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1-on-1 with the Widowmaker
Ali Shabestari, DO, Amr Badawy, DO, Mark Curato, DO.
Department of Emergency Medicine
St. Barnabas Hospital, 4422 3rd Avenue, Bronx, NY 10457
Case History
A 22 year old African-American male with a no past medical history was brought in by EMS after
he developed sudden chest pain while playing the basketball. The pain was described as
crushing, substernal, constant, nonradiating, and associated with shortness of breath, nausea,
and one episode of vomiting. The patient had no prior episodes of similar symptoms. The
patient reported his father had a heart attack in his 50's. He reported a history of occasional
marijuana use, and denied history of cocaine use. Physical exam revealed a young, athletic
male who was anxious and in moderate distress. He was diaphoretic, holding a clenched fist
over his chest and mildly tachypneic at rate of 24. The remainder of the exam and vital signs
were normal.
An electrocardiogram (EKG) was obtained (Figure 1).
Figure 1: ST elevations in the anterolateral leads with reciprocal depressions in the
inferior leads
The patient was given aspirin, sublingual nitroglycerin, heparin, and clopidogrel. Then taken
immediately for cardiac catheterization.
Background
In the United States, acute coronary syndrome (ACS) secondary to ischemic heart disease is
the leading cause of death among adults. ACS refers to a spectrum of disease ranging from
ST-segment elevation myocardial infarction (STEMI) to non-ST segment elevation myocardial
infarction (NSTEMI,) and unstable angina. Diagnosis is traditionally based on history, risk factor
1
stratification, EKG and cardiac biomarkers. There are many scoring tools that have been
developed to help aid the emergency provider in making the diagnosis, and more importantly
excluding those that are low-risk as candidates for discharge from the emergency department.
These scoring tools include the TIMI score, HEART score, Vancouver chest pain rule, and
EDACS score.
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3
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5
Discussion
Acute myocardial infarction in patients younger than 45 years is usually associated with low
mortality rates, less extensive coronary artery disease (CAD), and a favorable prognosis.
Studies reveal that risk profiles in young patients are typically different than older patients.
Younger patients more commonly have a smoking history and a family history of ischemic heart
disease. Some genetic polymorphisms affecting lipoprotein metabolism have also been
implicated. Other etiologies include anatomic anomalies and spontaneous coronary artery
dissection.
6,7,8,9
10,11
12,13
Using the available scoring tools, this patient would have had a TIMI score of 1, which is a lowrisk but still carries 4.7% risk of bad outcome. This patient had a HEART score of 4, which
would have placed the patient in the moderate risk, however the HEART score includes the
EKG in its scoring and with a normal or nonspecific repolarization disturbance the HEART score
would have been 2-3, or in the low-risk range This patient would have been excluded from the
Vancouver chest pain rule and EDACS score based on his initial ischemic EKG. If this patient
presented with an equivocal or nondiagnostic EKG, he would have been considered low-risk
and discharged from the emergency department with the support of the available risk
stratification scoring tools and potentially led to a bad outcome.
2
3
4,5
Conclusion
Our patient was found to have 100% occlusion of his proximal left anterior descending artery
which was successfully dilated and stented. Examination of the left ventricular wall motion
revealed akinesis of the anterolateral and apical walls. The initial troponin level was
undetectable, and after 6 hours was 77 ug/l. His LDL was slightly elevated at 178 mg/dL, while
the remainder of the lipid profile was within normal limits. Echocardiogram post-infarction
revealed ischemic cardiomyopathy with an ejection fraction of 35%. A post-PCI EKG was
obtained (Figure 2).
Figure 2: Markedly improved with some residual ST elevation in anterior leads
Rheumatological and hypercoagulability work-up did not reveal any abnormalities. Patient’s
myocardial infarction was attributed to premature atherosclerosis possible due to familial
dyslipidemia. Patient doing well at follow up with hopes of playing basketball once again.
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2011
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