Acute myocardial infarction in a 14-year-old male with normal coronary arteries.

To the Editor: Acute myocardial infarction may occur when the coronary arteries are normal or nearly normal. In patients with normal coronary arteries, there is strong evidence for the participation of thrombus formation in the pathogenesis of myocardial infarction. Coronary artery spasm may also play a role in initiating coronary occlusion and infarction. There is strong evidence to suggest that smoking is an important predisposing risk factor for myocardial infarction in the presence of normal coronary arteries. We report a case of acute myocardial infarction in a young patient, with smoking implicated as a precipitating factor. This case illustrates the relationship between cigarette smoking and myocardial infarction in the absence of coronary artery disease.

A 14-year-old boy presented to the hospital with the sudden onset of severe chest pain waking him from sleep in the early hours of the day. He smoked 30 cigarettes a day and there was no family history of premature coronary artery disease. There was no history of alcohol intake or illicit drug use. At admission to the hospital, his vital signs were normal and stable. The physical examination was entirely negative. Troponin I was significantly elevated. Complete blood cell count was normal. Cholesterol was 156 mg %, HDL was 52 mg %, LDL 90 mg %, and triglycerides were 68 mg %. Electrocardiography showed acute anterior myocardial infarction. He was treated with thrombolytic therapy and was placed on low-molecular-weight heparin, aspirin, metoprolol and nitroglycerin. Coronary angiography performed seven days after presentation showed no evidence of obstructive coronary artery disease. On echocardiography, wall motions were normal. The patient was discharged on the ninth day of hospitalization. Scintigraphic studies revealed slightly decreased uptake in the anteroapical area due to fibrosis, but no significant dyskinesia or perfusion deficits. A stress test performed at 1, 6, and 12 months after discharge were electro-cardiographically negative. After discharge, the patient's coagulation studies, which consisted of lupus anticoagulant, protein C activity, protein S activity, antithrombin III activity, and homosistein levels, were normal.

Discussion

The leading cause of myocardial infarction in patients with coronary artery disease is plaque rupture. The prevalence of myocardial infarction in young men, ages 14 to 40 years, is approximately 1%. (1) In adolescents, the diagnosis of acute myocardial infarction often requires evaluation to exclude numerous causes other than atherosclerosis and plaque rupture.

In our case, the coronary angiography revealed normal coronary arteries, or "MINC," (normal coronary arteries with myocardial infarction). The pathogenetic mechanism of myocardial infarction in patients with normal coronary arteries remains unknown. Smoking is a commonly identified risk factor in young patients with normal coronary arteries suffering from myocardial infarction. It has been shown that there is increased platelet consumption in young smokers without clinical evidence of coronary artery disease. This relation is presumably related to the mechanism of enhanced platelet aggregation and adhesion seen after smoking cigarettes that would be expected to increase the thrombotic risk in smokers with normal coronary arteries. (2) In people using cocaine and amphetamines as recreational drugs, there is evidence to suggest that cocaine-induced coronary spasm can lead to thrombosis and acute myocardial infarction in patients with normal coronary arteries. (3) Myocardial bridging is usually asymptomatic, but has been related to acute myocardial infarction in patients as young as 15 years in the absence of risk factors for coronary artery disease and without evidence of coronary atherosclerosis. (4) Coronary artery embolism secondary to infective endocarditis is a known etiologic factor in the production of acute myocardial infarction in the presence of normal coronary arteries, as is the situation of coronary arterial embolism resulting from passage of peripheral venous thromboemboli by way of a patent foramen ovale. Disorders of the coagulation system should be considered when any suspicion of idiopathic thrombosis or embolism appears possible, including a protein C deficiency, protein S and antithrombin III activity. (5) Protein C activity, protein S and antithrombin III activity was normal in our case.

In conclusion, coronary artery spasm related to endothelial effects of cigarette smoking is a possible mechanism of acute myocardial infarction. The diagnosis of acute myocardial infarction should be seriously considered in all young smokers. Failure to consider thrombolytic therapy may result in extensive myocardial infarction and impairment of left ventricular function. Evaluation requires extensive investigation into the various risk factors that may be involved, as well as the performance of invasive and noninvasive cardiovascular studies.

Ersan Tatli, MD

Huseyin Surucu, MD

Ozcelik Fatih, MD

Department of Cardiology

Trakya University School of Medicine

Edirne, Turkey

References

1. American Heart Association: 1999 Heart and Stroke: Statistical Update. Dallas, American Heart Association, 1999.

2. Giroux R, Giroux SK. [Myocardial infarction with normal or near normal coronary arteries: late outcome of seven patients]. Can J Cardiol 2000;16:162-166.

3. Carson P, Oldroyd K, Phadke K. Myocardial infarction due to amphetamine. Br Med J (Clin Res Ed) 1987;294:1525-1526.

4. Chee TP, Jensen DP, Padnick MB, et al. Myocardial bridging of the left anterior descending coronary artery resulting in subendocardial infarction. Arch Intern Med 1981;141:1703-1704.

5. Manzar KJ, Padder FA, Conrad AR, et al. Acute myocardial infarction with normal coronary artery: a case report and review of literature. Am J Med Sci 1997;314:342-345.