , 95% confidence limit (CL) –5.4 to 5.2, p = 0.97), cardiac index shift (0.12 ± 0.45, 95% CL –0.09 to 0.33 , p = 0.24 ) or any of the other 22 echocardigraphic measurements obtained. Therapy-duration was longer in the placebo arm, while more patients in the bosentan arm experienced adverse and serious AEs. Conclusion: In HF patients with left ventricular dysfunction and secondary pulmonary hypertension, bosentan did not provide any measurable hemodynamic benefit, and was associated with more frequent AEs, requiring drug discontinuation.