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Updated: Jan 16, 2026

Tachycardia-Induced Cardiomyopathy As a Chronic Heart Failure Model in Swine
Published on: February 17, 2018
Evidence for chronic inflammation in cats with cardiomyopathies
Martina Krofič Žel1, Kunho Song2, Alenka Nemec Svete1
1Veterinary Faculty, Small Animal Clinic, University of Ljubljana, Ljubljana, Slovenia.
None:
ObjectivesThe study aimed to investigate the extent and type of inflammation using the complete blood count (CBC) and selected CBC-derived inflammatory markers (neutrophil:lymphocyte ratio [NLR], monocyte:lymphocyte ratio [MLR] and systemic inflammation response index [SIRI]) in cats with cardiomyopathy stages American College of Veterinary Internal Medicine (ACVIM) B and ACVIM C vs healthy cats. The second aim was to find any differences in CBC and CBC-derived inflammatory markers between cardiogenic pleural effusion and cardiogenic pulmonary oedema.MethodsFor comparison between the control, ACVIM B and ACVIM C groups, one-way analysis of covariance (ANCOVA) or Quade's non-parametric ANCOVA, with age included as a covariate, was used. The independent t-test or Mann-Whitney test was used for comparison of data between cats with pulmonary oedema and those with pleural effusion. A value of P ⩽0.05 was considered significant.ResultsA total of 66 cats with cardiomyopathy (33 ACVIM B and 33 ACVIM C) and 24 healthy cats were included in the study. Cats in the ACVIM C group had a significantly higher white blood cell concentration than those in the ACVIM B control groups. Cats in the ACVIM C group had significantly higher neutrophil concentration, NLR, MLR and SIRI than healthy cats. Cats in the ACVIM B group had a significantly higher NLR and SIRI than healthy cats. Cats with pulmonary oedema and cats with pleural effusion did not differ significantly in any of the investigated CBC and selected CBC-derived inflammatory markers.Conclusions and relevanceThese results support the presence of inflammation in feline cardiomyopathies, particularly in the ACVIM C stage. With the parameters used, no differences in the extent or type of inflammation between cardiogenic pulmonary oedema and pleural effusion was demonstrable.
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