Acute Myocardial Infarction in a Young Man Complicated ... - J-Stage

Acute Myocardial Infarction in a Young Man Complicated With Left Ventricular Thrombi Chia-Pin LIN,1 MD, Feng-Chun TSAI,2 MD, Pao-Hsien CHU,1 MD, Shih-Ming JUNG,3 MD, Kun-Eng LIM,4 MD, Chi-Tai KUO,1 MD, and Ying-Shiung LEE,1 MD SUMMARY Premature coronary artery disease is very rare and complication with thrombus formation in the left ventricle is rarer still. A 23-year-old man was admitted to hospital for recent acute myocardial infarction after being struck by a basketball eight days previously. Echocardiography identified two peduncle thrombi at the apex of the left ventricle, which were confirmed with computed tomography. The proximal left anterior descending coronary artery was totally occluded. Following two weeks of treatment with heparin and warfarin, the patient agreed to undergo a coronary artery bypass graft and thrombectomy. The ecchymosed tissue around the coronary artery implied that a trauma injury might have been the cause of the coronary artery disease in this case. This work reviews the pathophysiology and natural history of coronary artery disease in a case of very young myocardial infarction. (Jpn Heart J 2004; 45: 1029-1035) Key words: Acute myocardial infarction, Young, Left ventricular thrombi, Trauma

PREMATURE coronary artery disease (CAD), variously defined as an age of onset from 30 to 45 years,1-6) recently has increased markedly. This work describes an unusually young case of acute myocardial infarction (AMI) complicated with left ventricular thrombi in a 23-year-old male who was treated successfully by anticoagulation, coronary artery bypass graft (CABG), and thrombectomy. The pathophysiology and natural history of premature CAD are also reviewed. CASE REPORT A previously healthy 23-year-old male complained of mild chest pain after being struck by a ball while playing basketball eight days previously. The patient experienced a transient ischemic attack (TIA) involving sudden loss of vision and From the 1Division of Cardiology, Department of Internal Medicine, 2Division of Thoracic & Cardiovascular Surgery, Department of Pathology, and 4Department of Radiology, Chang Gung Memorial Hospital, Taipei 105, Taiwan. Address for correspondence: Pao-Hsien Chu, MD, First Cardiovascular Division, Department of Internal Medicine, Chang Gung Memorial Hospital, 199 Tun-Hwa North Road, Taipei 105, Taiwan. Received for publication January 30, 2004. Revised and accepted July 2, 2004. 1029 3

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lasting for five minutes the day before admission. No exertional dyspnea, general malaise, abdominal fullness, nocturnal cough, strokes, fever, weight loss, or leg edema was noted. Moreover, his past and family history were free of smoking, hypertension, diabetes, anemia, renal disease, Kawasaki disease, drug addiction, hyperlipidemia, premature cardiovascular disease, and congenital heart disease. Physical examination revealed a body height of 170 cm, body weight of 78 kg, blood pressure of 130/85 mm Hg, and a pulse rate of 78 beats per minute. Electrocardiogram revealed significant Q waves in leads V1-V5 and low voltage in the limb leads. Cardiac isoenzymes were all normal (peak creatinine kinase of 58 U/ L, without MB fraction; and sequential cardiac troponin-I below 4 mg/dL). Abnormal serologic tests included slightly raised cholesterol of 204 mg/dL (normal range, below 200 mg/dL), LDL/HDL ratio of 3.60 (normal range, below 3.55 in males), high-sensitive CRP of 2.46 mg/L (normal range: 1.27 mg/L less than 50 years old) and homocysteine of 15 µmole/L (normal range, below 12 µmole/ L); and slightly depressed protein-C of 67% (normal range, 75-107%). Other laboratory findings were all normal, including protein-S, triglycerides, anti-ANA antibody, anticardiolipin antibody, and syphilis. There were no extracardiac sounds, but a grade 2/6 systolic murmur was heard at the left ventricular apex. No family history of coronary artery disease was identified. Two-dimensional echocardiography revealed mild mitral regurgitation, apical and anteroseptal wall motion akinesia, and adequate left ventricular systolic performance. No other evidence of pericarditis was found. Two peduncular, irregular thrombi were found at the apex of the left ventricle (Figures 1A and 1B). Emergent chest and brain computed tomography revealed apical thrombi (Figure 1C) without aortic dissection or brain stroke. Thrombolytic therapy was not administered because over 12 hours had passed since the onset of infarction and TIA, but heparin was administered to keep the activated partial thromboplastin time (aPTT) at 1.5 to 2.0 times normal. Initial baseline aPTT was normal. Cardiac catheterization was performed one day after admission. Coronary arteriography showed total stenosis from the proximal part of the left anterior descending (LAD) coronary artery with thrombi. The right coronary vessel was patent. Furthermore, aortography displayed a normal aorta and normal carotid, renal, and femoral arteries. The patient initially refused surgery or other intervention. Consequently, conservative treatment was given, involving aspirin and warfarin to dissolve the left ventricular thrombi. He suffered a transient attack of slurred speech three days after admission. Surgery was advised again two weeks after admission since the persisting mobile and split thrombi posed a high risk for recurrent systemic emboli. Surgery revealed two thrombi measuring 15 × 14 × 13 mm and 3 × 2 × 1 mm with granulation tissue and fibrosis (Figure 2). The left internal thoracic artery was grafted

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Figure 1. The two protruding thrombi (arrowhead and arrows) on the left ventricular apex were demonstrated based on a two dimensional echocardiogram (A: The apical four-chamber view; B: The parasternal long-axis view) and computed tomography. Ao = aorta; LV = left ventricle; RV = right ventricle.

