Alcohol-Induced Cardiomyopathy Presenting with Left Ventricular Apical Thrombus ()
1. Introduction
Chronic excessive alcohol consumption has been strongly associated with alcohol-induced cardiomyopathy (AC). AC comes under a large group of dilated cardiomyopathies [1]. This diagnosis becomes important when patients present with heart failure symptoms and have negative work-up for coronary artery disease (CAD). Among heart failure patients, the prevalence of alcoholic cardiomyopathy varies from 4% to 40% with the age group of 40 to 60 appears to be the most affected [2]. Higher disease burden has been documented in men; however, women develop AC at a lower total dose of ethanol [2] [3].
Similar to other cardiomyopathies and heart failure, AC is also associated with complications and significant impact on the quality of life. We report a case of dilated cardiomyopathy with associated complications, necessary work-up and management.
2. Case Presentation
A 44-year-old male was admitted to our hospital with progressively worsening exertional dyspnea, orthopnea, scrotal swelling and lower extremity edema started 3 - 4 weeks prior to presentation. He reported no chest pain, palpitations, dizziness or syncopal episodes. His medical history was unremarkable, and he was not taking any medications. Family history was significant for CAD in his mother. Social history was significant for consuming at least a pack of 12 beers every day and 30-pack-years smoking.
On presentation, his vitals were significant for a pulse of 109/minute and blood pressure of 174/106 mmHg with systolic more than his baseline systolic range of 110 - 125 mmHg. He was tachypneic and had diffuse crackles over all lung fields. Heart sounds were normal with no murmur or gallop. There was no jugular venous distension; however, he had an edematous abdominal wall, scrotal swelling and 3+ pitting edema of the legs.
Pertinent blood work showed a troponin of 0.038 ng/mL and elevated BNP of 12,700 pg/mL with normal chemistries, electrolytes and hemogram. Table 1 Electrocardiogram showed normal sinus rhythm, rate 110/minute and no ischemic changes (Figure 1). Chest x-ray revealed cardiomegaly and pulmonary edema (Figure 2). A chest computed tomography (CT) with intravenous (IV) contrast showed cardiomegaly with a filling defect in the left ventricle (LV) apical region suspicious for a thrombus (Figure 3). Transthoracic echocardiogram (TTE) revealed biatrial enlargement and dilated bilateral ventricles with severely reduced LV ejection fraction (EF) < 15%, moderate tricuspid regurgitation, and a filling defect (1.8 × 1.3 cm) at the LV apex consistent with a thrombus (Figure 4). A cardiac catheterization was unremarkable for CAD.
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Table 1. Pertinent laboratory results.
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Figure 1. Electrocardiogram showed normal sinus rhythm, no significant ischemic changes.
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Figure 2. Chest x-ray posterior-anterior view revealed cardiomegaly and pulmonary edema. Cardiothoracic ratio (CTR) 0.65.
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Figure 3. A chest CT with IV contrast showed cardiomegaly with a filling defect (arrows) in the left ventricle apical region suspicious for a thrombus.
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Figure 4. Transthoracic echocardiogram with contrast Definity revealed dilated LV with severely reduced LV ejection fraction (EF) < 15%, and a filling defect (1.8 × 1.3 cm) at the LV apex consistent with a thrombus.
Patient was initially treated with an IV diuretic including furosemide. For LV thrombus, unfractionated heparin (UFH) infusion was initiated. During the course of hospitalization, he had appropriate diuresis and lost significant weight. Subsequently, he was able to ambulate without dyspnea. He was started on guidelines-directed medical therapy (GDMT) for heart failure with reduced ejection fraction (HFrEF) including diuretic, beta-blocker and angiotensin receptor-neprilysin inhibitor. UFH was bridged with warfarin on which he was discharged. Detailed alcohol and tobacco cessation counseling was provided. On repeat TTE within 4 weeks of discharge, his EF improved and there was no evidence of LV thrombus, Figure 5.
3. Discussion
Excessive ethanol use has been established as one of the leading causes of secondary dilated cardiomyopathy contributing to about 10% of all cardiomyopathies [4] [5]. Subclinical changes in cardiac function may begin after at least 5 years of high alcohol consumption (defined as >80 g/day) [6]. Acetaldehyde, a toxic metabolite, from ethanol is thought to cause oxidative stress within myocardium and impairment of myocyte protein synthesis. Simultaneously, there is activation of renin-angiotensin system and arterial hypertension that may contribute to or worsen heart failure. Symptoms appear when there is ventricular dilation and decreased ejection function. Echocardiography is the key diagnostic test for chambers quantification.
Several prospective studies have reported J-shaped relationship between alcohol and heart failure. Increased risk was noted at higher levels of alcohol intake while reduced risk was associated with low to moderate levels of alcohol consumption [7] [8] [9] [10].
Diagnosis of Alcohol-induced cardiomyopathy requires all three of the following:
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Figure 5. Transthoracic echocardiogram with contrast Definity revealed dilated LV with the absence of a filling defect noted in Figure 4.
1) Long-term heavy alcohol consumption (defined as >80 g/day over a period of at least five years).
2) LV dilation defined as LV end-diastolic volume or LV diastolic dimension > 2 standard deviations above normal (by echocardiography, an LVDD > 58.4 mm in men and >52.2 mm in women). [11] & LVEF below normal (<50% an accepted threshold for dilated cardiomyopathy) [12] [13].
3) Absence of hypertensive disease, valvular, and CAD.
Our patient fulfills the criteria for AC that incudes long-term heavy alcohol consumption, reduced EF, dilated LV as evidenced on TTE and absence of CAD based on cardiac catheterization.
In our patient, AC was complicated by LV apical thrombus. This was observed both on CT angiogram and TTE, and was treated with anticoagulation initially with heparin and subsequently bridged with warfarin. LV thrombus was not observed on repeat TTE 4 weeks later suggesting resolution of the thrombus (Figure 5). Patients with AC and LV thrombus not only need GDMT for HFrEF but also require anticoagulation for 3 - 6 months [3]. Warfarin has been a well-studied agent for this purpose [14]. Intracardiac thrombus such as LV thrombus is a complication of blood stasis in a dilated ventricle. In similar passion, alcohol-related dilated cardiomyopathy may predispose these patients to intracardiac thrombus necessitating anticoagulation.
4. Conclusion
Chronic excessive alcohol use is detrimental to cardiac function leading to alcohol-induced cardiomyopathy. A careful approach to clinical history of alcohol consumption and diagnostic workup negative for ischemic causes may confirm the diagnosis. A prompt diagnosis is recommended due to the risk of intracardiac thrombus. Cardiac function improves with GDMT for heart failure and abstinence from alcohol.
Informed Consent
The case was reviewed by the Institutional Review Board and informed consent was obtained from the patient.