CCTA characteristics of vulnerable plaques preceding acute coronary syndromes-a comparative analysis between STE- and NSTE-ACS

Abstract

Abstract Funding Acknowledgements Type of funding sources: Public Institution(s). Main funding source(s): This work was supported by the University of Medicine, Pharmacy, Science and Technology „George Emil Palade“ of Târgu Mureș Research Grant number 510/13/17.01.2022. Background CCTA adverse plaque features, that illustrate increased vulnerability, have been established as significant predictors for adverse events in patients with coronary artery disease. Decades of research have benchmarked the implication of vulnerable plaques (VP) in the occurrence of acute coronary syndromes (ACS). Still, there is little information concerning the interrelation between VP features and the subsequent type of ACS. Aim We sought to identify specific characteristics of future culprit vulnerable plaques, in a comparative analysis between the type of ACS they trigger, in patients undergoing CCTA and plaque analysis for stable chest pain. Material and Methods We conducted a prospective analysis, with a 3 year follow-up, on 50 subjects who underwent CCTA evaluation for stable chest pain. Coronary plaques were analyzed at baseline, for lesions that presented moderate stenosis, with at least one vulnerability marker (LAP, PR, NRS, SCs), which became culprit lesions during follow-up. Patients were initially divided into 2 groups (gr.1 – with STE-ACS, n=13) gr.2 – patients with NSTE-ACS, n=37). The secondary analysis divided the population in 3 groups gr.1-patients with UA (n=28); gr.2- with STEMI (n=13); gr.2 –with NSTEMI (n=9). Results The time to the occurrence of an ACS was higher for STE-ACS compared to NSTE-ACS (169.9±177.4, p<0.001), which was similar when comparing NSTEMI vs. UA vs. STEMI (p = 0.0001). The lowest degree of stenosis was present for VP that had triggered NSTEMI (p = 0.03). Evaluation of plaque composition revealed that the STE-ACS group presented higher non-calcified (171.6±63 vs. 130.6±80.1 mm3 p = 0.04) and lipid rich (19.9±16.7 vs. 11.42±10.5 mm3, p = 0.04) volumes, with no other differences regarding plaque composition and morphology. Plaques that had triggered STEMI during follow-up, presented highest non-calcified (p = 0.01) and lipid rich (p = 0.01) volumes. The greatest number of plaques with over 2 vulnerability markers per lesions were found in NSTEMI precursor lesions compared to UA and STEMI (77.8% vs. 53.8% ±25%, p = 0.01). Conclusions Compared to NSTE-ACS triggering lesions, vulnerable plaques that precede STEMI-ACS present a more lipid rich, non-calcified phenotype. NSTEMI precursor lesions are heterogeneous, with a low calcium volume and increased number of vulnerability markers, while VPs triggering unstable angina are calcified, with a low lipid rich volume and spotty calcifications.