A Prothrombotic State in Patients With a History of Left Ventricular Thrombus

Left ventricular thrombus (LVT) is associated with a hypercoagulable state and occurs most frequently after myocardial infarction (MI). Blood prothrombotic alterations might predispose to LVT formation, its recurrence, and subsequent cerebrovascular events. We investigated 58 patients with a history of LVT unrelated to recent MI or LV ejection fraction <25% and 58 well-matched control subjects. We determined plasma clot permeability, fibrinolytic efficiency, thrombin generation, and endothelial markers after 3 to 6 months of anticoagulant treatment. During follow-up we recorded LVT and thromboembolic events. Patients with LVT more often had LV akinesia, congestive heart failure, and prothrombotic state as evidenced by increased endogenous thrombin potential, lower antithrombin, lower clot permeability, and longer clot lysis time associated with lower antiplasmin, higher plasminogen activator inhibitor-1, thrombin activatable fibrinolysis inhibitor, and von Willebrand factor. During follow-up (57.5 ± 8.1 months for LVT patients and 59.6 ± 5.3 months for controls) strokes, transient ischemic attacks, or LVT occurred in 18 (31%) LVT patients and in 6 (10.3%) control subjects (4.1 vs 1.4% per year, p = 0.006). LVT recurred in 10 (2.3%/year) patients, who had higher risk of stroke/transient ischemic attacks (relative risk = 4.73, 95% confidence interval 1.8 to 40.4). The most compact clot formation at baseline, defined as the lowest quartile of clot permeability (≤5.4 × 10−9 cm2) was a predictor of recurrent LVT (relative risk = 4.67, 95% confidence interval 1.32 to 18.37). This study shows that a persistent prothrombotic state involving enhanced thrombin generation, hypofibrinolysis, and formation of more compact fibrin clots characterizes patients who develop LVT not related to MI and those prone to its recurrence. Left ventricular thrombus (LVT) is associated with a hypercoagulable state and occurs most frequently after myocardial infarction (MI). Blood prothrombotic alterations might predispose to LVT formation, its recurrence, and subsequent cerebrovascular events. We investigated 58 patients with a history of LVT unrelated to recent MI or LV ejection fraction <25% and 58 well-matched control subjects. We determined plasma clot permeability, fibrinolytic efficiency, thrombin generation, and endothelial markers after 3 to 6 months of anticoagulant treatment. During follow-up we recorded LVT and thromboembolic events. Patients with LVT more often had LV akinesia, congestive heart failure, and prothrombotic state as evidenced by increased endogenous thrombin potential, lower antithrombin, lower clot permeability, and longer clot lysis time associated with lower antiplasmin, higher plasminogen activator inhibitor-1, thrombin activatable fibrinolysis inhibitor, and von Willebrand factor. During follow-up (57.5 ± 8.1 months for LVT patients and 59.6 ± 5.3 months for controls) strokes, transient ischemic attacks, or LVT occurred in 18 (31%) LVT patients and in 6 (10.3%) control subjects (4.1 vs 1.4% per year, p = 0.006). LVT recurred in 10 (2.3%/year) patients, who had higher risk of stroke/transient ischemic attacks (relative risk = 4.73, 95% confidence interval 1.8 to 40.4). The most compact clot formation at baseline, defined as the lowest quartile of clot permeability (≤5.4 × 10−9 cm2) was a predictor of recurrent LVT (relative risk = 4.67, 95% confidence interval 1.32 to 18.37). This study shows that a persistent prothrombotic state involving enhanced thrombin generation, hypofibrinolysis, and formation of more compact fibrin clots characterizes patients who develop LVT not related to MI and those prone to its recurrence.