Evaluation of neutrophil:lymphocyte and platelet:neutrophil ratios and their prognostic utility in cats with hypertrophic cardiomyopathy and cardiogenic arterial thromboembolism.

Abstract

ObjectivesThe aim of the study was to compare the neutrophil:lymphocyte ratio (NLR) and platelet:neutrophil ratio (PNR) in cats with or without hypertrophic cardiomyopathy (HCM) and cardiogenic arterial thromboembolism (CATE) and to evaluate their prognostic significance in cats with HCM.MethodsHealthy cats and cats with HCM and CATE were prospectively enrolled between 2018 and 2020. Complete blood count and echocardiogram were performed. NLR and PNR were compared between cats in healthy, HCM and CATE groups. Outcome data, including cause of death, time to death and progression of HCM, were collected via review of medical record and owner interviews. Associations between time to cardiac-related mortality, NLR and PNR were analyzed using Kaplan-Meier curves and the Cox proportional hazards regression model.ResultsA total of 110 cats were enrolled, including 42 healthy cats, 57 cats with HCM (37 stage B1, 9 stage B2, 11 stage C) and 11 cats with CATE. Cats with CATE had the highest NLR (5.8, range 3.1-12.7) compared with HCM ( = 0.03) and healthy cats ( ⩽0.0001), while NLR was higher in cats with HCM (3.3, range 1.8-5.1) compared with healthy controls ( = 0.04). PNR was lower in cats with CATE (16.6, range 13.2-27.9) compared with healthy cats ( = 0.0027). Although PNR did not differ between cats in the healthy and HCM groups (>0.9), HCM-affected cats with PNR below 40 had a significantly lower median survival time (1093-1185 days) compared with those with PNR above 40 ( = 0.03). Cats with PNR below 40 at the time of HCM diagnosis also had a significant risk (hazard ratio 9.8; = 0.03) of cardiac-related mortality.Conclusions and relevancePNR is an accessible and cost-effective hematological biomarker that outperforms NLR and echocardiographic findings in cats with early subclinical HCM. Alterations in NLR and PNR in cats with HCM and CATE suggest a potential role of systemic inflammation in feline HCM.