Pathophysiological Intersections Between Virchow's Triad and Type 2 Diabetes Mellitus: A Systematic Review
DOI:
https://doi.org/10.24859/SaberDigital.2026v19n2.1901Keywords:
Hypercoagulability, Inflammation, Insulin Resistance, Cardiovascular Risk, ThrombosisAbstract
Introduction: Type 2 Diabetes Mellitus (T2DM) is a chronic metabolic condition characterized by insulin resistance and persistent hyperglycemia, often associated with vascular complications. Virchow's Triad, composed of endothelial injury, blood stasis, and hypercoagulability, offers a conceptual model for understanding the mechanisms underlying thrombosis, which are frequently exacerbated in patients with T2DM. The interrelationship between these pathophysiological elements has relevant implications for cardiovascular and thromboembolic risk. Objective: This study aims to systematically review the scientific literature on the pathophysiological mechanisms connecting T2DM to Virchow's Triad, identifying shared risk factors and discussing clinical implications for the integrated management of these conditions. Method: A systematic review was conducted in the PubMed, Scopus, and Google Scholar databases, covering publications from the last ten years. Clinical studies, systematic reviews, and meta-analyses addressing the relationship between T2DM and the components of Virchow's Triad were included. Results and Discussion: Analysis of the studies revealed that T2DM is strongly associated with hypercoagulability, endothelial dysfunction, and changes in vascular hemodynamics. Insulin resistance, chronic low-grade inflammation, and oxidative stress contribute to the activation of thrombogenic pathways. The discussion emphasizes the importance of therapeutic strategies that simultaneously address glycemic control and the prevention of thromboembolic events, including the use of antithrombotic agents and lifestyle modifications. Conclusion: The intersection between T2DM and Virchow's Triad reinforces the need for a multidisciplinary and preventive approach in the care of patients at high cardiovascular risk. Understanding shared mechanisms can guide more effective and personalized interventions, with the potential to reduce vascular complications and improve clinical prognosis.
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