Syncope During Stress Testing
A 66-year-old male with a history of hyperlipidemia, hypertension, degenerative joint disorder, and gastroesophageal reflux disease (GERD), presented with shortness of breath and palpitation. Baseline electrocardiogram (ECG) showed sinus rhythm with T wave changes that could be related to lateral wall ischemia (Figure 1).
Figure 1: Baseline ECG sinus bradycardia with T wave abnormalities due to possible lateral wall ischemia
Echocardiogram showed mild dilated left ventricle (LV) and mild global LV systolic dysfunction with a left ventricular ejection fraction (LVEF) of 43%. He underwent a treadmill pharmacologic myocardial perfusion stress test that was aborted due to syncope associated with ventricular arrhythmia (VA). Post stress test, he became unresponsive with accelerated idioventricular rhythm (Figure 2) lasting 1 minute and 21 seconds. His rest myocardial perfusion images showed perfusion defect in the basal lateral wall. Urgent left heart catheterization (LHC) showed non-obstructive coronary artery disease (CAD) with a LVEF of 30-35%.
Figure 2: Accelerated idioventricular rhythm post stress test
He was seen at our electrophysiology clinic where he was prescribed a wearable cardioverter defibrillator (WCD) and was initiated on guideline directed medical therapy (GDMT) for the treatment of heart failure (HF). Due to syncope and VA in the setting of unexplained LV dysfunction and the presence of perfusion defects unexplained by CAD, he underwent further evaluation of possible infiltrative and inflammatory myocardial disease with cardiac magnetic resonance (CMR) and positron emission tomography (PET). CMR imaging showed basal lateral scars with corresponding myocardial edema with sarcoidosis suggested in the differential diagnosis. CMR imaging as showing in Figure 3 (Panel A-D) demonstrates thinning and hypokinesis of the inferior basal wall (Panel A1*-2), T2 signal elevation (Panel B1-2*) and transmural infarct scar in the basal inferolateral wall (Panel C1-2, D1-2*).
PET scan showed hypermetabolic uptake in the lateral wall (Figure 3, Panel E1-2; arrows). This finding could be related to cardiac sarcoidosis (CS). There was a nodal uptake within the chest that is likely to be related to sarcoidosis. Blood work showed high serum angiotensin converting enzyme (ACE) activity, elevated serum lysozyme level and high serum soluble interleukin-2 receptor (sIL‐2R) levels.
Panel 2 – Three chamber long axis images
Panel A – Cine images
Panel B – T2 mapping
Panel C – Late gadolinium enhancement imaging
Panel D – Short inversion time late gadolinium enhancement imaging
Panel E - 18F-fluorodeoxyglucose positron emission tomography
High resolution computed tomography (CT) of the chest was reported as no hilar lymphadenopathy. There was one symptomatic non-sustained ventricular tachycardia on his on WCD.
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