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Updated: Jun 12, 2025

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
Published on: September 9, 2012
A Rare Case of Left Ventricular Thrombus in a Normal Heart in a Patient With Factor V Leiden Disease
Rupesh Kshetri1, Pragya Pathak2, Prasanna Sugathan3
1Internal Medicine, University of Iowa Hospitals and Clinics, Iowa City, USA.
Insights
A left ventricular thrombus (LVT) was found in a patient with Factor V Leiden (FVL) disease, highlighting the need for anticoagulation. Early diagnosis and treatment of cardiac thrombosis are crucial for reducing complications.
Area of Science:
- Cardiology
- Hematology
Background:
- Left ventricular thrombus (LVT) is often linked to myocardial infarction and reduced ejection fraction.
- Hypercoagulable states, including Factor V Leiden (FVL) disease, also increase LVT risk.
- FVL disease elevates the risk of thromboembolism, such as pulmonary embolism and deep vein thrombosis.
Observation:
- A 60-year-old female with a history of heterozygous FVL and deep vein thrombosis presented with neurological and cardiac symptoms.
- Brain CT ruled out stroke; EKG showed sinus rhythm with T-wave inversion; troponin was mildly elevated.
- Transthoracic echocardiogram revealed a left ventricular mass causing outflow tract obstruction, despite normal ventricular function.
Findings:
- Surgical intervention confirmed the left ventricular mass as a thrombus.
- A normal-sized and functional left ventricle does not exclude the possibility of LVT.
- This case underscores the potential for LVT in patients with hypercoagulable conditions like FVL.
Implications:
- Long-term anticoagulation may prevent recurrent thromboembolic events in FVL patients with additional risk factors.
- Prompt diagnosis and management of cardiac thrombosis can significantly reduce patient morbidity and mortality.
- Consideration of LVT in patients with unexplained neurological or cardiac symptoms and hypercoagulable states is essential.
Abstract:
Left ventricular thrombus (LVT) is mostly associated with anterior wall myocardial infarction and reduced ejection fraction. It can also be associated with cardiomyopathy, myocarditis, and hypercoagulable states such as cancer, antiphospholipid syndrome, and protein C or protein S deficiency. Factor V Leiden (FVL) disease is one of the hypercoagulable states where mutant factor V is insensitive to natural anticoagulation factor protein C, and FVL disease increases the risk of peripheral thromboembolism such as pulmonary embolism (PE) and deep vein thrombosis (DVT). We report a 60-year-old female patient with a history of heterozygous factor V Leiden and a remote history of deep vein thrombosis who presented with left-sided weakness and intermittent chest pain. Computed tomography (CT) of the brain ruled out stroke, electrocardiogram (EKG) showed sinus rhythm and some new T-wave inversion, and troponin was mildly elevated. Other laboratory results were unremarkable. A transthoracic echocardiogram showed a left ventricular mass with left ventricular outflow tract (LVOT) obstruction in systole with normal systolic and diastolic function and no wall motion abnormalities. Emergent surgery proved to be a thrombus. The learning objectives of our case are that a normal-sized and functional left ventricle does not preclude left ventricular thrombosis, long-term anticoagulation therapy in patients with factor V Leiden and a first episode of thromboembolism with additional risk factors may prevent further serious thromboembolic event, and timely diagnosis and treatment of cardiac thrombosis may reduce morbidity and mortality.
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