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Patient initials or identifier number
Relevant clinical history and physical exam
A 48 year-old man visited emergency room with effort chest pain for 3 days. He had history of dyslipidemia and smoking as cardiovascular risk factors. Initial blood pressure was 137/88 mmHg and heart rate was 83/min.
Relevant test results prior to catheterization
The electrocardiogram revealed normal sinus rhythm without ST segment or T wave abnormality. Cardiac enzymes including of CK, CK-MB and troponin I were all within normal range.
Relevant catheterization findings
Coronary angiography demonstrated that left anterior descending artery (LAD) had 64% eccentric narrowing at proximal segment and 55% diffuse narrowing at middle segment. Left circumflex artery had multiple intermediate lesions. Right coronary artery showed significant up to 80% stenosis at proximal segment. (movie 1, 2 and 3).
First, the stenotic lesion at pRCA was treated with 4.0 x 15 mm Orsirostent. For LAD lesions, fractional flow reserve was performed to decide intervention. Adenosine induced hyperemic FFR was of 0.77 and continuous pull-back analysis showed greater pressure gradient across pLAD lesion rather than mLAD lesion. Index of micro vascular resistance (INR) was 19 (Fig. 1-A). We performed intracoronary imaging study with Intravascular ultrasound and Near-infrared spectroscopy (LipiScan, InfraReDx, Inc, Burlington, MA, USA) to evaluate the lesion at pLAD. The combined image revealed an echo-attenuated plaque with a large lipid core and the measured minimal lumen area (MLA) was 3.81 mm2 and the maximum 4-mm subsegment lipid-core burden index (maxLCBI4 mm) 332 (Fig. 2-A, B). For the lesion atpLAD, 3.5 x 18 mm Resolute Integrity stent was deployed at 16 atmospheres after dilating with 2.0/20 mm Genoss balloon at 9 atmospheres. The subsequent coronary angiography showed no-reflow phenomenon distal to the lesion site. After intracoronary adenosine bolus injection, coronary blood flow was restored (Fig 3). Post-stent imaging showed a reduced amount of yellow area with maxLCBI4 mm 248 and the IMR was increased to 84 (Fig. 1-B and Fig. 2-C, D). After PCI, a peak of CK, CK-MB, and Troponin I were elevated up to 528 U/L, 72.7 ug/L, and 29.8 ng/mL, respectively.
Distal embolization of disrupted lipid-rich plaque might be one potential mechanism of myocardial injury after stenting and the no-reflow phenomenon. Detection of lipid-rich plaque by combined near-infrared spectroscopy and IVUS could predict high risk of peri-procedural injury.