(Circulation. 1997;96:3201-3204.)
© 1997 American Heart Association, Inc.
Articles |
Myocardial Infarction Associated With Physical Exertion in a Young Man
From the Cardiology Service, Walter Reed Army Medical Center (A.J.T., M.F.), and the Department of Cardiovascular Pathology, Armed Forces Institute of Pathology (A.F., R.V.), Washington, DC.
Correspondence to Renu Virmani, MD, Chairperson, Cardiovascular Division, Armed Forces Institute of Pathology, Washington, DC 20306. E-mail virmani{at}mail.afip.ods.mil
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History (Michael Ferguson, MD) |
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 Top History (Michael Ferguson, MD) Initial Clinical FindingsSubsequent Hospital CourseClinical Discussion (Allen J....Pathological Findings (Andrew...Summary (Allen J. Taylor,...Final DiagnosisReferences |
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A 20-year-old man was admitted to an outside institution with chest pain, shortness of breath, and a syncopal episode. He had previously been in good health until 2.5 years earlier, when he developed presyncope associated with chest pain and shortness of breath during an army training exercise. An emergency room evaluation, which included a chest radiograph and an ECG, was normal. He continued to be bothered by fatigue and poor exercise capacity after this initial evaluation.
On the day of admission, the patient developed dizziness, palpitations,
central chest pressure, and shortness of breath after playing
basketball for 30 minutes. After leaving the court, he lost
consciousness for 
2 minutes, with spontaneous recovery. The patient
was transported to a nearby hospital with persistent chest pain.
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Initial Clinical Findings |
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TopHistory (Michael Ferguson, MD)Initial Clinical FindingsSubsequent Hospital CourseClinical Discussion (Allen J....Pathological Findings (Andrew...Summary (Allen J. Taylor,...Final DiagnosisReferences |
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On initial examination, the patient was diaphoretic and anxious. He had a blood pressure of 70/30 mm Hg, a heart rate of 103 beats per minute, and respirations of 24 breaths per minute. Physical examination revealed a well-developed man in mild distress. The lungs were clear. The cardiovascular examination revealed tachycardia, with a regular rhythm. On cardiac auscultation, the S1 and S2 were normal, and an S4 gallop was present. There was no jugular venous distension, and the carotid upstrokes were normal. The remainder of his physical examination was unremarkable. The initial ECG showed normal sinus rhythm with marked and diffuse ST segment depression and widening of the QRS complex in the precordial leads (Fig 1
). Continuous rhythm monitoring showed
occasional nonsustained ventricular ectopy. The patient's
hypotension rapidly resolved after resuscitation with
intravenous fluids. A diagnosis of an acute
coronary ischemic syndrome was made, and treatment with
intravenous heparin, intravenous
nitroglycerin, and lidocaine was begun. After gradual
resolution of his chest pain over several hours, the ECG reverted to
normal. On the next hospital day, physical examination revealed no new
findings. Serial creatine kinase determinations showed a peak creatine
kinase of 5326 IU/dL, including an MB fraction of 465 IU/dL (8.7%).
The patient was transferred to Walter Reed Army Medical Center.
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Subsequent Hospital Course |
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TopHistory (Michael Ferguson, MD)Initial Clinical FindingsSubsequent Hospital CourseClinical Discussion (Allen J....Pathological Findings (Andrew...Summary (Allen J. Taylor,...Final DiagnosisReferences |
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On transfer to our institution, the patient complained of chest pain with inspiration without recurrent angina pectoris or shortness of breath. Vital signs upon transfer showed a blood pressure of 138/78 mm Hg and a pulse of 93 beats per minute. Physical examination remained remarkable for the presence of an S4 gallop. Laboratory evaluation at the time of transfer included a creatine kinase of 6214 IU/dL (MB fraction, 315 IU/dL [5%]). Urine and serum drug screens were negative. An ECG showed normal sinus rhythm with new Q waves in leads V1 through V3 but no active ischemic changes.
The lidocaine infusion was stopped, and intravenous heparin
and nitroglycerin were continued. A bedside
echocardiogram showed severely depressed left ventricular
systolic function with relative sparing of the
inferior wall. The estimated left ventricular
ejection fraction was 15%. Shortly after arrival, the patient
developed dyspnea and bibasilar rales, which rapidly progressed and
required intubation and mechanical ventilation because of hypoxemia. An
ECG during this episode was unchanged. A Swan-Ganz catheter was placed,
with the following results: central venous pressure, 13 mm Hg;
pulmonary capillary wedge pressure, 14 mm Hg; and cardiac
index, 3.1 L · min-1 ·
m-2. The patient subsequently became
hypotensive and tachycardic, with an associated 2 mm of ST-segment
depression in the inferolateral leads. An intravenous
infusion of dopamine was begun, and emergent cardiac
catheterization was performed. Before coronary
angiography, an intra-aortic balloon pump was placed. Coronary
angiography demonstrated an anomalous origin of the left main
coronary artery (LMCA) from the right coronary cusp
(Fig 2). Important angiographic features
included a superior and anterior course of the anomalous LMCA in the
right anterior oblique projection, suggesting that the LMCA passed
between the aorta and pulmonary trunk. The crescent shape of
the coronary ostium indicated the presence of an ostial
valve–like ridge. Attenuation of the angiographic density of contrast
within the LMCA (so-called "gray banding") suggested
arterial narrowing along the aortic intramural course. The
coronary arteries were otherwise normal.
