tetano
Editor, Senior Moderator
Am J Case Rep
. 2025 Sep 19:26:e949609.
doi: 10.12659/AJCR.949609. Severe Left Ventricular Thrombus in the Context of Heart Failure and COVID-19: A Case Report
Jochebet Irene[SUP] 1 [/SUP], Teuku Muhammad Haykal Putra[SUP] 2 [/SUP], Wahyu Aditya Soedarsono[SUP] 2 [/SUP], Wishnu Aditya Widodo[SUP] 2 [/SUP], Raja Ezman Raja Shariff[SUP] 3 [/SUP]
Affiliations
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.
. 2025 Sep 19:26:e949609.
doi: 10.12659/AJCR.949609. Severe Left Ventricular Thrombus in the Context of Heart Failure and COVID-19: A Case Report
Jochebet Irene[SUP] 1 [/SUP], Teuku Muhammad Haykal Putra[SUP] 2 [/SUP], Wahyu Aditya Soedarsono[SUP] 2 [/SUP], Wishnu Aditya Widodo[SUP] 2 [/SUP], Raja Ezman Raja Shariff[SUP] 3 [/SUP]
Affiliations
- PMID: 40968506
- DOI: 10.12659/AJCR.949609
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.