Posters
Academic Level (Author 1)
Resident
Discipline/Specialty (Author 1)
Internal Medicine
Academic Level (Author 2)
Medical Student
Discipline Track
Clinical Science
Abstract
Introduction: Ischemic cardiomyopathy is defined by the American Heart Association (AHA) as cardiomyopathy caused by ischemic heart disease. The most common complication of ischemic cardiomyopathy is systolic congestive heart failure. Heart failure patients are in a hypercoagulable state that predisposes them to develop intracardiac thrombus. The incidence of LV thrombus in patients with dilated cardiomyopathy and sinus rhythm is 13% with the clot in the left atrial appendage in 68% of these cases. The thrombus formation results from impaired blood flow within the 4 chambers of the heart and can present as a life-threatening complication of end stage heart failure. Herein, we present a case of a 61-year-old gentleman with ischemic cardiomyopathy who presented with multiple intracardiac thrombi.
Case: 61-year-old man with known history of ischemic cardiomyopathy from severe two-vessel coronary artery disease with chronic occlusion of the proximal LAD and proximal RCA presented to the emergency department due do dyspnea. Physical examination remarkable for JVD and bibasilar crackles. ECG was remarkable for sinus rhythm with evidence of old anterior wall myocardial infarction which was asymptomatic. An echocardiogram showed evidence of a severe ischemic cardiomyopathy and severely impaired systolic function with an ejection fraction of 20% and multiple thrombus including a 2.7x 3.6 cm LV apical mural thrombus, 1.3x 3.3 cm RV apical mural thrombus, and a 1.6x 2.2 cm left atrial mural thrombus. The patient was admitted for acute decompensated biventricular heart failure with signs of pulmonary congestion and poor tissue perfusion. The hypercoagulable workup for antithrombin, homocysteine levels, factor 5 Leiden, antiphospholipid, protein c, protein s states were unremarkable. The patient was treated with diuretics, heparin and was eventually bridged to warfarin. Patients' dyspnea improved and he was discharged with warfarin with recommendations to follow up closely with his cardiologist. Follow up 2D Echo with contrast demonstrated an LVEF of 20-25% and complete resolution of all thrombi.
Conclusion: The management of ischemic cardiomyopathy with multiple intracardiac thrombi requires an individualized approach. The specific treatment plan will depend on various factors, including the size and location of the thrombi, the underlying cause, and the patient's overall health. Diagnosing multiple thrombi in ischemic cardiomyopathy is important for risk assessment, treatment planning, prevention of embolic events, and long-term monitoring to optimize patient care and prevent complications. Further studies in patients with sinus rhythm and ischemic cardiomyopathy with reduced left ventricular function should be done to see if they benefit from being treated with anticoagulation.
Presentation Type
Poster
Recommended Citation
Garcia Cruz, Jian and Perez Rodriguez, Julio, "Multiple Intracardiac Thrombi in a patient with Ischemic Cardiomyopathy" (2024). Research Colloquium. 46.
https://scholarworks.utrgv.edu/colloquium/2024/posters/46
Included in
Multiple Intracardiac Thrombi in a patient with Ischemic Cardiomyopathy
Introduction: Ischemic cardiomyopathy is defined by the American Heart Association (AHA) as cardiomyopathy caused by ischemic heart disease. The most common complication of ischemic cardiomyopathy is systolic congestive heart failure. Heart failure patients are in a hypercoagulable state that predisposes them to develop intracardiac thrombus. The incidence of LV thrombus in patients with dilated cardiomyopathy and sinus rhythm is 13% with the clot in the left atrial appendage in 68% of these cases. The thrombus formation results from impaired blood flow within the 4 chambers of the heart and can present as a life-threatening complication of end stage heart failure. Herein, we present a case of a 61-year-old gentleman with ischemic cardiomyopathy who presented with multiple intracardiac thrombi.
Case: 61-year-old man with known history of ischemic cardiomyopathy from severe two-vessel coronary artery disease with chronic occlusion of the proximal LAD and proximal RCA presented to the emergency department due do dyspnea. Physical examination remarkable for JVD and bibasilar crackles. ECG was remarkable for sinus rhythm with evidence of old anterior wall myocardial infarction which was asymptomatic. An echocardiogram showed evidence of a severe ischemic cardiomyopathy and severely impaired systolic function with an ejection fraction of 20% and multiple thrombus including a 2.7x 3.6 cm LV apical mural thrombus, 1.3x 3.3 cm RV apical mural thrombus, and a 1.6x 2.2 cm left atrial mural thrombus. The patient was admitted for acute decompensated biventricular heart failure with signs of pulmonary congestion and poor tissue perfusion. The hypercoagulable workup for antithrombin, homocysteine levels, factor 5 Leiden, antiphospholipid, protein c, protein s states were unremarkable. The patient was treated with diuretics, heparin and was eventually bridged to warfarin. Patients' dyspnea improved and he was discharged with warfarin with recommendations to follow up closely with his cardiologist. Follow up 2D Echo with contrast demonstrated an LVEF of 20-25% and complete resolution of all thrombi.
Conclusion: The management of ischemic cardiomyopathy with multiple intracardiac thrombi requires an individualized approach. The specific treatment plan will depend on various factors, including the size and location of the thrombi, the underlying cause, and the patient's overall health. Diagnosing multiple thrombi in ischemic cardiomyopathy is important for risk assessment, treatment planning, prevention of embolic events, and long-term monitoring to optimize patient care and prevent complications. Further studies in patients with sinus rhythm and ischemic cardiomyopathy with reduced left ventricular function should be done to see if they benefit from being treated with anticoagulation.