Pancoronary Plaque Characteristics in STEMI Caused by Culprit Plaque Erosion Versus Rupture: 3-Vessel OCT Study

ObjectivesThis study sought to investigate nonculprit plaque characteristics in patients with ST-segment elevation myocardial infarction (STEMI) presenting with plaque erosion (PE) and plaque rupture (PR). Pancoronary vulnerability was considered at nonculprit sites: 1) the CLIMA (Relationship Between OCT Coronary Plaque Morphology and Clinical Outcome) study (NCT02883088) defined high-risk plaques with simultaneous presence of 4 optical coherence tomography (OCT) features (minimum lumen area <3.5 mm²; fibrous cap thickness [FCT] <75 μm; maximum lipid arc >180º; and macrophage accumulation); and 2) the presence of plaque ruptures or thin-cap fibroatheromas (TCFA).BackgroundPE is a unique clinical entity associated with better outcomes than PR. There is limited evidence regarding pancoronary plaque characteristics of patients with culprit PE versus culprit PR.MethodsBetween October 2016 and September 2018, 523 patients treated by 3-vessel OCT at the time of primary percutaneous intervention were included with 152 patients excluded from final analysis.ResultsOverall, 458 nonculprit plaques were identified in 202 STEMI patients with culprit PE; and 1,027 nonculprit plaques were identified in 321 STEMI patients with culprit PR. At least 1 CLIMA-defined OCT nonculprit high-risk plaque was seen in 11.4% of patients with culprit PE, but twice as many patients were seen with culprit PR (25.2%; p < 0.001). This proportion was also seen when individual high-risk features were analyzed separately. When patients with PE were divided by a heterogeneous substrate (fibrous or lipid-rich plaque) underlying the culprit site, the prevalence of nonculprits with FCT <75 μm, macrophages, and TCFA showed a significant gradient from PE_(Fibrous) to PE_{lipid-rich plaque (LRP)} to PR. Interestingly, nonculprit rupture was rarely found in patients with culprit PE_(Fibrous) (1.9%), although it was exhibited with comparable prevalence in patients with culprit PE_(LRP) (16.3%) versus PR (17.8%). Culprit PE predicted decreased pancoronary vulnerability independent of conventional risk factors.ConclusionsSTEMI patients with culprit PE have a limited pancoronary vulnerability that may explain better outcomes in these patients than in STEMI patients with culprit PR.     

Association between food and nutrients intakes and coronary plaque vulnerability in patients with coronary heart disease: An optical coherence tomography study

Background and aimsDietary intakes play important roles in the prevention and treatment of coronary heart disease (CHD). Coronary plaque vulnerability is the key mechanism leading to CHD progression. We aimed to explore the association between dietary intakes and plaque vulnerability via optical coherence tomography (OCT).Methods and resultsA total of 314 CHD patients were included in this study. Dietary intake status was assessed by semi-quantitative food frequency questionnaire and plaque vulnerability was measured by OCT. The results showed that vegetables were negatively associated with macrophage infiltration, thin cap fibroatheroma (TCFA) and thrombus [odds ratio (OR) = 0.48, 0.38, 0.38, 95% confidence interval (95% CI) = 0.24–0.93, 0.17–0.84, 0.15–0.94, all P < 0.05]; fruits were negatively associated with lipid plaque, TCFA, rupture and thrombus (OR = 0.17, 0.11, 0.12, 0.20, 95% CI = 0.07–0.39, 0.04–0.29, 0.05–0.28, 0.08–0.55, all P < 0.05); salt was positively associated with lipid plaque and TCFA (OR = 2.59, 2.83, 95% CI = 1.14–5.90, 1.23–6.51, all P < 0.05). Regarding nutrients intakes, dietary fiber was negatively associated with macrophage infiltration (OR = 0.34, 95% CI = 0.14–0.85, P = 0.021); folate was negatively associated with lipid plaque, TCFA and rupture (OR = 0.22, 0.16, 0.20, 95% CI = 0.09–0.58, 0.06–0.41, 0.08–0.51, all P < 0.05); vitamin C was negatively associated with TCFA, rupture and thrombus (OR = 0.26, 0.22, 0.05, 95% CI = 0.07–0.95, 0.07–0.65, 0.01–0.25, all P < 0.05); sodium was positively associated with lipid plaque, TCFA, rupture and thrombus (OR = 3.43, 3.96, 2.73, 4.84, 95% CI = 1.51–7.80, 1.66–9.45, 1.18–6.27, 1.76–9.28, all P < 0.05).ConclusionSalt and sodium were dietary risk factors for plaque vulnerability, whereas vegetables, fruits, dietary fiber, folate and vitamin C were dietary protective factors for plaque vulnerability.     