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Figure 2. The histological studies of thrombi (T) demonstrate ventricular cardiomyocytes (C) with granulation tissue (G) with fibrosis (F) (A, × 100; B and C is the higher-magnification view from the punch and asterisk sign area each from A, ×200, hematoxylin and eosin stain)

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to the mid-LAD, and some ecchymosis was demonstrated around the vessel. The postoperative course was uneventful and the patient was discharged on warfarin and aspirin therapy. The patient remained free of thrombi throughout the series of follow-up echocardiographs. DISCUSSION Young onset AMI is increasing, and commonly has a favorable prognosis in the short- and medium-term.3,5,6) One-third of patients with acute anterior wall infarction develop left ventricular apical thrombi, but this condition previously has only been rarely reported among youth.7) This report describes an unusually young case of AMI complicated by left ventricular thrombi that was treated successfully using CABG and thrombectomy. Male sex and smoking are two key risk factors for premature CAD.1-6) Additionally, the unique etiologies of premature CAD should be considered in cases of young AMI, including congenital coronary abnormality, Kawasaki's disease, and systemic lupus erythematosus (Table I).8-11) The ecchymosed tissue around the LAD in this patient might hint at the trauma caused by the basketball even without direct evidence. The slightly elevated homocysteine and depressed protein-C in this patient also require follow-up despite the lack of evidence of a family history of premature coronary disease. Most previous investigations have found a high incidence of single-vessel disease among young patients.1-6) Angioplasty combined with stenting or CABG is safely and effectively applied in most cases. The importance of hemostasis in the pathogenesis of AMI has been firmly established, and the gene polymorphisms involved in the premature CAD have been elucidated (Table II).12-22) However, the interpretation of polymorphism for premature onset AMI requires further evaluation. Left ventricular thrombus is a common complication of AMI. Mobile thrombi have the highest risk of systemic embolization, especially during the early phase following AMI.7,23-26) Therapeutic options for such thrombi include antithrombotic, anticoagulant therapy, thrombolysis, or surgical removal of the thrombus. Protruding thrombi are associated with high incidences of embolization.24,25) Thrombectomy following AMI complicated by protruding thrombosis is well recognized but limited among youth. However, recurrence of thrombosis and embolism following surgical thrombectomy is rare.7) The present patient was treated by thrombectomy due to recent recurrent minor strokes, the presence of two large protruding mobile thrombi, and the need for CABG. His postoperative course was uneventful and warfarin therapy was maintained. We have recommended that the patient remain on anticoagulants for life to prevent recurrence.

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Table I. Etiologies of Coronary Artery Disease in the Young Atherosclerosis Spasm or myocardial bridges Embolism or thrombosis 1. Nephrotic syndrome 2. Sickle cell anemia 3. Essential thrombocytosis 4. Myxoma 5. Pheochromocytoma 6. Infective endocarditis 7. Protein S and/or protein C deficiency Coronary dissection 1. Spontaneous 2. Trauma Drugs and intoxicants 1. Cocaine 2. Pills and hormone supplements 3. Glue sniffing Coronary arteritis 1. Kawasaki’s disease 2. Takayasu’s disease 3. Systemic lupus erythematosus 4. Primary antiphospholipid syndrome 5. Mycotic arteritis Congenital coronary abnormality 1. Coronary aneurysm 2. Coronary artery fistulas 3. Origin of the left coronary artery from the pulmonary artery 4. Congenital coronary stenosis or atresia 5. Origin of the coronary artery from the contralateral sinus with passage between the aorta and the right ventricular outflow tract Others 1. Radiation 2. Heart transplantation 3. Human immunodeficiency virus 4. Electrocution 5. William’s syndrome 6. Bland-White-Garland syndrome 7. Thyrotoxicosis 8. Trauma

Conclusion: The analytical results presented in this study indicate that early

thrombectomy should be considered for a left ventricular protruded, mobile thrombus in youth. The etiologies of premature CAD still require further evaluation.

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Table II. Possible Relationship Between Prothrombotic Gene Polymorphism and Myocardial Infarction in Youth 1. Angiotensin-converting enzymes 2. Angiotensin receptor 3. Apolipoprotein 4. Coagulation 5. Endothelial nitric oxide 6. Fibrinolysis 7. Glycoprotein 8. Homocysteine metabolism 9. Matrix metalloproteinase-3 promoter 10. Platelet function 11. Tumor growth factor-beta

ACKNOWLEDGEMENT Dr Chu was supported by grants NHRI-EX91-9108SC, NHRI-EX92-9108SC, and NHRI-EX93-9108SC from the National Health Research Institutes, Taiwan.

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