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Severe Left Ventricular Thrombus in the Context of Heart Failure and COVID-19: A Case Report
Jochebet Irene1, Teuku Muhammad Haykal Putra2, Wahyu Aditya Soedarsono2
1Clinical Research Unit, Jakarta Heart Center, Jakarta, Indonesia.
Insights
Left ventricular thrombus (LVT) can severely impair heart function and increase mortality. This case highlights how large LVTs, potentially linked to COVID-19, can worsen heart failure despite anticoagulation, leading to fatal outcomes.
Area of Science:
- Cardiology
- Internal Medicine
Background:
- Left ventricular thrombus (LVT) is a serious complication of heart failure and myocardial infarction.
- LVT significantly impairs cardiac function and increases mortality risk.
- Poor hemodynamics and blood stasis are key factors in LVT development.
Purpose of the Study:
- To report a case of massive LVT in a patient with acute decompensated heart failure.
- To illustrate the clinical course and challenges in managing large LVTs.
- To explore the potential role of COVID-19 in LVT formation.
Main Methods:
- Transthoracic echocardiography for LVT identification and volume estimation.
- Clinical assessment of heart failure symptoms and response to treatment.
- Review of patient history, including recent COVID-19 infection.
Main Results:
- A 59-year-old woman presented with severe dyspnea and a massive LVT (140 mL).
- Diuretics improved congestive symptoms, but anticoagulation failed to resolve the thrombus.
- The patient's condition deteriorated, leading to death from low cardiac output syndrome.
Conclusions:
- Large LVTs significantly worsen heart failure and hemodynamics, contributing to mortality.
- COVID-19 infection may increase the risk of hypercoagulable states and thrombus formation.
- Management of massive LVT in heart failure remains challenging.
Abstract:
BACKGROUND Left ventricular thrombus (LVT) is a common complication of heart failure and acute myocardial infarction. A peak mortality rate of 27.9% for LVT has been reported, especially among patients with severe LV systolic dysfunction. Poor hemodynamics and blood stasis contribute to the development of LVT by disrupting normal blood flow, which promotes thrombus formation. Conversely, LVT significantly impairs cardiac function, resulting in reduced stroke volume, decreased cardiac output, and an increased risk of systemic embolism, stroke, cardiovascular events, and mortality. CASE REPORT We report a case of a 59-year-old woman presenting with severe dyspnea. Acute decompensated heart failure was diagnosed. A massive LVT occupying over half of the left ventricle was identified on transthoracic echocardiography. The estimated volume of the thrombus was 140 mL, calculated using the end-diastolic volume formula from echocardiography. Presumably, the condition was precipitated by a previous infection of COVID-19. An aggressive diuretic strategy relieved her congestive symptoms. However, intravenous anticoagulation, overlapped with oral anticoagulant, did not alter the thrombus. The patient's condition deteriorated significantly, resulting in multiple episodes of rehospitalizations and eventual death due to low cardiac output syndrome in her last 3 months of follow-up. CONCLUSIONS This case underscores the impact of large thrombi on LV performance and hemodynamics exacerbating heart failure symptoms, and finally leading to severe complications and mortality. The patient's SARS-CoV-2 infection likely contributed to the hypercoagulable state and thrombus formation.
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