Lei Xing

Distinct Morphological Features of Ruptured Culprit Plaque for Acute Coronary Events Compared to Those With Silent Rupture and Thin-Cap Fibroatheroma : A Combined Optical Coherence Tomography and Intravascular Ultrasound Study

OBJECTIVESnThe study sought to identify specific morphological characteristics of ruptured culprit plaques (RCP) responsible for acute events, and compare them with ruptured nonculprit plaques (RNCP) and nonruptured thin-cap fibroatheroma (TCFA) in patients presenting with acute coronary syndromes (ACS).nnnBACKGROUNDnNonruptured TCFA and multiple ruptured plaques are detected in the same patients with ACS. It remains unknown whether certain morphological characteristics determine rupture of TCFA and subsequently result in ACS.nnnMETHODSnWe analyzed 126 plaques (RCP = 49, RNCP = 19, TCFA = 58) from 82 ACS patients using optical coherence tomography (OCT) and intravascular ultrasound (IVUS). Fibrous cap thickness was determined by OCT. Plaque burden and lumen area were measured with IVUS.nnnRESULTSnFibrous cap was thinner in RCP (43 ± 11 μm) and RNCP (41 ± 10 μm) than in TCFA (56 ± 9 μm, p < 0.001 and p < 0.001, respectively). Plaque burden was greater in RCP (82 ± 7.2%), compared with RNCP (64 ± 7.2%, p < 0.001) and TCFA (62 ± 12.5%, p < 0.001). Lumen area was smaller in RCP (2.1 ± 0.9 mm(2)), compared with RNCP (4.6 ± 2.3 mm(2), p = 0.001) and TCFA (5.1 ± 2.7 mm(2), p < 0.001). The fibrous cap thickness <52 μm had good performance in discriminating ruptured plaque from TCFA (area under the curve [AUC] = 0.857, p < 0.001), and plaque burden >76% and lumen area <2.6 mm(2) had good performance in discriminating RCP from RNCP and TCFA (AUC = 0.923, p < 0.001 and AUC = 0.881, p < 0.001, respectively).nnnCONCLUSIONSnFibrous cap thickness is a critical morphological discriminator between ruptured plaques and nonruptured TCFA, while plaque burden and lumen area appear to be important morphological features of RCP. These findings suggest that plaque rupture is determined by fibrous cap thickness, and a combination of large plaque burden and luminal narrowing result in ACS.

Effective anti-thrombotic therapy without stenting: intravascular optical coherence tomography-based management in plaque erosion (the EROSION study)

AimsnPlaque erosion, compared with plaque rupture, has distinctly different underlying pathology and therefore may merit tailored therapy. In this study, we aimed to assess whether patients with acute coronary syndrome (ACS) caused by plaque erosion might be stabilized by anti-thrombotic therapy without stent implantation.nnnMethods and resultsnThis was a single-centre, uncontrolled, prospective, proof-of concept study. Patients with ACS including ST-segment elevation myocardial infarction were prospectively enrolled. If needed, aspiration thrombectomy was performed. Patients diagnosed with plaque erosion by optical coherence tomography (OCT) and residual diameter stenosis <70% on coronary angiogram were treated with anti-thrombotic therapy without stenting. OCT was repeated at 1 month and thrombus volume was measured. The primary endpoint was >50% reduction of thrombus volume at 1 month compared with baseline. The secondary endpoint was a composite of cardiac death, recurrent ischaemia requiring revascularization, stroke, and major bleeding. Among 405 ACS patients with analysable OCT images, plaque erosion was identified in 103 (25.4%) patients. Sixty patients enrolled and 55 patients completed the 1-month follow-up. Forty-seven patients (47/60, 78.3%; 95% confidence interval: 65.8-87.9%) met the primary endpoint, and 22 patients had no visible thrombus at 1 month. Thrombus volume decreased from 3.7 (1.3, 10.9) mm3 to 0.2 (0.0, 2.0) mm3. Minimal flow area increased from 1.7 (1.4, 2.4) mm2 to 2.1 (1.5, 3.8) mm2. One patient died of gastrointestinal bleeding, and another patient required repeat percutaneous coronary intervention. The rest of the patients remained asymptomatic.nnnConclusionnFor patients with ACS caused by plaque erosion, conservative treatment with anti-thrombotic therapy without stenting may be an option.