Radiomics-Based Precision Phenotyping Identifies Unstable Coronary Plaques From Computed Tomography Angiography

ObjectivesThe aim of this study was to precisely phenotype culprit and nonculprit lesions in myocardial infarction (MI) and lesions in stable coronary artery disease (CAD) using coronary computed tomography angiography (CTA)-based radiomic analysis.BackgroundIt remains debated whether any single coronary atherosclerotic plaque within the vulnerable patient exhibits unique morphology conferring an increased risk of clinical events.MethodsA total of 60 patients with acute MI prospectively underwent coronary CTA before invasive angiography and were matched to 60 patients with stable CAD. For all coronary lesions, high-risk plaque (HRP) characteristics were qualitatively assessed, followed by semiautomated plaque quantification and extraction of 1,103 radiomic features. Machine learning models were built to examine the additive value of radiomic features for discriminating culprit lesions over and above HRP and plaque volumes.ResultsCulprit lesions had higher mean volumes of noncalcified plaque (NCP) and low-density noncalcified plaque (LDNCP) compared with the highest-grade stenosis nonculprits and highest-grade stenosis stable CAD lesions (NCP: 138.1 mm³ vs 110.7 mm³ vs 102.7 mm³; LDNCP: 14.2 mm³ vs 9.8 mm³ vs 8.4 mm³; both P_trend < 0.01). In multivariable linear regression adjusted for NCP and LDNCP volumes, 14.9% (164 of 1,103) of radiomic features were associated with culprits and 9.7% (107 of 1,103) were associated with the highest-grade stenosis nonculprits (critical P < 0.0007) when compared with highest-grade stenosis stable CAD lesions as reference. Hierarchical clustering of significant radiomic features identified 9 unique data clusters (latent phenotypes): 5 contained radiomic features specific to culprits, 1 contained features specific to highest-grade stenosis nonculprits, and 3 contained features associated with either lesion type. Radiomic features provided incremental value for discriminating culprit lesions when added to a machine learning model containing HRP and plaque volumes (area under the receiver-operating characteristic curve 0.86 vs 0.76; P = 0.004).ConclusionsCulprit lesions and highest-grade stenosis nonculprit lesions in MI have distinct radiomic signatures compared with lesions in stable CAD. Within the vulnerable patient may exist individual vulnerable plaques identifiable by coronary CTA-based precision phenotyping.     

Predictors of Rapid Plaque Progression: An Optical Coherence Tomography Study

ObjectivesThis study sought to identify morphological predictors of rapid plaque progression.BackgroundTwo patterns of plaque progression have been described: slow linear progression and rapid step-wise progression. The former pattern will cause stable angina when the narrowing reaches a critical threshold, whereas the latter pattern may lead to acute coronary syndromes or sudden cardiac death.MethodsPatients who underwent optical coherence tomography (OCT) imaging during the index procedure and follow-up angiography with a minimum interval of 6 months were selected. Nonculprit lesions with a diameter stenosis of ≥30% on index angiography were assessed. Lesion progression was defined as a decrease of angiographic minimum lumen diameter ≥0.4 mm at follow-up (mean, 7.1 months). Baseline morphological characteristics of plaques with rapid progression were evaluated by OCT. In a subgroup with follow-up OCT imaging for plaques with rapid progression, morphological changes from baseline to follow-up were assessed.ResultsAmong 517 lesions in 248 patients, 50 lesions showed rapid progression. These lesions had a significantly higher prevalence of lipid-rich plaque (76.0% vs. 50.5%, respectively), thin-cap fibroatheroma (TCFA) (20.0% vs. 5.8%, respectively), layered plaque (60.0% vs. 34.0%, respectively), macrophage accumulation (62.0% vs. 42.4%, respectively), microvessel (46.0% vs. 29.1%, respectively), plaque rupture (12.0% vs. 4.7%, respectively), and thrombus (6.0% vs. 1.1%, respectively) at baseline compared with those without rapid progression. Multivariate analysis identified lipid-rich plaque (odds ratio [OR]: 2.17; 95% confidence interval [CI]: 1.02 to 4.62; p = 0.045]), TCFA (OR: 5.85; 95% CI: 2.01 to 17.03; p = 0.001), and layered plaque (OR: 2.19; 95% CI: 1.03 to 4.17; p = 0.040) as predictors of subsequent rapid lesion progression. In a subgroup analysis for plaques with rapid progression, a new layer was detected in 25 of 41 plaques (61.0%) at follow-up.ConclusionsLipid-rich plaques, TCFA, and layered plaques were predictors of subsequent rapid plaque progression. A new layer, a signature of previous plaque disruption and healing, was detected in more than half of the lesions with rapid progression at follow-up. (Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538)     

