Atrial involvement in feline hypertrophic cardiomyopathy suggests a need for stage-anchored therapy decisionsHeart disease in cats may start in the upper chambers

Hypertrophic cardiomyopathy is the most common heart disease of cats and is conventionally characterised by its ventricular phenotype. The clinical events that determine quality and duration of life in affected cats, however, are atrial in their proximate pathophysiology. Congestive heart failure arises from elevated left atrial pressure transmitted to the pulmonary venous bed, arterial thromboembolism arises from blood stasis in a remodelled and dysfunctional left atrial appendage, and survival tracks left atrial size and function independently of left ventricular wall thickness. Recent longitudinal evidence indicates that lower left atrial fractional shortening can be detected before the diagnostic threshold for left ventricular hypertrophy is met, suggesting the atrium registers the disease before the ventricular wall-thickness criterion does. Despite this body of evidence, contemporary diagnostic frameworks, prognostic models, and the regulatory endpoint underpinning the recent conditional approval of delayed-release rapamycin remain anchored on the ventricle. This narrative review examines the atrial contribution to feline hypertrophic cardiomyopathy through five themes: atrial pathobiology, atrial imaging, atrial-driven outcomes, the implications for emerging disease-modifying therapy, and the practical implications for the cardiology consultation. We outline a framework for stage-anchored therapy decisions and a research agenda prioritising atrial trial endpoints and multicentre replication. In a disease affecting 14.7% of apparently healthy cats, with an 11.3% 10-year thromboembolic risk in preclinical cohorts, we propose that the atrium should now be at the centre of feline hypertrophic cardiomyopathy rather than at its periphery.