This case highlights the rare but devastating complication of coronary and systemic embolization from intracardiac thrombi in severe dilated cardiomyopathy.
We present the case of a 25-year-old man with a 3-week history of worsening dyspnea, generalized weakness, and palpitations. Thyroid function tests showed thyrotoxicosis, and he was started on thyrostatic treatment. Electrocardiography (ECG) findings showed normal sinus rhythm with incomplete right bundle branch block and unspecific ST changes. Transthoracic echocardiography demonstrated a moderately dilated left ventricle, severe global hypokinesis with a left ventricular ejection fraction of 10%, and an apical thrombus (Figure). Echocardiography demonstrated a moderately dilated left ventricle, severe global hypokinesis, left ventricular ejection fraction 10%, and an apical thrombus (A, arrows). After readmission with decompensated heart failure, transthoracic echocardiography showed a large left atrial appendage thrombus (B, arrow) with unchanged left ventricular function. Coronary angiography demonstrated a normal, left dominant coronary circulation (C). One day later, the patient developed an acute ST-segment elevation myocardial infarction, and repeat angiography demonstrated an occluded proximal circumflex coronary artery with a rounded filling defect consistent with an embolus (D, arrow). The patient was noncompliant with anticoagulation and medical treatment and was readmitted 1 month after his initial presentation with decompensated heart failure (HF) (international normalized ratio [INR] 1.1). Transthoracic echocardiography now showed a large left atrial appendage thrombus and a left ventricular apical thrombus; left ventricular function remained severely depressed despite being biochemically euthyroid (Figure). Myocardial biopsy demonstrated nonspecific findings with no evidence of myocarditis. Coronary angiography demonstrated a normal, left dominant coronary circulation (Figure). Catheterization of the left ventricle was avoided. The following day, the patient developed severe chest pain. ECG showed changes of an acute inferoposterior ST-segment elevation myocardial infarction (MI). Emergent coronary angiography revealed an occluded proximal circumflex coronary artery with a rounded filling defect consistent with a coronary embolus (Figure). Intracoronary lytic therapy was not considered due to concerns over a systemic lytic state and further embolization from intracardiac thrombi. Revascularization was performed through direct coronary artery stenting using a bare metal stent with resolution of chest pain and ECG abnormalities. The patient had several subsequent admissions with HF, a low cardiac output state, and abdominal pain. During one of the admissions, abdominal computed tomographic findings showed embolic infarcts of the spleen and kidneys. Despite intensive efforts including counseling and psychiatric support, patient compliance remained inconsistent and he declined further interventions including right heart catheterization for tailored therapy as well as an implantable cardiac-defibrillator. He was not deemed to be a candidate for mechanical circulatory support or cardiac transplant due to his disruptive behavior and psychosocial problems. One year after the initial presentation, the patient presented with severe abdominal pain, respiratory distress, and altered mental status with a therapeutic INR. Abdominal computed tomographic findings showed multiple new embolic infarcts in his kidneys and spleen. Magnetic resonance imaging revealed embolic infarcts to the brain and atrophic cerebral degeneration. The patient developed multiorgan failure and died of cardiogenic shock several days later. Postmortem examination confirmed the presence of embolic infarcts to multiple organs, severely dilated cardiomyopathy, left ventricular thrombi, and multilobar pneumonia. Anticoagulation is not routinely recommended in patients with congestive HF, but is reserved for high-risk patients such as those with concomitant atrial fibrillation, previous thromboembolic events, severely impaired left ventricular function, and left ventricular thrombus and aneurysm.1 Evidence does not support the use of antiplatelet therapy to reduce the risk of stroke and thromboembolism in HF patients who are in sinus rhythm.2 The results of 2 ongoing studies will help to further define the antithrombotic management of patients with left ventricular dysfunction. The Heart Failure Long-Term Antithrombotic Study (HELAS) enrolled 6000 patients with New York Heart Association class II through IV HF secondary to MI, idiopathic dilated cardiomyopathy, or hypertensive heart disease and an ejection fraction of <35%.3 Patients with ischemic cardiomyopathy were randomized to warfarin (INR=2.0–3.0) or aspirin (325 mg) and patients with nonischemic cardiomyopathy were randomized to warfarin (INR=2.0–3.0) or placebo. Composite endpoints include death, MI, peripheral or pulmonary embolism, and nonfatal cardiogenic stroke. Another major study, the Warfarin vs Aspirin in Reduced Cardiac Ejection Fraction (WARCEF) trial aims to recruit 2860 patients with a left ventricular ejection fraction <30% randomized to aspirin (325 mg) or warfarin (INR=2.5–3.0), where primary endpoints include death, recurrent stroke, and intracranial hemorrhage.4 This case provides a rare direct demonstration of a coronary artery embolus and MI that arose in the setting of a dilated cardiomyopathy with known large intracardiac thrombi accompanied by subsequent multiorgan embolization. Systemic embolization remains an uncommon but potentially devastating complication of HF. Ongoing studies will clarify the role of anticoagulation in preventing thromboembolic events in these patients.
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Schulze et al. (2009) studied this question.
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