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

Abstract

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. We compared NT-proBNP and cTnI concentrations as well as POCUS findings in dogs presented with cNHA and ncNHA. Dogs (n = 60) were enrolled based on identification of NHA with an effusion packed cell volume < 10%. 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). 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). NT-proBNP concentration and POCUS help distinguish between cNHA and ncNHA.