Abstract

Background Non-ST elevation acute coronary syndromes (NSTE-ACS) may arise from moderately stenosed atherosclerotic lesions that suddenly undergo transformation to vulnerable plaques complicated by rupture and thrombosis. Objective Assessment and tissue characterization of the coronary atherosclerotic lesions among NSTE-ACS patients compared to those with stable angina. Methodology Evaluation of IVUS studies of 312 coronary lesions was done by 2 different experienced IVUS readers, 216 lesions in 66 patients with NSTE-ACS (group I) versus 96 lesions in 50 patients with stable angina (group II). Characterization of coronary plaques structure was done using colored-coded iMap technique. Results The Syntax score was significantly higher in group I compared to group II (18.7 ± 7.8 vs. 8.07 ± 2.5, p=0.001). Body mass index (BMI) was significantly higher in group II while triglycerides levels were higher in group I (P=0.01 & P=0.04, respectively). History of previous MI and PCI was significantly higher in group I (P=0.016 & P=0.001, respectively). The coronary lesions of NSTE-ACS patients had less vessel area (9.86 ± 3.8 vs 11.36 ± 2.9, p=0.001), stenosis percentage (54.7 ± 14.9% vs 68.6 ± 8.7%, p=0.001), and plaque burden (54.4 ± 14.7 vs 67.8 ± 9.8, p=0.001) with negative remodeling index (0.95 ± 20 vs 1.02 ± 0.14, p=0.008) compared to the stable angina group. On the other hand, they had more lipid content (21.8 ± 7.03% vs 7.26 ± 3.47%, p=0.001), necrotic core (18.08 ± 10.19% vs 15.83 ± 4.9%, p=0.02), and calcifications (10.4 ± 5.2% vs 4.19 ± 3.29%, p=0.001) while less fibrosis (51.67 ± 7.07% vs 70.37 ± 11.7%, p=0.001) compared to the stable angina patients. Syntax score and core composition especially calcification and lipid content were significant predictors to NSTE-ACS. Conclusions The vulnerability rather than the stenotic severity is the most important factor that predisposes to non-ST segment elevation acute coronary syndromes. The vulnerability is related to the lesion characteristics especially lipidic core and calcification while lesion fibrosis favours lesion stability.

Highlights

  • Acute coronary syndromes frequently arise from erosion of vulnerable plaques and subsequent thrombosis [1, 2] while stable coronary atherosclerotic plaques progress to stenosis causing stable angina [3]

  • Body mass index (BMI) was significantly higher in the stable angina (SA) group while the triglyceride level was higher in the NSTE-ACS group

  • LM lesions were higher in the NSTE-ACS patients compared to SA patients. e Syntax score was significantly higher in the NSTE-ACS group compared to the SA group (Table 2)

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Summary

Introduction

Acute coronary syndromes frequently arise from erosion of vulnerable plaques and subsequent thrombosis [1, 2] while stable coronary atherosclerotic plaques progress to stenosis causing stable angina [3].Previous studies have noted that histologic thumbprints of these vulnerable plaques were characterized by thincapped atheroma with a lipid-rich core, few smooth muscle cells, numerous macrophages, adventitial inflammation, and positive remodeling [4,5,6].e main challenge faced was that ACS often arises from lesions with only mild to moderate stenosis. Non-ST elevation acute coronary syndromes (NSTE-ACS) may arise from moderately stenosed atherosclerotic lesions that suddenly undergo transformation to vulnerable plaques complicated by rupture and thrombosis. Assessment and tissue characterization of the coronary atherosclerotic lesions among NSTE-ACS patients compared to those with stable angina. E coronary lesions of NSTE-ACS patients had less vessel area (9.86 ± 3.8 vs 11.36 ± 2.9, p 0.001), stenosis percentage (54.7 ± 14.9% vs 68.6 ± 8.7%, p 0.001), and plaque burden (54.4 ± 14.7 vs 67.8 ± 9.8, p 0.001) with negative remodeling index (0.95 ± 20 vs 1.02 ± 0.14, p 0.008) compared to the stable angina group. They had more lipid content (21.8 ± 7.03% vs 7.26 ± 3.47%, p 0.001), necrotic core (18.08 ± 10.19% vs 15.83 ± 4.9%, p 0.02), and calcifications (10.4 ± 5.2% vs 4.19 ± 3.29%, p 0.001) while less fibrosis (51.67 ± 7.07% vs 70.37 ± 11.7%, p 0.001) compared to the stable angina patients. Conclusions. e vulnerability rather than the stenotic severity is the most important factor that predisposes to non-ST segment elevation acute coronary syndromes. e vulnerability is related to the lesion characteristics especially lipidic core and calcification while lesion fibrosis favours lesion stability

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