Plasma renin activity (PRA; >4 ng/mL/hour) was used as a surrogate of effective arterial blood volume. Patients were followed up for 12 months. Thirty-seven patients had LVDD (19 with grade 1 and

18 with grade 2). Left ventricular hypertrophy, left atrial volume, AEVS, and natriuretic peptide levels were significantly greater in patients with LVDD than without LVDD. Patients with grade 2 LVDD, compared to grade 1 LVDD and without LVDD, had significantly lower mean arterial pressure and higher Model for End-Stage Liver Disease (MELD) score, E-wave transmitral/early diastolic mitral annular velocity (E/e’ ratio), cardiopulmonary pressures, PRA, and AP24534 supplier natriuretic peptide levels. Systolic and cardiac chronotropic function were significantly lower in patients with grade 2 LVDD than without LVDD. LVDD was more frequent in patients with ascites and increased PRA than patients without ascites or with ascites Talazoparib molecular weight but normal PRA. Fourteen patients with LVDD developed hepatorenal syndrome (HRS) type 1 on follow-up. Survival was different according to degree of LVDD (without LVDD: 95%; grade 1 LVDD: 79%; grade 2 LVDD: 39%; P < 0.001). Independent predictive factors of mortality were MELD score and E/e' ratio. Conclusion:

LVDD occurs simultaneously with other changes in cardiac structure and function and is associated with an impairment of effective arterial blood volume. LVDD is a sensitive marker of advanced cirrhosis, type 1 HRS development, and mortality. (Hepatology 2013;58:1732–1741) Cirrhosis is associated with a specific subclinical cardiomyopathy[1-4] characterized by diminished systolic responsiveness to stress stimuli,[5, 6] impaired diastolic relaxation,[7, 8] electrophysiological abnormalities,[9]

and enlargement and hypertrophy of cardiac chambers,[10, 11] all in the absence of known cardiac disease. However, evidence suggests that patients with cirrhosis display primarily left ventricular diastolic dysfunction (LVDD) with normal systolic function at rest.[7] Doppler examination of mitral inflow has been the most common technique used in the evaluation of left ventricular (LV) diastolic selleck compound function in cirrhosis.[7, 8, 10, 11] However, conventional Doppler echocardiographic indices (E/A ratio) have clear limitations (age and load conditions) and rarely allow the accurate differentiation between normal from pseudonormal pattern. Currently, the most sensitive and reproducible echocardiographic technique for the assessment of LV filling dynamics is tissue Doppler imaging (TDI), because TDI can overcome some of these factors. TDI is an ultrasound modality that applies the Doppler principle to record velocities within the myocardium. TDI velocities have demonstrated a significant correlation with invasive indices of LV relaxation and minimal effect of preload in the setting of impaired relaxation.