A 80-year-old male with a history of smoking and a family history of myocardial infarction presented with chest pain during exercise.There were no additional coronary risk factors, such as dyslipidemia, hypertension, or diabetes mellitus.

The electrocardiogram revealed no abnormalities, and echocardiography showed an ejection fraction (EF) of 64% with normal wall motion.Blood tests, including lipid levels, revealed no significant abnormalities.However, coronary CT angiography revealed diffuse, severe stenotic lesions with extensive calcification in all three main coronary arteries.

Coronary angiography revealed severe, heavily calcified stenosis in the proximal LAD. After stent implantation, OCT showed marked incomplete stent apposition at the proximal segment. During the OCT run, contrast extravasation emerged at the stent’s proximal edge, indicating perforation.

Lesion preparation was performed with rotational atherectomy (1.5mm burr) and 3.0mm balloon predilation were performed, followed by implantation of a 3.0×32mm Synergy drug-eluting stent (DES) in the proximal LAD. Post-stent OCT demonstrated notable incomplete stent apposition, so post-dilation with a 4.0-mm non-compliant balloon was undertaken, focusing on the proximal portion. During the subsequent OCT angiography run, new contrast extravasation was seen at the proximal stent edge consistent with coronary perforation. Immediate inflation of a 3.5-mm perfusion balloon across the injured segment secured hemostasis while maintaining distal flow. Extravascular hemorrhage gradually subsided, and the patient remained hemodynamically stable. Comparative OCT frames before and after the event revealed epicardial-side wall detachment and signal-free zones within perivascular adipose tissue. Notably, pre-dilation OCT at the same site showed loss of the normal three-layer architecture, suggesting local fragility that, combined with aggressive post-dilation in a calcified segment, predisposed the vessel to perforation.

OCT revealed the mechanism of perforation and its warning signs. These include wall detachment and extravascular signal loss at the perforation site, as well as pre-existing weakening of the arterial tri-laminar structure at the injury site. Recognizing these patterns may allow for more cautious post-dilatation management during the use of debulking devices for calcified coronary lesions.