Healed Culprit Plaques in Patients With Acute Coronary Syndromes

BackgroundHealed plaques, morphologically characterized by a layered phenotype, are frequently found in subjects with sudden cardiac death. However, in vivo data are lacking.ObjectivesThe purpose of this study was to determine the prevalence, morphological characteristics, and clinical significance of healed culprit plaques in patients with acute coronary syndromes (ACS) using optical coherence tomography (OCT).MethodsA total of 376 ACS patients (252 ST-segment elevation myocardial infarction [MI] and 124 non–ST-segment elevation acute coronary syndrome) who had undergone pre-intervention OCT imaging of the culprit lesion were enrolled. Patients were stratified according to the presence of layered phenotype, defined as layers of different optical density at OCT. Clinical and laboratory data, OCT characteristics, and 1-year outcome were compared between the 2 groups.ResultsAmong 376 patients, 108 (28.7%) healed plaques were identified. Hyperlipidemia, diabetes, and history of MI were more frequent in patients with healed plaques (44.4% vs. 33.2%; p = 0.041; 35.2% vs. 23.5%; p = 0.021; and 15.7% vs. 6.3%; p = 0.009, respectively). High-sensitivity C-reactive protein was significantly higher in patients with healed plaques (median 4.98 mg/l [interquartile range: 1.00 to 11.32 mg/l] vs. 3.00 mg/l [interquartile range: 0.30 to 10.15 mg/l]; p = 0.029). Plaque rupture (64.8% vs. 53.0%; p = 0.039), thin cap fibroatheroma (56.5% vs. 42.5%; p = 0.016), and macrophage accumulation (81.1% vs. 63.4%; p = 0.001) were common in the layered group. OCT also revealed greater area stenosis in plaques with layered phenotype (79.2 ± 9.5% vs. 74.3 ± 14.3%; p = 0.001). The incidence of major adverse cardiovascular events was similar between the 2 groups, except that the all-cause rehospitalization rate was higher among healed plaques (32.7% vs. 16.5%; p = 0.013).ConclusionsHealed plaques, a signature of prior plaque destabilization, were found at the culprit site in more than one-quarter of ACS patients. Such patients more frequently were diabetic, were hyperlipidemic, or had a history of MI. Healed plaques frequently showed OCT features of vulnerability with evidence of local and systemic inflammation. The combination of plaque vulnerability, local inflammation, and greater plaque burden in addition to systemic inflammation may outweigh the protective mechanism of plaque healing and predispose those plaques to develop occlusive thrombus.     

Air Pollution and Coronary Plaque Vulnerability and Instability: An Optical Coherence Tomography Study

ObjectivesWe assessed the relationship between exposure to air pollutants and mechanisms of coronary instability evaluated by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS).BackgroundAir pollution is an emerging key player in determining the residual risk of coronary events. However, pathophysiological mechanisms linking air pollution and coronary events have been not adequately investigated.MethodsPatients with ACS undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT, and the presence of macrophage infiltrates (MØI) and thin-cap fibroatheroma (TCFA) at the culprit site was also assessed. Based on each case’s home address, exposure to several pollutants was evaluated, including particulate matter 2.5 (PM2.5), PM10, and carbon monoxide (CO). Only patients with >2 years of available data on air pollution exposure prior to ACS were enrolled.ResultsWe included 126 patients (median age: 67.0 years of age; IQR: 55.5-76.0; 97 male patients [77.0%]). Sixty-six patients (52.4%) had PR as the mechanism of plaque instability. Patients with PR were exposed to significantly higher PM2.5 levels than to IFC, and PM2.5 was independently associated with PR (odds ratio: 1.194; 95% CI: 1.036 to 1.377; P = 0.015). Moreover, exposure to higher levels of PM2.5 was independently associated with the presence of TCFA and of MØI at the culprit site. Interestingly, PM2.5, PM10, and Co levels were positively and significantly correlated with serum levels of C-reactive protein.ConclusionsWe provide novel insights into the missing link between air pollution and increased risk of coronary events. In particular, exposure to higher concentrations of air pollutants is associated with the presence of vulnerable plaque features and with plaque rupture as a mechanism of coronary instability. An enhanced systemic and plaque inflammatory activation may explain these findings.     

