Optical Coherence Tomography (OCT) evaluation of culprit lesions in patients with Non-ST Elevation Acute Coronary Syndromes (NSTE-ACS)

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Background OCT is an excellent tool to determine plaque morphology in Acute Coronary Syndromes. While plaque rupture has been determined to be the dominant morphology in ST Elevation Myocardial Infarction, there is paucity of literature in NSTE-ACS, which includes Non–ST Segment Elevation Myocardial Infarction (NSTEMI) and Unstable angina (UA). Purpose To characterize culprit lesion morphology by OCT in NSTE-ACS and to evaluate the frequency of each type of lesion in patients presenting with NSTEMI and UA. Methods In this single-centre observational study, OCT imaging of culprit lesion was acquired during coronary angioplasty of culprit lesions of 50 patients presenting with NSTE-ACS between August 2020 to July 2021. A comparison of the frequency of each type of lesion between NSTEMI and UA was performed. Results OCT of culprit vessel in the entire cohort of NSTE-ACS showed plaque erosion in 32% (n=16), plaque rupture in 32% (n=16), tight stenosis in 26% (n=13) and calcific nodule in 10% (n= 5) patients. Lipid plaque was seen in a higher number of patients with plaque erosion and plaque rupture (93.8% and 87.5% respectively). Comparison of the frequency of these lesions in NSTEMI and UA, revealed that among NSTEMI patients (n=25), 48% had plaque erosion, 36% had plaque rupture, 12% had tight stenosis and 4% had calcific nodule whereas, among UA patients (n=25), 16% had plaque erosion, 28% had plaque rupture, 40% had tight stenosis and 16% had calcific nodule. There was a statistically significant increase in plaque erosion in NSTEMI compared to UA (p=0.015) while tight stenosis was significantly more common in UA (p=0.024). Similarly, red thrombus and spotty calcium (p=0.002 and 0.008 respectively) were higher in NSTEMI compared to UA. There was no significant difference in frequency of thin cap fibroatheroma, macrophages, cholesterol crystals, white thrombus, and neovascularization among the two groups. Conclusions OCT provides unique insights into the mechanisms of NSTE-ACS. In our study plaque erosion and plaque rupture were both equally seen in patients presenting with NSTE- ACS. However, NSTEMI patients had a higher frequency of plaque erosion, red thrombus, and spotty calcium when compared to UA. While UA patients had a higher incidence of tight stenosis.