CBS 2019
CBSMD教育中心
中 文

DAPT Duration

Abstract

Recommended Article

Ticagrelor versus clopidogrel in elective percutaneous coronary intervention (ALPHEUS): a randomised, open-label, phase 3b trial ISAR-SAFE: a randomized, double-blind, placebo-controlled trial of 6 vs. 12 months of clopidogrel therapy after drug-eluting stenting 6-Month Versus 12-Month Dual-Antiplatelet Therapy Following Long Everolimus-Eluting Stent Implantation: The IVUS-XPL Randomized Clinical Trial 'Ticagrelor alone vs. dual antiplatelet therapy from 1 month after drug-eluting coronary stenting among patients with STEMI': a post hoc analysis of the randomized GLOBAL LEADERS trial Dual-antiplatelet treatment beyond 1 year after drug-eluting stent implantation (ARCTIC-Interruption): a randomised trial Long-term dual antiplatelet-induced intestinal injury resulting in translocation of intestinal bacteria into blood circulation increased the incidence of adverse events after PCI in patients with coronary artery disease Patient-tailored antithrombotic therapy following percutaneous coronary intervention Cost-Effectiveness of Different Durations of Dual-Antiplatelet Use After Percutaneous Coronary Intervention

Original Research2018 Mar 1;3(3):207-214.

JOURNAL:JAMA Cardiol. Article Link

Nonculprit Plaque Characteristics in Patients With Acute Coronary Syndrome Caused by Plaque Erosion vs Plaque Rupture: A 3-Vessel Optical Coherence Tomography Study

Sugiyama T, Yamamoto E, Bryniarski K et al. Keywords: nonculprit plaque; ACS; plaque erosion; plaque rupture;

ABSTRACT


IMPORTANCE - Patients with culprit plaque rupture are known to have pancoronary plaque vulnerability. However, the characteristics of nonculprit plaques in patients with acute coronary syndromes caused by plaque erosion are unknown.


OBJECTIVE - To investigate the nonculprit plaque phenotype in patients with acute coronary syndrome according to culprit plaque pathology (erosion vs rupture) by 3-vessel optical coherence tomography imaging.

DESIGN, SETTING, AND PARTICIPANTS - In this observational cohort study, between August 2010 and May 2014, 82 patients with acute coronary syndrome who underwent preintervention optical coherence tomography imaging of all 3 major epicardial coronary arteries were enrolled at the Massachusetts General Hospital Optical Coherence Tomography Registry database. Analysis of the data was conducted between November 2016 and July 2017. Patients were classified into 2 groups based on the culprit lesion pathology: 17 patients with culprit plaque erosion and 34 patients with culprit plaque rupture. Thirty-one patients with the absence of culprit rupture or erosion were excluded from further analysis.

EXPOSURES - Preintervention 3-vessel optical coherence tomography imaging.

MAIN OUTCOMES AND MEASURES - Plaque characteristics at the culprit and nonculprit lesions evaluated by optical coherence tomography.

RESULTS - In 51 patients (37 men; mean age, 58.7 years), the characteristics of 51 culprit plaques and 216 nonculprit plaques were analyzed. In patients with culprit erosion, the mean (SD) number of nonculprit plaques per patient was smaller (3.4 [1.9] in erosion vs 4.7 [2.1] in rupture, P = .05). Patient-based analysis showed that none of 17 patients with culprit plaque erosion had nonculprit plaque rupture, whereas 26% of the patients (9 of 34) with culprit plaque rupture had nonculprit plaque rupture (P = .02). Plaque-based analysis showed that, compared with the culprit rupture group (n = 158), the culprit erosion group (n = 58) had lower prevalence of plaque rupture (0% vs 8%; P < .001), macrophage accumulation (29% vs 53%; P = .01), microvessels (21% vs 42%; P = .003), and spotty calcium (5% vs 22%; P = .006) in the nonculprit lesions. The prevalence of lipid-rich plaque, thin-cap fibroatheroma, and thrombus did not differ between the groups.

CONCLUSIONS AND RELEVANCE - Compared with those with culprit plaque rupture, patients with acute coronary syndrome caused by culprit plaque erosion had a smaller number of nonculprit plaques and the lower levels of panvascular instability, affirming that distinct pathophysiologic mechanisms operate in plaque erosion and plaque rupture.