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At the conclusion of the catheterization procedure, ventricular fibrillation occurred. After a prolonged attempt at resuscitation, sinus rhythm was restored, and the patient was placed on femoral cardiopulmonary support. Despite maximal attempts at stabilization with intravenous and mechanical hemodynamic support, progressive coagulopathy and hypotension developed, and the patient died later that evening.
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Clinical Discussion (Allen J. Taylor, MD) |
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TopHistory (Michael Ferguson, MD)Initial Clinical FindingsSubsequent Hospital CourseClinical Discussion (Allen J....Pathological Findings (Andrew...Summary (Allen J. Taylor,...Final DiagnosisReferences |
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This young man developed chest pain and loss of consciousness during physical exertion, followed by evolution of an extensive myocardial infarction leading to cardiogenic shock and death. Numerous potential causes for sports-related cardiac death in the young have been identified, with severe atherosclerosis being most common, followed closely by hypertrophic cardiomyopathy.1 Other cardiac disorders associated with chest pain, sudden death, and possibly ECG changes in the young include myocarditis and both hypertrophic and dilated cardiomyopathy.1 2 3 In the present case, however, the findings of transient and extensive ECG changes, followed by evidence for extensive myocardial necrosis, are highly suggestive of ischemia arising from obstruction of the LMCA.
There are several potential causes of myocardial infarction associated with the LMCA in a young patient. Although obstructive coronary artery disease is the most important cause of myocardial infarction in the young, it would be unlikely in a 20-year-old man in the absence of familial hypercholesterolemia or history of tobacco use.4 5 Coronary spasm with or without associated cocaine use has been associated with myocardial infarction,6 7 although the toxicology screen was negative in this case. Other potential causes of LMCA obstruction include spontaneous coronary dissection,8 9 which is more common in women and often involves the left anterior descending coronary artery, and ascending aortic dissection involving the takeoff of the LMCA. Less common causes include traumatic thrombosis,10 coronary artery embolism,11 or arteritis involving either the coronary artery or aorto-ostial junction.12 No data are available to compare the relative importance of these potential, yet uncommon, causes of LMCA obstruction in the young.
Coronary angiography revealed the presence of an anomalous LMCA arising from the right coronary sinus. This particular anomaly is unique among coronary artery anomalies identified in adults because of its low prevalence13 14 but frequent association with sudden cardiac death. In a previous autopsy series published from our institution,15 an anomalous LMCA from the right coronary sinus was overrepresented as a cause of sudden cardiac death relative to other coronary artery anomalies. Although acute myocardial infarction can be a presenting manifestation of this anomaly, we have found sudden cardiac death, particularly associated with exercise, to be most common. Before presentation, patients with this anomaly have frequently (50%) been asymptomatic. When present, symptoms most commonly include chest pain and syncope, but they are not indicative of clinical outcome. The risk for sudden death when the LMCA arises from the right coronary sinus is perhaps the greatest of any coronary anomaly, involving 57% of patients in our series.
The most likely mechanism of sudden death in cases of anomalous LMCA arising from the right coronary sinus and coursing between the great vessels is due to impaired coronary flow reserve. This is postulated to occur secondary to one or more abnormalities in the initial coronary artery course, including a narrowed, slitlike coronary orifice, an acute angle of takeoff, and an aortic intramural course. To assess the relative importance of these various pathological variables, we recently performed a retrospective analysis of these anatomic features in cases of an anomalous coronary artery arising from the contralateral coronary sinus and coursing between the great vessels, including cases with and without associated sudden death.16 Because of marked interpatient variability of the pathological features, there was no single characteristic of the initial coronary artery course on postmortem pathological analysis, which was related primarily to clinical outcome. However, the overall importance of anomalous coronary arteries arising from the contralateral coronary sinus and coursing between the great vessels in causing sudden death is not in question, because these abnormalities have been found to be associated with sudden cardiac death, even in the absence of a coronary anomaly.17 Thus, when prospectively identified in a young patient (<30 years old), surgical repair is warranted. For the older patient with a similar coronary anomaly, the risk of sudden death seems to be less,15 and thus decisions on prophylactic surgical correction should be made on an individual basis, considering associated symptoms, the patient's desire to participate in competitive sports, concomitant coronary artery disease, and comorbidity, which may influence cardiac surgical risk.
