A 50-year-old male patient visited Chonnam National University Hospital with a complaint of chest discomfort, exertional dyspnea, and nocturnal dyspnea for 6 months. Chest discomfort was aggravated with exertion, and relieved by rest. He had no past history of hypertension, diabetes mellitus, and familial history of coronary artery disease. He was an ex-smoker with 30-pack years. With the impression of stable angina pectoris, he checked cardiac CT at other hospital, which showed middle right coronary artery (RCA) dissection with soft plaque (Fig. 1). Initial laboratory finding showed elevated serum levels of creatine kinase 337 U/L, AST 65 U/L, and ALT 142 U/L. Lipid profile showed elevated serum levels of triglyceride 532 mg/dL, total cholesterol 209 mg/dL, low density lipoprotein-cholesterol (LDL-C) 121 mg/dL, and decreased serum level of high density lipoprotein-cholesterol (HDL-C) 26 mg/dL. Myocardial Single Photon Emission Computed Tomography (M-SPECT) showed reversible myocardial ischemia in inferolateral wall (Fig. 2). For the further evaluation and definitive treatment, coronary angiography (CAG) was planned.
CAG demonstrated type I coronary ectasia in RCA with focal dissection in mid part (Fig. 3). Focal dissection also seemed as double lumen coronary artery or plaque rupture in ectatic coronary artery. For the further evaluation, Intravascular ultrasound (IVUS) was performed. IVUS showed two large lumens in middle RCA. Intracoronary saline test performed to evaluate communication at each lumen and differentiate coronary artery dissection. It showed simultaneous saline passage at each lumen, which ruled out coronary artery dissection. Also further serial images showed huge plaque rupture in mid portion of ectatic RCA (Fig. 4). Fortunately, he had not developed acute myocardial infarction even with huge plaque rupture. Because he suffered from chest discomfort, and M-SPECT showed reversible myocardial ischemia in inferolateral wall which corresponded to RCA territory, we decided to perform percutaneous coronary intervention (PCI) in that lesion. Direct stenting with 5.0 x 24 mm bare metal stent (Liberte®, Boston-Scientific, US) was performed. Follow-up CAG and IVUS showed good stent apposition and expansion after stenting (Fig.5).
At discharge, the patient did not complain of chest discomfort any more. He was prescribed aspirin 300mg, clopidogrel 75 mg daily. Also he was prescribed rosuvastatin 10 mg plus nicotinic acid for dysplipidemia.
We report the presenting interesting PCI case, which initially seemed as spontaneous coronary artery dissection, and finally diagnosed as huge plaque rupture provoking myocardial ischemia.