ReviewFrontiers in veterinary science2026
Early activation of Virchow's triad in feline hypertrophic cardiomyopathy: beyond spontaneous echo contrast and insights into translational thromboembolism.
Review 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, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Cardiovascular biomarkers in feline hypertrophic cardiomyopathy phenotype: evidence from the last decade.Veterinary research communications · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.