A Recreational Athlete with Sudden Cardiac Arrest and Coronary Artery Disease: Part I

A 29-year-old recreationally athletic male, prior collegiate basketball player and current high school physical education teacher, presented to his local hospital with chest pain exacerbated after exercise. Past medical history was notable only for Factor V Leiden heterozygous status (though no thromboembolic history and no family history of cardiovascular or thromboembolic disease). Evaluation included elevated troponin-I levels (peak 4.38 ng/mL, normal range 0.00 – 0.10 ng/mL), normal serial electrocardiograms (ECGs), and a normal trans-thoracic echocardiogram with normal left ventricular (LV) systolic function. A cardiac magnetic resonance (CMR) study revealed small, patchy areas of mid-wall late gadolinium enhancement (LGE) in the apical lateral segments , with LGE versus blood pool artifact in the basal septum and anterolateral papillary muscle (Figure 1). He was diagnosed with probable myocarditis and was discharged home with anticipation of clinical improvement and resolution of myocardial inflammation.

Figure 1: CMR scan at time of initial presentation, with LGE sequence demonstrating small, patchy areas of midwall LGE in the apical lateral segments, with LGE versus blood pool artifact in the basal septum and anterolateral papillary muscle.

Figure 1

Two months later, he developed chest pain after playing recreational soccer followed by cardiac arrest. He was shocked twice, restoring spontaneous circulation. At the emergency department (ED), an ECG showed anterolateral ST segment elevation. Emergent coronary angiography showed an occluded ostial left anterior descending (LAD) coronary artery with thrombus extending into the distal left main (LM) and ostial left circumflex (LCx) coronary arteries. Ventriculography revealed an ejection fraction (LVEF) of 30%. Aspiration thrombectomy was partially successful in removing the thrombus burden. Percutaneous coronary intervention was performed in the ostial/proximal LAD with placement of a drug-eluting stent.

He had a protracted hospital course, including prolonged intensive care unit (ICU) stay requiring extracorporeal membrane oxygenation (ECMO). On repeat catheterization, the LM thrombus was once again demonstrated but multiple attempts at aspiration were incompletely successful. A definitive etiology of the coronary thrombus was never identified. Review of intravascular ultrasound (IVUS) images from his catheterization suggested proximal LAD atherosclerosis with positive remodeling, raising the likelihood of his acute coronary syndrome being secondary to plaque pathology. Repeat echocardiograms showed LVEF in the mid-30s%, severe hypokinesis of the anterior, septal, and apical walls and no LV thrombus.

After a month-long hospitalization, a regadenoson stress CMR showed the LVEF improved to 38%, no ischemia, and less than 50% gadolinium enhancement in the LAD territory, suggestive of residual viability (Figure 2). As the patient was readied for transfer to an acute rehabilitation facility, the plan for risk stratification and safe rehabilitation/eventual return to participation in physical activity was discussed.

Figure 2: CMR scan at time of discharge post-myocardial infarction, demonstrating LVEF 38%, anterior/anteroseptal/apical hypokinesis and subendocardial LGE in the LAD territory comprising 25-50% of wall thickness, suggesting viable myocardium. The LGE noted in the previous CMR appeared to have resolved on this scan, with equivocal LGE versus blood pool artifact remaining in the anterolateral papillary muscle.

Figure 2

Given the reduced LVEF, residual LM thrombus post STEMI, and a possible episode of myocarditis 3 months ago, what would be the appropriate recommendation on rehabilitation (rehab) and return to his prior activities?

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