Comparison of nonculprit coronary plaque characteristics between patients with and without diabetes: a 3-vessel optical coherence tomography study.

OBJECTIVESnThe aim of the present study was to compare the characteristics of nonculprit coronary plaques between diabetes mellitus (DM) and non-DM patients using 3-vessel optical coherence tomography (OCT) imaging.nnnBACKGROUNDnDM patients have a higher recurrent cardiovascular event rate.nnnMETHODSnPatients who had undergone 3-vessel OCT imaging were identified from the Massachusetts General Hospital OCT Registry. Characteristics of nonculprit plaques were compared between DM and non-DM patients.nnnRESULTSnA total of 230 nonculprit plaques were identified in 98 patients. Compared with non-DM patients, DM patients had a larger lipid index (LI) (averaged lipid arc × lipid length; 778.6 ± 596.1 vs. 1358.3 ± 939.2, p < 0.001) and higher prevalence of calcification (48.4% vs. 72.2%, p = 0.034) and thrombus (0% vs. 8.3%, p = 0.047). DM patients were divided into 2 groups based on glycated hemoglobin (A(1C)) levels of ≤7.9% and ≥8.0%. LI was significantly correlated with diabetic status (778.6 ± 596.1 [non-DM] vs. 1,171.5 ± 708.1 [A(1C) ≤7.9%] vs. 1,638.5 ± 1,173.8 [A(1C) ≥8%], p value for linear trend = 0.005), and fibrous cap thickness was inversely correlated with the A(1C) level (99.4 ± 46.7 μm [non-DM] vs. 91.7 ± 29.6 μm [A(1C) ≤7.9%] vs. 72.9 ± 22.7 μm [A(1C) ≥8%], p value for linear trend = 0.014). Patients with A(1C) ≥8% also had the highest prevalence of thin-cap fibroatheroma (TCFA) and macrophage infiltration.nnnCONCLUSIONSnCompared with non-DM patients, DM patients have a larger LI and a higher prevalence of calcification and thrombus. The LI was larger and TCFA and macrophage infiltration were frequent in patients with A(1C) ≥8%.

Comparison of Intensive Versus Moderate Lipid-Lowering Therapy on Fibrous Cap and Atheroma Volume of Coronary Lipid-Rich Plaque Using Serial Optical Coherence Tomography and Intravascular Ultrasound Imaging.

Despite marked clinical benefit, reduction in atheroma volume with statin therapy is minimal. Changes in plaque composition may explain this discrepancy. We aimed in the present study to assess the effect of statin therapy on coronary plaque composition and plaque volume using serial multimodality imaging. From an open-label, single-blinded study, patients with angiographically mild-to-moderate lesion were randomized to receive atorvastatin 60 (AT 60) mg or atorvastatin 20 (AT 20) mg for 12 months. Optical coherence tomography was used to assess fibrous cap thickness (FCT) and intravascular ultrasound to assess atheroma burden at 3 time points: baseline, at 6 months, and at 12 months. Thirty-six lipid-rich plaques in 27 patients with AT 60 mg and 30 lipid-rich plaques in 19 patients with AT 20 mg were enrolled in this study. Low-density lipoprotein cholesterol level was significantly decreased at 6 months without further reduction at 12 months. AT 60 mg induced greater reduction in low-density lipoprotein cholesterol compared with AT 20 mg. Optical coherence tomography revealed continuous increase in FCT from baseline to 6 months and to 12 months in both groups. AT 60 mg induced greater increase in FCT compared with AT 20 mg at both follow-up points. The prevalence of thin-cap fibroatheroma and the presence of macrophage at 6 months were significantly lower in AT 60 mg compared with AT 20 mg. Plaque burden did not change significantly in both groups. In conclusion, both intensive and moderate statin therapy stabilizes coronary plaques, with a greater benefit in the intensive statin group. However, no significant changes in plaque volume were observed over time regardless of the intensity of statin therapy.

