Early activation of Virchow's triad in feline hypertrophic cardiomyopathy: beyond spontaneous echo contrast and insights into translational thromboembolism.

The hypertrophic cardiomyopathy (HCM) phenotype is closely associated with arterial thromboembolism (ATE). The pathophysiology of ATE is linked to activation of Virchow's triad, characterized by endothelial injury, blood stasis, and hypercoagulability. Together, these factors create a prothrombotic microenvironment that may precede overt clinical manifestations. Although spontaneous echocardiographic contrast (SEC) is widely used in clinical practice as a marker of thromboembolic risk, it should be regarded as a late finding. This review explores the early activation of Virchow's triad in cats with HCM phenotype, with emphasis on atrial remodeling, hemodynamic alterations, and endothelial dysfunction preceding detectable SEC. Evidence suggests that changes in left atrial appendage dynamics contribute to localized stasis, while systemic mechanisms, including platelet activation, thrombin generation, and inflammatory processes, promote a hypercoagulable state. Additionally, the presence of SEC should be interpreted as a biomarker of blood stasis rather than a causal factor. Reliance on SEC for thrombotic risk assessment reflects limitations in identifying the pre-thrombotic state, particularly due to the lack of standardized biomarkers for routine clinical use. Therefore, improved thromboembolic risk stratification in cats with HCM phenotype is needed. Overall, thrombogenesis in cats with cardiac disease is a dynamic, multifactorial, and progressive process that begins prior to detectable echocardiographic changes. A clearer understanding of these mechanisms may enable earlier identification of high-risk patients and support preventive therapeutic strategies. This review analyzes the early activation of Virchow's triad in cats with HCM phenotype and its relationship with atrial thrombus formation, with emphasis on thrombogenic mechanisms preceding SEC and their implications for ATE.