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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.
Insights
Inflammation is present in feline cardiomyopathies, especially in advanced stages (ACVIM C). Complete blood count markers like neutrophil:lymphocyte ratio (NLR) indicate this inflammation, but don
Area of Science:
- Veterinary Internal Medicine
- Cardiology
- Immunology
Background:
- Feline cardiomyopathy is a significant cardiac disease in cats.
- Inflammation is suspected to play a role in the pathogenesis of feline cardiomyopathies.
- Complete blood count (CBC)-derived inflammatory markers may offer insights into disease activity.
Purpose of the Study:
- To investigate inflammation using CBC and derived markers (neutrophil:lymphocyte ratio [NLR], monocyte:lymphocyte ratio [MLR], systemic inflammation response index [SIRI]) in cats with American College of Veterinary Internal Medicine (ACVIM) stages B and C cardiomyopathy versus healthy controls.
- To compare CBC and derived inflammatory markers between cats with cardiogenic pleural effusion and cardiogenic pulmonary edema.
Main Methods:
- Comparative study involving 66 cats with cardiomyopathy (ACVIM B and C) and 24 healthy cats.
- Statistical analysis included ANCOVA (with age as covariate) for group comparisons and t-tests/Mann-Whitney tests for effusion type comparisons.
- Evaluated white blood cell count, neutrophil count, NLR, MLR, and SIRI.
Main Results:
- Cats in ACVIM C stage showed significantly higher white blood cell and neutrophil concentrations than ACVIM B and control groups.
- ACVIM C cats had significantly elevated NLR, MLR, and SIRI compared to healthy cats.
- ACVIM B cats exhibited significantly higher NLR and SIRI than healthy cats. No significant differences in inflammatory markers were found between pleural effusion and pulmonary edema.
Conclusions:
- Results support the presence of systemic inflammation in feline cardiomyopathies, particularly in advanced (ACVIM C) stages.
- CBC-derived inflammatory markers, including NLR and SIRI, are elevated in feline cardiomyopathy.
- The type of fluid accumulation (pleural effusion vs. pulmonary edema) did not correlate with differences in measured inflammatory markers.
Abstract:
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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