17-year-old male athlete

  • Achiahu Ludomirsky, MD
  • +Author Affiliations

    1. From the Division of Cardiology, Departments of Pediatrics (D.B.H., G.K.S., E.K.R., A.L.) and Internal Medicine (J.B.), Washington University School of Medicine, St. Louis, Mo.
    1. Correspondence to Gautam K. Singh, MD, Division of Pediatric Cardiology, Campus Box 8116, One Children’s Place, St. Louis, MO 63110. E-mailsingh_g@kids.wustl.edu

    A previously asymptomatic 17-year-old male athlete presented with acute onset of left-sided chest pain that awakened him from sleep. The pain was described as “crushing,” radiated to the left arm and jaw, and associated with diaphoresis. He was evaluated in the emergency department of our hospital and was found to have an abnormal ECG with ST-segment elevation in the anterolateral leads (Figure 1A). Initial troponin I and creatine kinase-MB (CK-MB) were elevated, 5.7 ng/mL (0 to 1.4) and 29 ng/mL (0 to 7), respectively. Urine toxicity screen was negative, and chest x-ray was unremarkable. Supplemental oxygen, aspirin, and morphine sulfate were administered for cessation of chest pain. Approximately 6 hours after admission, he experienced a second episode of similar chest pain, which did not respond to morphine sulfate but did subside with sublingual nitroglycerin. An echocardiogram at that time confirmed a structurally normal heart but wall motion abnormality by tissue synchronization imaging of the apical segments of the left ventricle, indicative of ischemia in the left anterior descending artery territory (Figure 2A). Emergent cardiac catheterization demonstrated normal coronary arteries by angiography (Figure 3) and no evidence of myocarditis by endomyocardial biopsy and viral serologies.

     

    Figure 1. Selected electrocardiograms demonstrate (A) ST-segment elevation during and (B) return of ST segment to baseline with T wave inversion after resolution of chest pain in lateral chest leads.

    Figure 2. Two-chamber 2D echocardiographic view and tissue synchronization imaging demonstrate (A) abnormal systolic segmental wall motion during acute chest pain in left anterior descending perfusion territory represented by orange color map in comparison with synchronous wall motion of the rest of left ventricle represented by uniform green color map. Velocity traces from multiple regions of interest confirm asynchrony of apical segment of left ventricle (violet). (B) Return of synchrony of segmental wall motion of left ventricle during systole, represented by uniform green color map and velocity traces in all segments after resolution of chest pain.

    Figure 3. Normal (A) left and (B) right selective coronary angiograms.

    Successful treatment included nitroglycerin and calcium channel blocker. Cardiac enzymes gradually returned to normal, and follow-up ECG and echocardiogram demonstrated resolution of ST elevation (Figure 1B) and normal segmental wall motion (Figure 2B), respectively. This was a rare case of Prinzmetal (variant) angina in an adolescent.