Coronary Artery Dissection Associated with Exercise Myocardial Perfusion Scintigraphy

摘要

Exercise myocardial perfusion scintigraphy (MPS) is commonly performed to assess for ischaemic heart disease. The risks of MPS are primarily related to those of an exercise stress test (EST). The overall cardiac complication rate from maximal EST is very low and is estimated at 0.8 complications per 10, 000 tests1. Spontaneous coronary artery dissection (SCAD) is an infrequent cause of acute myocardial ischaemia with fewer than 300 cases described in the literature2. We describe a male patient with acute myocardial infarction from SCAD associated with MPS. Case report A 72-year-old man presented with recent onset of brief episodes of nocturnal crushing central chest pain. He had been generally well and active (undertaking regular walking exercise). Apart from age, his only other cardiac risk factor was previous heavy smoking history. He reached stage IV of conventional Bruce-protocol treadmill EST with total exercise duration of 9 min 30 sec, peak heart rate of 150 bpm (105% of predicted maximum heart rate (PMHR)) without chest pain. Stress ECG response was mildly abnormal with ST depression up to 1 mm at V4-V6.Further evaluation with rest/stress Tc-99m sestamibi MPS was performed 10 days later using a one-day protocol. He exercised on the treadmill using the same Bruce protocol for 6 minutes attaining a heart rate of 132 bpm (89% PMHR) with appropriate rise in blood pressure up to 170/80 mmHg. The test was terminated due to dyspnoea, fatigue and satisfactory heart rate response. The stress ECG showed equivocal abnormal response with slowly upsloping ST depression up to 1 mm in V3-V6, which normalised in recovery. Stress / rest SPECT images revealed a moderate sized, mainly fixed inferior perfusion defect from apex to base, of mild to moderate severity (green arrows, Fig. 1). Post-stress gated SPECT demonstrated normal-sized left ventricle with satisfactory wall motion and thickening. LVEF = 60%. The appearances could represent attenuation artefact in the inferior wall although a prior non-transmural myocardial infarct at this site could not be entirely excluded. No significant inducible myocardial ischaemia was evident.