- Case Report
- Open Access
Acute myocardial infarction and syncope in an 18-year-old athlete with an abnormal origin of the left coronary artery: a case report
© licensee BioMed Central Ltd. 2009
- Received: 3 June 2009
- Accepted: 19 August 2009
- Published: 10 September 2009
We report a case of acute myocardial infarction and syncope in an 18-year-old athlete during high-performance exercise. A coronary arteriography and an angiographic computed tomography scan subsequently revealed a left coronary arterial origin from the right aortic sinus along with an intramural course of the left main stem. The patient was successfully treated with surgical unroofing of the left main stem from inside the aorta. To our knowledge, this is the first report demonstrating this type of anomaly pre- and postoperatively by use of angiographic computed tomography scan in the context of acute coronary syndrome.
- Angiographic Compute Tomography
- Sudden Cardiac Death
- Left Coronary Artery
- Left Main
- Coronary Arteriography
Coronary anomalies with a left coronary arterial origin from the right aortic sinus along with an intramural course of the left main stem have previously been described in autopsy materials from patients suffering a sudden cardiac death during high-performance exercise . Here, we report a case of exercise-related acute myocardial infarction in which this type of anomaly was demonstrated by means of angiographic CT scanning.
An 18-year-old Danish man of Ghanesian ancestry was admitted due to acute chest pain and a syncope occurring during vigorous exercise playing basket ball. The patient was unconscious for approximately one minute, and complained from sustained chest pain and dyspnea after regaining consciousness. There was no history of smoking or drug abuse. He had no previous medical history and no familial history of cardiovascular disease or sudden death; however, he had previously experienced episodes of chest pain and dyspnea without syncope during exercise.
Upon admission the patient had ongoing chest pain. Values for capillary oxygen saturation fluctuated between 82 and 94% with nasal oxygen supply. The arterial blood pressure was 70/40 mmHg, increasing to 125/75 mmHg after the administration of intravenous saline. There was no fever, and other vital signs were unremarkable. Chest examination demonstrated a regular heart rate (pulse 85) with no murmurs and normal breath sounds. The patient did not exhibit cyanosis or edema.
There were increases in coronary enzymes with a troponin T (TNT) of 0.25 μg/L (affirmative for myocardial infarction above 0.01 μg/L) and creatine kinase MB (CKMB) of 25 μg/L (affirmative for myocardial infarction above 5 μg/L). 12 hours later TNT and CKMB had increased further to 2.85 μg/L and 185 μg/L, and at 24 hours they had decreased to 1.80 μg/L and 68 μg/L, respectively. The leucocyte count was 15 × 109 cells/L, and CRP was normal. There were no signs of thrombophilia or coagulopathy.
A chest radiograph showed a mild enlargement of the heart and a minor diffuse infiltrate near the apex of the left lung. Subsequent chest radiographs were normal. Bedside transthoracal echocardiography showed no abnormalities.
Myocardial ischemia is generally believed to be the underlying cause of sudden cardiac death in relation to coronary anomalies [1, 3]-. The mechanistic link between a coronary anomaly and myocardial ischemia has been a matter of dispute -; both kinking of the coronary artery, flap-like closure of the abnormal slit-like coronary lumen, and compression of the coronary artery between the aorta and the pulmonary trunk have been suggested -. In the present case, the LM was located intramurally in the aortic tunica media, and the aortic expansion during exercise would therefore expectedly aggravate the narrowing of the LM and, in synergy with an increased myocardial oxygen demand, lead to myocardial ischemia.
A left coronary arterial origin from the right aortic sinus, and a right coronary arterial origin from the left coronary sinus are the most common congenital coronary malformations that have been described in autopsy materials from previously healthy athletes who suffered a sudden death [1, 6]. Furthermore, an intramural course of the left coronary artery in the aorta has been noted in several of the cases , and has previously been demonstrated in the context of exercise-related acute myocardial infarction . These malformations are associated with sudden cardiac death to a wider extent in competitive athletes than in non-athletes . This lends further support to the hypothesis that compression of the coronary artery during workout is a common pathogenetic link in exercise related death in these patients. In this context, the present case is unique, as it demonstrates this concept in the clinical setting of acute coronary syndrome with myocardial infarction by means of angiographic CT scanning.
The incidence of athletic field deaths ranges between 0.5 and 1.6 out of 100.000 young competitive athletes per year [6, 8]. The underlying diseases are mainly hypertrophic cardiomyopathy, arrythmogenic right ventricular dysplasia and congenital coronary malformations [6, 8]. As the latter is amenable to surgical correction, it is crucial to be aware of this cause of exercise-induced chest pain, dyspnea and syncope in healthy young subjects.
Written informed consent could not be obtained because the patient was lost to follow-up. Despite repeated attempts we were unable to trace the patient or his family. We believe this case report holds a worthwhile clinical lesson which could not be communicated effectively in any other way. Every effort has been made to keep the patient's identity anonymous. We would not expect the patient or his family to object to publication.
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