Cardiopulmonary changes and its association with clinical features in noncirrhotic portal hypertension

Cardiopulmonary changes in noncirrhotic portal hypertension (NCPH) are poorly understood.

To investigate cardiopulmonary changes using transthoracic echocardiography (TTE) in NCPH and their correlation with clinical features.

Prospective cohort including 10 preclinical NCPH [without portal hypertension (PH)] and 32 NCPH subjects who underwent TTE with agitated saline injection and comprehensive clinical evaluation were assessed. PH was defined by presence of either varices, ascites or portosystemic shunting. Intrapulmonary vascular dilatation (IPVD) is defined as appearance of microbubbles in the left atrium after three heartbeats. Right ventricular systolic pressure (RVSP) > 38 mmHg was used to identify possible porto-pulmonary hypertension. Cardiomyopathy is defined using cirrhotic cardiomyopathy consortium criteria.

Among 42 subjects, 17 (40%) had IPVD, 4 (9.5%) had RVSP > 38 mmHg, and 6 (14%) had cardiomyopathy. Aspartate aminotransferase to alanine aminotransferase (AST/ALT) (1.3 vs 1, P = 0.04) and liver stiffness measurement (LSM) (12.4 kPa vs 7.1 kPa, P = 0.03) were higher in those with IPVD. Presence of either LSM > 10 or AST/ALT > 1.2 aided in identifying subjects with IPVD-sensitivity, specificity, and accuracy of 76%. RVSP correlated with oxygen saturation (r = -0.33), and free right hepatic vein pressure (r = 0.43). Those with PH had higher left atrial volume (LAV) (62 mL vs 48 mL, P < 0.01), and LAV index (LAVI) (35 m² vs 23 m², P < 0.01) compared to those without PH. Total bile acids, especially primary bile acids positively correlated with LAV (r = 0.36), and LAVI (r = 0.41).

Similar to cirrhotic patients, cardiopulmonary changes are prevalent in NCPH, especially among those with PH. In NCPH, cardiopulmonary changes occur despite preserved synthetic function, suggesting the NCPH model's value in understanding cardiopulmonary dysfunction in liver disease.