Prognostic value of characteristics of plaque combined with residual syntax score among patients with STEMI undergoing primary PCI: an intravascular optical coherence tomography study

Abstract

Aim: The present study aimed to explore these characteristics, particularly thin-cap fibroatheroma (TCFA), in relation to residual syntax score (rSS) in patients who presented with acute MI.

Methods and outcomes: A total of 434 consecutive patients with MI aged ≥18 years who had STEMI underwent primary PCI. Notably, compared with other subgroups, the presence of TCFA in culprit lesions and a higher level of rSS, were significantly associated with MACE. When rSS was divided into three groups, high rSS levels were associated with a higher incidence of MACE, in the subgroups of without TCFA (P = 0.005), plaque erosion (P = 0.045), macrophage infiltration (P = 0.026), and calcification (P = 0.002). AUC of ROC curve was 0.794 and 0.816, whereas the AUC of the survival ROC was 0.798 and 0.846.

Conclusion: The results of this study could be used in clinical practice to support risk stratification.

Trial registration: This study was registered at ClinicalTrials.gov as NCT03593928 .

Keywords: Optical coherence tomography; Prognosis value; Residual syntax score; Thin-cap fibroatheroma.

Fig. 1

Representative cross-sectional optical coherence tomography images. A Thin-cap fibroatheroma was defined as a lipid-rich plaque (lipid identified as signal poor and attenuating) of more than two quadrants of vessel lumen with a fibrous cap (identified as signal rich, or brightly reflecting, with low attenuation) thickness measuring 65 um or less. (arrow). B Lipid plaque (arrow) most often appears as diffusely bordered, signal-poor regions with overlying signal-rich bands. C Calcification identified by the presence of a well-delineated, low-backscattering heterogeneous region (asterisk). D Plaque rupture identified by disruption of the fibrous cap and cavity formation (asterisk). E Plaque erosion identified by the presence of attached thrombus (asterisk) overlying an intact plaque. F Microvessels defined as tubule luminal structures that do not generate a signal, with no connection to the vessel lumen (arrow). G Red thrombus consists mainly of red blood cells; relevant OCT images are characterized as high-backscattering protrusions with signal free shadowing (asterisk). H. Cholesterol crystal (arrow) identified by linear, highly backscattering structures without remarkable backward shadowing

Fig. 2

Flow chart 2 Study flow chart. OCTAMI, Optical Coherence Tomography Examination in Acute Myocardial Infarction; OCT optical coherence tomography, AMI acute myocardial infarction

Fig. 3

ROC curve, survival ROC curve for rSS with traditional risk factors, TCFA and microstructure of culprit lesion by OCT in predicting 2-year MACE and K-M curve of performance of the model III and IV. A, Model I, predictor of traditional risk factors including sex, age, ejection fraction, hypertension, hyperlipidemia, diabetes mellitus, history of myocardial infarction, history of PCI, history of CABG, Killip classification, cTnI of baseline, peak level of cTnI, brain natriuretic peptide (BNP) of baseline, peak level of BNP, white blood cell, hemoglobin, platelet, creatine kinase, glucose, glycosylated hemoglobin, C-reactive protein, total cholesterol, triglyceride, low density lipoprotein, high density lipoprotein, triglyceride/ low density lipoprotein, lipse activator, aspirin, Ticagrelor, clopidogrel. Model II, Model I plus rSS. Model III, Model II plus TCFA. Model IV, Model III plus microstructure of culprit lesion by OCT including macrophage, thrombus, plaque rupture or erosion, mixed plaque, lipid plaque, fibrous plaque, calcification, max lipid-arc, fibrous cap thickness, minimal lumen area, micro-vessels. AUC, areas under the ROC curve; CI, 95% confidence interval. B Survival ROC curve, the confounding factors of model I, II, III, IV are as same as the (A). C Model III cutoff value=0.5970; 0, predictors of model III< cutoff value; 1, predictors of model III≥ cutoff value; D Model IV cutoff value=0.6493. 0, predictors of model III< cutoff value; 1, predictors of model III≥ cutoff value

Fig. 4

Kaplan-Meier curves showing cumulative MACE rates for up to median 1.98 years stratified by the level of rSS and TCFA characteristic among subgroups. Group=0 represent the patients with low level of rSS (rSS≤4) and without characteristic of TCFA in the culprit lesion. Group=1 represent the patients with low level of rSS (rSS≤4) and characteristic of TCFA in the culprit lesion. Group=2 represent the patients with low level of rSS (rSS>4) and without characteristic of TCFA in the culprit lesion. Group=3 represent the patients with low level of rSS (rSS>4) and characteristic of TCFA in the culprit lesion. DM, diabetes mellitus; WBC, white blood cell; EF, ejective fraction. A Kaplan-Meier curves showing cumulative MACE rates stratified by the level of rSS and TCFA among subgroups without hypertension. B Kaplan-Meier curves showing cumulative MACE rates stratified by the level of rSS and TCFA among subgroups with hypertension. C Kaplan-Meier curves showing cumulative MACE rates stratified by the level of rSS and TCFA among subgroups without DM. D Kaplan-Meier curves showing cumulative MACE rates stratified by the level of rSS and TCFA among subgroups with DM. E Kaplan-Meier curves showing cumulative MACE rates stratified by the level of rSS and TCFA among subgroups WBC>10 10*9/L. F Kaplan-Meier curves showing cumulative MACE rates stratified by the level of rSS and TCFA among subgroups WBC≤10 10*9/L. G Kaplan-Meier curves showing cumulative MACE rates stratified by the level of rSS and TCFA among subgroups of EF≥50%. H Kaplan-Meier curves showing cumulative MACE rates stratified by the level of rSS and TCFA among subgroups of EF<50%