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A Prothrombotic State in Patients With a History of Left Ventricular Thrombus
Michał Ząbczyk1, Rafal Meus1, Krzysztof Piotr Malinowski2
1Institute of Cardiology, Jagiellonian University Medical College, Cracow, Poland.
Insights
Patients with left ventricular thrombus (LVT) not linked to heart attacks exhibit a persistent prothrombotic state, increasing risks for recurrent LVT and cerebrovascular events. Compact clot formation predicts LVT recurrence.
Area of Science:
- Cardiology
- Hematology
- Thrombosis Research
Background:
- Left ventricular thrombus (LVT) is linked to hypercoagulable states, often following myocardial infarction (MI).
- Prothrombotic alterations in blood may predispose individuals to LVT formation, recurrence, and cerebrovascular events.
Purpose of the Study:
- To investigate the prothrombotic state in patients with LVT unrelated to recent MI.
- To identify predictors of LVT recurrence and associated thromboembolic events.
Main Methods:
- Studied 58 patients with LVT history (excluding recent MI or low ejection fraction) and 58 controls.
- Assessed plasma clot permeability, fibrinolytic efficiency, thrombin generation, and endothelial markers.
- Monitored LVT and thromboembolic events during follow-up.
Main Results:
- LVT patients showed more LV akinesia, heart failure, and a prothrombotic state (increased thrombin potential, lower antithrombin, lower clot permeability, longer lysis time).
- Recurrent LVT occurred in 10 patients (2.3%/year), associated with a higher stroke/TIA risk (RR=4.73).
- Compact clot formation (low clot permeability) predicted recurrent LVT (RR=4.67).
Conclusions:
- A persistent prothrombotic state characterizes patients with non-MI-related LVT.
- This state involves enhanced thrombin generation, hypofibrinolysis, and compact clot formation.
- These factors predispose to LVT recurrence and subsequent thromboembolic events.
Abstract:
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.
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