ArticleFrontiers in veterinary science2026
Prevalence of iron deficiency and its association with cardiac function in dogs with various stages of myxomatous mitral valvular disease.
Article in Frontiers in veterinary science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Quantitative mitral regurgitation and conventional echocardiographic variables in canine myxomatous mitral valve disease.Frontiers in veterinary science · 2026Article
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7 authors.
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Abstract
Introduction: Iron deficiency (ID) is known to increase cardiac workload and contribute to cardiac dysfunction in humans. However, its prevalence in canine heart disease remains poorly understood. Methods: This retrospective cohort study aimed to determine the prevalence of ID in dogs with myxomatous mitral valvular disease (MMVD) and evaluate its association with cardiac function. Dogs diagnosed with MMVD at the Veterinary Teaching Hospital of Nippon Veterinary and Life Science University between August 2020 and December 2025 were retrospectively evaluated. ID was assessed using transferrin saturation (TSAT) as a marker of iron metabolism. Dogs were stratified into three groups according to TSAT levels. Data from physical examinations, hematological and biochemical analyses, and echocardiographic assessments were analyzed. Statistical analyses were conducted to evaluate intergroup differences and correlations between TSAT levels and clinical variables. Results: ID was identified in 12% (9/84) of the dogs. Dogs in the ID group demonstrated significantly higher stroke volume and cardiac output compared with those in the normal-TSAT group. In addition, TSAT was significantly and inversely correlated with cardiac output. Discussion: These findings indicate that ID is present in a subset of dogs with MMVD and is associated with increased cardiac output, likely reflecting reduced systemic vascular resistance. This hemodynamic alteration may represent a potential risk factor for the development of high-output heart failure in this population.
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