Plaque Rupture,Compared With Plaque Erosion,Is Associated With a Higher Level of Pancoronary Inflammation

ObjectivesThe aim of this study was to compare the level of coronary inflammation between plaque rupture and plaque erosion using pericoronary adipose tissue (PCAT) attenuation.BackgroundVascular inflammation plays a key role in plaque rupture, while the role of inflammation in plaque erosion remains less well defined. PCAT attenuation determined using computed tomography has emerged as a marker specific for coronary artery inflammation.MethodsPatients with non–ST-segment elevation acute coronary syndromes who underwent preintervention coronary computed tomographic angiography and optical coherence tomographic culprit lesion imaging were enrolled. PCAT attenuation was measured around the culprit lesion and in the proximal 40 mm of all coronary arteries.ResultsAmong 198 patients, plaque rupture was the underlying mechanism in 107 (54.0%) and plaque erosion in 91 (46.0%). Plaque rupture had higher PCAT attenuation than plaque erosion both at the culprit plaque level (?65.8 ± 7.5 HU vs ?69.5 ± 11.4 HU; P = 0.010) and at the culprit vessel level (?67.1 ± 7.1 HU vs ?69.6 ± 8.2 HU; P = 0.024). The mean PCAT attenuation of all 3 coronary arteries was also significantly higher in patients with plaque rupture than in plaque erosion, indicating a higher level of inflammation (?67.9 ± 5.7 HU vs ?69.9 ± 6.8 HU; P = 0.030). In multivariable analysis, plaque rupture was significantly associated with high PCAT attenuation.ConclusionsPCAT attenuation in culprit plaque, culprit vessel, and all 3 coronary arteries was higher in plaque rupture than in plaque erosion. The results suggest that pancoronary inflammation plays a more significant role in plaque rupture than in plaque erosion. (Massachusetts General Hospital and Tsuchiura Kyodo General Hospital Coronary Imaging Collaboration; NCT04523194)     

Identification of High-Risk Plaques Destined to Cause Acute Coronary Syndrome Using Coronary Computed Tomographic Angiography and Computational Fluid Dynamics

ObjectivesThe authors investigated the utility of noninvasive hemodynamic assessment in the identification of high-risk plaques that caused subsequent acute coronary syndrome (ACS).BackgroundACS is a critical event that impacts the prognosis of patients with coronary artery disease. However, the role of hemodynamic factors in the development of ACS is not well-known.MethodsSeventy-two patients with clearly documented ACS and available coronary computed tomographic angiography (CTA) acquired between 1 month and 2 years before the development of ACS were included. In 66 culprit and 150 nonculprit lesions as a case-control design, the presence of adverse plaque characteristics (APC) was assessed and hemodynamic parameters (fractional flow reserve derived by coronary computed tomographic angiography [FFR_CT], change in FFR_CT across the lesion [△FFR_CT], wall shear stress [WSS], and axial plaque stress) were analyzed using computational fluid dynamics. The best cut-off values for FFR_CT, △FFR_CT, WSS, and axial plaque stress were used to define the presence of adverse hemodynamic characteristics (AHC). The incremental discriminant and reclassification abilities for ACS prediction were compared among 3 models (model 1: percent diameter stenosis [%DS] and lesion length, model 2: model 1 + APC, and model 3: model 2 + AHC).ResultsThe culprit lesions showed higher %DS (55.5 ± 15.4% vs. 43.1 ± 15.0%; p < 0.001) and higher prevalence of APC (80.3% vs. 42.0%; p < 0.001) than nonculprit lesions. Regarding hemodynamic parameters, culprit lesions showed lower FFR_CT and higher △FFR_CT, WSS, and axial plaque stress than nonculprit lesions (all p values <0.01). Among the 3 models, model 3, which included hemodynamic parameters, showed the highest c-index, and better discrimination (concordance statistic [c-index] 0.789 vs. 0.747; p = 0.014) and reclassification abilities (category-free net reclassification index 0.287; p = 0.047; relative integrated discrimination improvement 0.368; p < 0.001) than model 2. Lesions with both APC and AHC showed significantly higher risk of the culprit for subsequent ACS than those with no APC/AHC (hazard ratio: 11.75; 95% confidence interval: 2.85 to 48.51; p = 0.001) and with either APC or AHC (hazard ratio: 3.22; 95% confidence interval: 1.86 to 5.55; p < 0.001).ConclusionsNoninvasive hemodynamic assessment enhanced the identification of high-risk plaques that subsequently caused ACS. The integration of noninvasive hemodynamic assessments may improve the identification of culprit lesions for future ACS. (Exploring the Mechanism of Plaque Rupture in Acute Coronary Syndrome Using Coronary CT Angiography and Computational Fluid Dynamic [EMERALD]; NCT02374775)     

