Association of myocardial parasitic load with cardiac biomarkers and other selected variables in 10 dogs with advanced Canine Leishmaniasis

Abstract

Background: The association between myocardial parasitic load (MPL) and cardiac biomarkers in Canine Leishmaniasis (CanL) has not been studied. Methods: Dogs with advanced CanL were prospectively recruited and were included if they were euthanised. Prior to euthanasia these variables were assessed: hematocrit, globulin, creatinine, N‐terminal‐pro brain natriuretic peptide (NT‐proBNP), cardiac troponin I (cTnI), blood pressure, urine protein/creatinine ratio and echocardiographic parameters. A left ventricular (LV) sample was taken for histopathology and MPL evaluation by quantitative PCR. Correlation of MPL with all variables was analysed. Dogs with lower and higher histopathology scores were compared. Results: Ten dogs were included. NT‐proBNP was 6946 pmol/ (interquartile range [IQR] 3751–9268 pmol/L) and cTnI 4.56 ng/mL (IQR 0.46–13.1 ng/mL). In all dogs, echocardiography showed an increase in LV thickening, and histopathology revealed moderate to severe lympho‐plasmocytic myocarditis and/or myocardial cell degeneration. MPL was 215.53 parasites/gram (IQR 21.2–1372.63 parasites/gram). A strong correlation (p < 0.001; R = 0.90; R20.81) with cTnI was observed but correlation with any of the other variables or differences between the two histopathological scores, were not detected. Conclusions: MPL in dogs with advanced CanL shows variable but generally high levels. A strong association between MPL and cTnI was observed, which encourages the exploration of cTnI as a marker in CanL.

Evaluation of heart fatty acid‐binding protein as a biomarker for canine leishmaniosis

“…HFABPc was not significantly different between healthy control dogs and dogs with leishmaniosis, and importantly, HFABPc was not elevated in dogs with very severe disease (stage IV of LeishVet). While it could be argued that dogs with milder forms of the disease might have variable myocardial involvement and therefore have less consistent results, it is well documented that most dogs at LeishVet stage IV have lymphoplasmacytic myocarditis 4,5,7–10 and parasitic presence in the myocardium as detected by myocardial PCR 10 . The absence of consistent elevation of HFABPc in these dogs with advanced disease, a group in which approximately 70% of dogs in this study had values below the elected reference threshold, discourages the exploration of this marker as a clinical tool for CanL.…”

“…This type of remodelling was observed for most dogs in this study. The cardiac remodelling in these cases is thought to be primarily due to myocarditis, with the myocardium being altered by inflammation and myocardial infiltration of inflammatory cells 9,10,22 . However, the presence of increased afterload due to systemic arterial hypertension and/or pseudohypertrophy in hypovolaemic patients may also play a role 9,10,22 .…”

“…The principal cardiac alteration in CanL is myocarditis (mostly lymphoplasmacytic), 4,5,7,8,10 which leads to a variable degree of myocardial damage 4,5,7,8,10,12 and makes HFABP a potentially adequate biomarker in CanL. An increase in left ventricular thickening and increased left ventricular mass (LVM) have been consistently reported in dogs with advanced CanL 9,10,22 . This is suspected to be secondary to myocarditis (oedema and inflammatory cell infiltration), although systemic arterial hypertension may also play a role 4,5,9,10,22 …”

“…An increase in left ventricular thickening and increased left ventricular mass (LVM) have been consistently reported in dogs with advanced CanL 9,10,22 . This is suspected to be secondary to myocarditis (oedema and inflammatory cell infiltration), although systemic arterial hypertension may also play a role 4,5,9,10,22 …”

“…Cardiac troponin I (cTnI) is a marker of myocardial damage 14 and has been shown to increase as the disease advances, 7,12 to be elevated in most dogs with advanced cardiac disease 6,7,10,12 and to correlate very strongly with the degree of myocardial parasitic load. 10 It is a promising biomarker in CanL, and further clinical field research is required to best define its clinical role. N-terminal proB type natriuretic peptide (NT-proBNP), a marker of acute and chronic increments of ventricular stress, 13,15 has also been shown to be increased in CanL, 9,12 although it is less consistently elevated at early stages of the disease.…”