Key result
The pathophysiology of acute coronary syndromes correlates with Virchow's triad, leading to the identification of novel pharmacological agents targeting thrombus formation and plaque vulnerability.
Understanding ACS pathophysiology through the lens of Virchow's triad helps identify novel pharmacological targets for altering thrombus formation and plaque vulnerability.
May inform novel ACS antithrombotic strategies; leaves open prospective validation of targeted agents.
The acute coronary syndromes (ACS), which include unstable angina, non-ST-segment and ST-segment elevation acute myocardial infarction, all share common pathophysiology processes that are characterized by coronary plaque disruption with superimposed thrombus formation, leading to myocardial ischaemia. A greater understanding of these processes has enable us to correlate the abnormalities in arterial vessel wall substrates ('vessel abnormalities'), rheologic and biomechanical conditions ('abnormal flow'), and blood thrombogenicity ('abnormal blood constituents') to the contribution of coronary plaque disruption and subsequent thrombosis, with the basic concepts of Virchow's triad for thrombus formation (thrombogenesis) described about 150 years ago. This improved understanding has led to the identification of newer therapeutic targets and, hence, novel pharmacological agents targeting different components of Virchow's triad, particularly in altering thrombus formation and plaque vulnerability.
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Lee et al. (2003) conducted a review in Acute coronary syndromes. The pathophysiology of acute coronary syndromes correlates with Virchow's triad, leading to the identification of novel pharmacological agents targeting thrombus formation and plaque vulnerability.
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