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Pathological Findings (Andrew Farb, MD, and Renu Virmani, MD) |
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TopHistory (Michael Ferguson, MD)Initial Clinical FindingsSubsequent Hospital CourseClinical Discussion (Allen J....Pathological Findings (Andrew...Summary (Allen J. Taylor,...Final DiagnosisReferences |
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At autopsy, the heart weighed 445 g. Examination of the coronary arteries revealed an anomalous origin of the LMCA from the anterior portion of the right sinus of Valsalva. No thrombi or intimal disruptions were found. Features of the initial coronary artery course included an acute angle of takeoff and an ostial ridge of aortic wall tissue overlying and partially obstructing the LMCA orifice (Fig 3A
).
The LMCA coursed anteriorly between the aorta and main
pulmonary artery (Fig 3B).
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The heart was perfusion-fixed via the aortic stump for 30 minutes with
10% neutral buffered formalin from a height of 130 cm (equivalent to
100 mm Hg) and then sectioned. Gross examination after perfusion
fixation disclosed a large region of poor fixation, corresponding to
the perfusion bed supplied by the LMCA (Fig 3C
). The myocardial
sections were then fixed by immersion in formalin for 24 hours. Further
gross examination showed an acute, near-circumferential, focally
transmural myocardial infarction extending from base to apex involving
both papillary muscles, with relative sparing of the posterior left
ventricular wall (Fig 3D). The regions of poor perfusion
fixation and myocardial infarction were identical (Figs 3C and 3D).
Myocardial histological sections demonstrated
coagulation necrosis with areas of extensive contraction band necrosis
and focal neutrophil infiltration in the infarcted regions.
The precise mechanism of myocardial ischemia is uncertain in
this type of coronary artery anomaly. The regional myocardial pattern
of the initial perfusion fixation (Fig 3C) in the present case
offers insights into the relative significance of the acute-angle
takeoff and ostial ridge. Distension of the aortic root by perfusion
fixation at physiological pressure resulted in
fixation only of the epicardial surface (outer one third) of the
interventricular septum, anterior wall, and lateral wall;
the subendocardial and midmyocardial walls in these areas were
nonperfused and nonfixed. These myocardial regions of no flow during
perfusion fixation were consistent with the vascular bed of the
LMCA and corresponded precisely with the areas of infarction seen after
further immersion fixation. This finding indicates that compression of
the LMCA by the pulmonary trunk (which was not pressurized
during perfusion fixation), which is another proposed mechanism for
reduced coronary blood flow in this anomaly, is not necessary
to reduce myocardial blood flow. Rather, abnormalities in the initial
coronary artery course, which are subject to aortic pressure,
are of greater relative importance. Whether the course of the LMCA
between the aorta and the pressurized pulmonary trunk during
life can further compromise flow is unknown.
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Summary (Allen J. Taylor, MD) |
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TopHistory (Michael Ferguson, MD)Initial Clinical FindingsSubsequent Hospital CourseClinical Discussion (Allen J....Pathological Findings (Andrew...Summary (Allen J. Taylor,...Final DiagnosisReferences |
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Clinical findings suggesting widespread ischemia in a young patient should raise concern for an anomalous LMCA arising from the contralateral coronary sinus. The pathological findings in this case illustrate the mechanistic importance of abnormalities of the initial coronary artery course in these anomalies. The specific triggers contributing to the eventual clinical manifestations of this congenital anomaly remain to be elucidated.
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Final Diagnosis |
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TopHistory (Michael Ferguson, MD)Initial Clinical FindingsSubsequent Hospital CourseClinical Discussion (Allen J....Pathological Findings (Andrew...Summary (Allen J. Taylor,...Final DiagnosisReferences |
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Extensive myocardial infarction secondary to anomalous origin of the LMCA from the right coronary sinus.
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Footnotes |
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Presented at the Cardiovascular Pathology Conference, Cardiology Service, Walter Reed Army Medical Center, Washington, DC, February 22, 1997.
The Editor of Clinicopathological Conferences is Herbert L. Fred, MD, St Luke's Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, Room B524 (MC1-267), Houston, TX 77030-2697.
The opinions or assertions contained herein are the private views of the authors and are not to be construed as reflecting the views of the Department of the Army, the Air Force, or the Department of Defense.
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References |
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TopHistory (Michael Ferguson, MD)Initial Clinical FindingsSubsequent Hospital CourseClinical Discussion (Allen J....Pathological Findings (Andrew...Summary (Allen J. Taylor,...Final DiagnosisReferences |
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