A 36-year-old man presented with continuous chest pain for one hour. He had been treated in Nephrology for acute renal infarction. No thrombotic or embolic source was found on trans-esophageal echocardiography, abdominal CT angiography, and serologic tests including protein C, protein S, anti-phospholipid antibody and anti-nuclear antibody. His initial EKG showed pathologic Q wave and ST elevation in lead II, III, and aVF (Fig.1). The levels of cardiac enzymes were elevated: CK 1,537 U/L (35-172), CK-MB 36.6 U/L (2.3-9.5) and troponin-I 0.58 ng/mL (0-0.05). Emergent coronary angiography (CAG) revealed diffuse spastic narrowing of the left anterior descending coronary artery (LAD) and right coronary artery (RCA), but no significant stenosis was detected (Fig. 2A and 2B). There was no regional wall motion abnormality and his ejection fraction was 69.8% on echocardiography. On follow angiogram for ergonovine stimulation test, diffuse stenosis in left main to distal-LAD with spontaneous type B dissection of proximal LAD extending to left main and mid-LAD were detected (Fig. 3), These finding was also existed in IVUS (Fig.4A), and cardiac CTA (Fig. 4B, 4C). We decided to treat with medical therapy because he had no chest pain. Three days later, he complained of severe chest pain with 3-fold increase of CK-MB (4 U/L ' 14.1 U/L) and markedly troponin-I (0.03 ng/mL ' 2.20 ng/mL). His EKG showed tall T wave in V2-4 with Q wave in II, III, aVF. Emergency CAG revealed dissection in LM to m-LAD and p-LCx with poor distal flow and spasm in distal LAD. We decided to perform percutaneous coronary intervention (PCI) for these lesions, deployed Cypher stents (Cordis Corp, Johnson & Johnson, Miami Lakes, Fla) 3.5 x 18mm for p-LCx, 3.5 x 28mm for LM to p-LAD, 3.5 x 33mm for m-LAD and 3.0 x 33mm for d-LAD. Final CAG remained small dissection in d-LAD stent edge (Fig. 5A and 5B). Apico-septal wall akinesia was detected and his ejection fraction was 60% on echocardiogram after PCI. The follow up CAG and renal angiogram was performed 6 months later. CAG showed patent Cypher stents, and no significant stenosis in both renal artery.
The incidence of spontaneous coronary artery dissection (SCAD) was very rare. SCAD was frequently occurred in young women with peripartal period. There are a few reports about SCAD associated with vasospasm. Mark et al reported a patient with variant angina combined with SCAD in RCA lesion. In other reported case, SCAD occurred in the LAD with vasospasm in RCA. In our case, spontaneous dissection was present in both LAD and RCA, which were considered as culprit for vasospastic angina. However, dissection of LAD could be considered as procedure-related because the first angiogram showed no definite dissection in LAD. There are some reasons that we consider spontaneous dissection rather than iatrogenic origin. The first of all, spontaneous dissection was also present in proximal RCA, which was far from catheter engaged site. Dissection flow was started in proximal LAD, which also far from catheter engaged site, and then extended to left main, and mid-LAD.