Abstract

Background:

Point-of-care echocardiography (POC-Echo) can be used to evaluate Cirrhotic Cardiomyopathy (CCM) and inferior vena cava (IVC) dynamics. The impact of cardiac function and IVC dynamics on cirrhosis progression towards refractory ascites and HRS-AKI is yet to be defined. This study aims to evaluate the utility of CCM markers and IVC changes, assessed by POC-Echo, in predicting adverse outcomes in patients with cirrhosis and ascites.

Methods:

Serial POC-Echo was done at presentation, at 1 week following 1^st paracentesis, and subsequently at 3 & 6 months from 1^st assessment in decompensated patients with ascites. Clinical data, diuretic response, cardiac & renal biomarkers were prospectively collected at presentation, and at 6 & 12 months. CCM was defined as per CCM consortium 2020 criteria. Refractory ascites and HRS-AKI were diagnosed as per International Ascites Club 2015 criteria. Patients with coronary artery disease, valvular heart disease, those on dialysis, uncontrolled thyroid disease, portopulmonary hypertension, dilated cardiomyopathy, and hepatocellular carcinoma were excluded. (Figure 1)

Results:

We enrolled 130 cirrhotic patients with ascites at presentation [(62% men, aged 50± 12years, 61.5% alcohol-related, median MELD-Na 18.8 (16.3- 24.3)]. There were 34(28.3%) patients with CCM at presentation. Twenty-four patients subsequently developed refractory ascites (18.4%), and 22(16.9%) patients developed at least 1 episode of HRS-AKI on 1-yr follow up. Overall mortality was 22(17%) at 1 year. When adjusted for age, gender, presence of diabetes, and etiology of liver disease, MELD-Na (aHR 1.3,95%CI: 1.2-2.4, P<0.001), NT-proBNP (aHR 1.1, 95% CI: 1.01-1.31, P=0.032), low Cardiac index at presentation (aHR 0.9, 95%CI:0.7-0.9, P=0.022) and Cystatin C (aHR 1.2, 95%CI: 1.1-3.2, P<0.001) predicted 1-year mortality. IVC dynamics showed poor association with diuretic response or HRS-AKI. CCM markers, namely, septal E/e’ representing filling pressures (aHR 1.3, 95%CI: 1.3-4.3, P=0.033) and e’ representing myocardial relaxation (aHR 0.98, 95%CI 0.7-0.9, P=0.045) were predictive of development of HRS-AKI on follow up. A reduction in cardiac index by 24% at 7 days predicted poor diuretic response, and preceded fall in mean arterial pressure. On adjustment for MELDNa, presence of CCM at baseline was associated with subsequent HRS-AKI [OR 3.2, 95%CI: 1.9-6.8, P<0.001) and mortality [OR 4.1, 95%CI: 1.4-9.6, P=0.012), but did not predict risk of refractory ascites.

Conclusion:

Cirrhotic cardiomyopathy is independently associated with HRS-AKI and 1-year mortality in patients with cirrhosis and ascites. Impaired cardiac index, which can represent undiagnosed CCM, may limit the potential for resolution of ascites. POC-Echo can predict prognosis and may inform therapeutic strategies in cirrhosis with ascites.