Does Residual Thrombus After Aspiration Thrombectomy Affect the Outcome of Primary PCI in Patients With ST-Segment Elevation Myocardial Infarction? : An Optical Coherence Tomography Study

OBJECTIVESnThe aim of this study was to evaluate if residual thrombus burden after aspiration thrombectomy affects the outcomes of primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction (STEMI).nnnBACKGROUNDnRecent studies failed to show clinical benefit of aspiration thrombectomy in STEMI patients. This might be due to insufficient removal of thrombus at the culprit lesion.nnnMETHODSnA total of 109 STEMI patients who underwent aspiration thrombectomy followed by stenting within 24 h from symptom onset were included. Optical coherence tomography was performed after thrombectomy to measure residual thrombus burden. Patients were divided into tertiles based on the amount of residual thrombus and the outcomes were compared.nnnRESULTSnMyocardial no reflow, defined as TIMI (Thrombolysis In Myocardial Infarction) flow grade ofxa0≤2 and/or myocardial blush grade ofxa0≤1 after stenting, was more observed frequently in patients in the highest tertile compared with those in the lowest tertile (44.4% vs. 16.7%; pxa0= 0.001). Patients in the highest tertile also had greater myocardial damage measured by creatine kinase MB compared with those in the lowest tertile (pxa0= 0.002).nnnCONCLUSIONSnSTEMI patients with greater residual thrombus burden after aspiration thrombectomy had worse microvascular dysfunction and greater myocardial damage compared with those with smaller residual thrombus burden.

Association between cholesterol crystals and culprit lesion vulnerability in patients with acute coronary syndrome: An optical coherence tomography study.

BACKGROUNDnCholesterol Crystals (ChCs) are recognized as a hallmark of advanced atherosclerotic lesions. Previous animal and histopathology studies have revealed that Cholesterol crystallization trigger a local inflammatory response and plaque rupture. We sought to investigate the in vivo relationship between ChCs and culprit lesion vulnerability in patients with acute coronary syndrome (ACS).nnnMETHODSn206 culprit lesions from 206 patients with ACS who underwent optical coherence tomography (OCT) imaging were divided into 2 groups based on the presence or absence of ChCs. Culprit lesions characteristics were compared between ChCs and Non-ChCs groups.nnnRESULTSnFor overall ACS patients, culprit lesions with ChCs had higher incidence of macrophages accumulation (77.8% vs. 40.0%, p < 0.001), microchannel (67.9% vs. 24.8%, p < 0.001), plaque rupture (58.0% vs. 36.0%, p = 0.001), thrombosis (66.7% vs. 49.6%, p = 0.016) and spotty calcification (35.8% vs. 10.4%, p < 0.001). In addition, the mean lipid arc (274.2 ± 57.6° vs. 228.1 ± 66.3°, p < 0.001) was larger and the lipid index (3826.1 ± 2111.4 vs. 2855.0 ± 1753.0, p = 0.001) was greater. The frequency of ChCs was significantly higher in patients with STEMI, as compared with NSTEACS (50.8% vs. 34.7%, p = 0.032). Larger lipid arc, higher incidence of macrophages accumulation and that of microchannel were observed in culprit lesions with ChCs in both STEMI (p = 0.028, p < 0.001, and p = 0.002 respectively) and NSTEACS (p < 0.001, p < 0.001, and p < 0.001 respectively) subgroups.nnnCONCLUSIONnChCs were frequently associated with characteristics of vulnerable plaques in ACS culprit lesions as well as in STEMI and NSTEACS subgroups. ChCs and vulnerable plaque features were more often observed in culprit lesions of STEMI patients compared to NSTEACS patients.

In vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction: a clinical, angiographical, and intravascular optical coherence tomography study

AimsnPlaque erosion is a significant substrate of acute coronary thrombosis. This study sought to determine in vivo predictors of plaque erosion in patients with ST-segment elevation myocardial infarction (STEMI).nnnMethods and resultsnA prospective series of 822 STEMI patients underwent pre-intervention optical coherence tomography. Using established diagnostic criteria, 209 had plaque erosion (25.4%) and 564 had plaque rupture (68.6%). Plaque erosion was more frequent in women <50u2009years when compared with those ≥50u2009years of age (Pu2009=u20090.009). There was a similar, but less striking, trend in men (Pu2009=u20090.011). Patients with plaque erosion were more frequently current smokers but had fewer other coronary risk factors (dyslipidaemia, hypertension, chronic kidney disease, and diabetes mellitus) than those with plaque rupture. There was a preponderance of plaque erosion in the left anterior descending artery (LAD; 61.2%), whereas plaque rupture was more equally distributed in both the LAD (47.0%) and right coronary artery (43.3%). Despite the similar spatial distribution of erosions and ruptures over the lengths of the coronary arteries, plaque erosion occurred more frequently near a bifurcation (Pu2009<u20090.001). In the multivariable analysis, age <50u2009years, current smoking, absence of other coronary risk factors, lack of multi-vessel disease, reduced lesion severity, larger vessel size, and nearby bifurcation were significantly associated with plaque erosion. Nearby bifurcation and current smoking were especially notable in men, while age <50u2009years was most predictive in women.nnnConclusionsnPlaque erosion was a predictable clinical entity distinct from plaque rupture in STEMI patients, and gender-specific role of risk factors in plaque erosion should be considered.

Lipid-lowering therapy stabilizes the complexity of non-culprit plaques in human coronary artery: a quantitative assessment using OCT bright spot algorithm.

To quantitatively evaluate the change of plaque complexity with cholesterol lowering therapy. A total of 44 non-culprit plaques from 30 patients who had serial image acquisition at baseline, 6-months, and 12-months by both optical coherence tomography (OCT) and intravascular ultrasound (IVUS) were included. Patients were treated with atorvastatin 60xa0mg (AT60, nu2009=u200916) or 20xa0mg (AT20, nu2009=u200914). We applied an OCT bright spot algorithm, which identifies a variety of plaque components including macrophages. The density of bright spot was measured within the superficial 250xa0µm of the vessel wall. Significant reduction of bright spot density was observed from baseline to 12-months [−0.49% (−0.95, −0.20), pu2009<u20090.001], particularly during the second 6 months [first 6 months: −0.01% (−0.57, 0.60), pu2009=u20090.939; second 6 months: −0.49% (−0.98, 0.14), pu2009<u20090.001]. Although there was no significant difference at 12 months in the reduction of bright spot density between plaques with acute coronary syndrome (ACS, nu2009=u200933) and those with stable angina (nu2009=u200911) [−0.49% (−0.93, −0.19) vs. −0.39% (−1.01, −0.21), pu2009=u20090.748], a significant reduction of bright spot density during the first 6 months was observed only in plaques with ACS. There was no significant difference in the change of bright spot density between the AT60 group (nu2009=u200922) and AT20 group (nu2009=u200922) [−0.61% (−0.93, −0.34) vs. −0.41% (−0.98, −0.19), pu2009=u20090.483]. Coronary plaque complexity evaluated by a quantitative OCT algorithm significantly decreased with 12 month atorvastatin therapy irrespective of the dose and initial clinical presentation.

Association between leukocyte telomere length and drug-eluting stent strut coverage by optical coherence tomography.

To the Editor:nnAfter coronary stent placement, the vascular response to injury includes re-endothelialization by resident and circulating bone marrow–derived endothelial progenitor cells ([1][1]). Delayed re-endothelialization after drug-eluting stent (DES) implantation may lead to uncovered

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

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, Pu2009=u2009.05). 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 (Pu2009=u2009.02). Plaque-based analysis showed that, compared with the culprit rupture group (nu2009=u2009158), the culprit erosion group (nu2009=u200958) had lower prevalence of plaque rupture (0% vs 8%; Pu2009<u2009.001), macrophage accumulation (29% vs 53%; Pu2009=u2009.01), microvessels (21% vs 42%; Pu2009=u2009.003), and spotty calcium (5% vs 22%; Pu2009=u2009.006) 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.