N-terminal brain natriuretic peptide, cardiac troponin-I, and point-of-care ultrasound in dogs with cardiac and noncardiac causes of nonhemorrhagic ascites

Background: Nonhemorrhagic ascites (NHA) can be caused by cardiac diseases (cNHA) and noncardiac diseases (ncNHA). N-terminal brain natriuretic peptide (NT-proBNP), cardiac troponin-I (cTnI), and point-of-care ultrasound (POCUS) may differentiate between cNHA and ncNHA. Hypothesis/Objectives: We compared NT-proBNP and cTnI concentrations as well as POCUS findings in dogs presented with cNHA and ncNHA. Animals: Dogs (n = 60) were enrolled based on identification of NHA with an effusion packed cell volume < 10%. Methods: Blood samples were collected and POCUS was performed on all dogs. Dogs were diagnosed with cNHA (n = 28) or ncNHA (n = 32) based on echocardiography. The cNHA group was subdivided into cardiac non-pericardial disease (n = 17) and pericardial disease (n = 11). Results: The NT-proBNP concentration (median; range pmol/L) was significantly higher in the cNHA group (4510; 250-10 000) compared to the ncNHA group (739.5; 250-10 000; P =.01), with a sensitivity of 53.8% and specificity of 85.7% using a cut-off of 4092 pmol/L. The NT-proBNP concentrations were significantly higher in the cardiac non-pericardial disease group (8339; 282-10 000) compared with the pericardial disease group (692.5; 250-4928; P =.002). A significant difference in cTnI concentration (median; range ng/L) between the cNHA group (300; 23-112 612) and ncNHA group (181; 17-37 549) was not detected (P =.41). A significantly higher number of dogs had hepatic venous and caudal vena cava distension in the cNHA group compared to the ncNHA group, respectively (18/28 vs 3/29, P <.0001 and 13/27 vs 2/29, P <.001). Gall bladder wall edema was not significantly different between groups (4/28 vs 3/29, P =.74). Conclusions and Clinical Importance: NT-proBNP concentration and POCUS help distinguish between cNHA and ncNHA.