• BNP3-32;
  • B-type natriuretic peptide biology;
  • Dilated cardiomyopathy;
  • Myxomatous mitral valve disease


In congestive heart failure (HF), plasma B-type natriuretic peptide (BNP) seems devoid of biological effectiveness. BNP1–32 could be truncated into BNP3–32 by dipeptidyl peptidase IV (DPP4), and BNP3–32 has reduced biological activities.


Increased DPP4 activity is associated with pathophysiology of HF.


One hundred twenty-eight client-owned dogs and 9 experimental Beagles from the Clinical Veterinary Unit of the University of Liège.


We prospectively measured plasma DPP4 activity in 5 groups of dogs: normal growing dogs (n = 21), normal adult dogs (n = 60), healthy Beagle (n = 9), dogs with myxomatous mitral valve disease (n = 35), and dogs with dilated cardiomyopathy (n = 12). The final diagnosis and the severity of HF were determined by Doppler echocardiography. Plasma DPP4 activity was measured kinetically by a fluorimetric method.


In growing dogs, DPP4 activity was higher than in adults (P < .001) and inversely correlated with age (r = −0.57, P < .01). In adults, DPP4 activity increased linearly with body weight (r = 0.39, P < .01), but there was no influence of age or sex. No effect of the circadian rhythm was noted. DPP4 activity was significantly higher in HF ISACHC I (16.3 ± 1.14 U/L) compared with healthy adults (12.4 ± 0.65 U/L, P < .05) and HF ISACHC III (11.0 ± 1.50 U/L, P < .05). Mean DPP4 activity in ISACHC II was 15.1 ± 1.4 U/L.

Conclusion and Clinical Importance

We did not find evidence that plasma DPP4 activity is responsible for the “BNP resistance” in overt congestive HF, but it may be implicated in early stages.