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Nonculprit Plaque Characteristics in Patients With Acute Coronary Syndrome Caused by Plaque Erosion vs Plaque Rupture: A 3-Vessel Optical Coherence Tomography Study Association of Improvement in Fractional Flow Reserve With Outcomes, Including Symptomatic Relief, After Percutaneous Coronary Intervention A randomized trial of bifurcation stenting technique in chronic total occlusions percutaneous coronary intervention A prediction model of simple echocardiographic variables to screen for potentially correctable shunts in adult patients with pulmonary arterial hypertension associated with atrial septal defects: a cross-sectional study New Volumetric Analysis Method for Stent Expansion and its Correlation With Final Fractional Flow Reserve and Clinical Outcome An ILUMIEN I Substudy Coronary CT Angiographic and Flow Reserve-Guided Management of Patients With Stable Ischemic Heart Disease Streamlined reverse wire technique for the treatment of complex bifurcated lesions Individual Lesion-Level Meta-Analysis Comparing Various Doses of Intracoronary Bolus Injection of Adenosine With Intravenous Administration of Adenosine for Fractional Flow Reserve Assessment

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.