Association of plasma trimethylamine N-Oxide level with healed culprit plaques examined by optical coherence tomography in patients with ST-Segment elevation myocardial infarction

Background and aimsHealed plaque is a hallmark of previous regional plaque rupture or erosion. We hypothesized that the plasma level of trimethylamine N-oxide (TMAO) is related to healed culprit plaque in ST-segment elevation myocardial infarction (STEMI) patients.Methods and resultsA prospective cohort of 206 patients with STEMI, who were examined by optical coherence tomography (OCT) was enrolled in our study. After exclusion, 156 patients were categorized into healed plaque (n = 54) and nonhealed plaque (n = 102) groups. Plasma TMAO levels were detected by stable isotope dilution liquid chromatography tandem mass spectrometry in these two groups. Increased age and low BMI were more common in patients with healed plaques than in those without healed plaques. Through OCT observation, plaque rupture (81.5% vs. 45.1%, p < 0.001), thin cap fibroatheroma (TCFA) and macrophages (42.6% vs. 20.6%, p = 0.004, 70.4% vs. 26.5%, p < 0.001, respectively) were more frequently seen in patients with healed plaques than in those without healed plaques. The TMAO level in patients with healed plaques was significantly higher than that in patients with nonhealed plaques (3.9 μM [2.6–5.1] vs. 1.8 μM [1.0–2.7], p < 0.001). Furthermore, the receiver operating characteristic curve showed that TMAO can be used as a potential biomarker to predict healed plaque presence with a cutoff value of 2.9 μM (AUC = 0.810, sensitivity: 72.2%, specificity: 81.4%).ConclusionsHealed plaque in STEMI patients is associated with a high level of plaque vulnerability and inflammation. A high level of plasma TMAO can be a useful biomarker to differentiate STEMI patients with healed culprit plaques.     

Cardiac Magnetic Resonance for Evaluating Nonculprit Lesions After Myocardial Infarction: Comparison With Fractional Flow Reserve

ObjectivesThis study sought to determine the agreement between cardiac magnetic resonance (CMR) imaging and invasive measurements of fractional flow reserve (FFR) in the evaluation of nonculprit lesions after ST-segment elevation myocardial infarction (STEMI). In addition, we investigated whether fully quantitative analysis of myocardial perfusion is superior to semiquantitative and visual analysis.BackgroundThe agreement between CMR and FFR in the evaluation of nonculprit lesions in patients with STEMI with multivessel disease is unknown.MethodsSeventy-seven patients with STEMI with at least 1 intermediate (diameter stenosis 50% to 90%) nonculprit lesion underwent CMR and invasive coronary angiography in conjunction with FFR measurements at 1 month after primary intervention. The imaging protocol included stress and rest perfusion, cine imaging, and late gadolinium enhancement. Fully quantitative, semiquantitative, and visual analysis of myocardial perfusion were compared against a reference of FFR. Hemodynamically obstructive was defined as FFR ≤0.80.ResultsHemodynamically obstructive nonculprit lesions were present in 31 (40%) patients. Visual analysis displayed an area under the curve (AUC) of 0.74 (95% confidence interval [CI]: 0.62 to 0.83), with a sensitivity of 73% and a specificity of 70%. For semiquantitative analysis, the relative upslope of the stress signal intensity time curve and the relative upslope derived myocardial flow reserve had respective AUCs of 0.66 (95% CI: 0.54 to 0.77) and 0.71 (95% CI: 0.59 to 0.81). Fully quantitative analysis did not augment diagnostic performance (all p > 0.05). Stress myocardial blood flow displayed an AUC of 0.76 (95% CI: 0.64 to 0.85), with a sensitivity of 69% and a specificity of 77%. Similarly, MFR displayed an AUC of 0.82 (95% CI: 0.71 to 0.90), with a sensitivity of 82% and a specificity of 71%.ConclusionsCMR and FFR have moderate-good agreement in the evaluation of nonculprit lesions in patients with STEMI with multivessel disease. Fully quantitative, semiquantitative, and visual analysis yield similar diagnostic performance.     

NIRS-IVUS for Differentiating Coronary Plaque Rupture,Erosion, and Calcified Nodule in Acute Myocardial Infarction

ObjectivesThis study sought to investigate the ability of combined near-infrared spectroscopy and intravascular ultrasound (NIRS-IVUS) to differentiate plaque rupture (PR), plaque erosion (PE), or calcified nodule (CN) in acute myocardial infarction (AMI).BackgroundMost acute coronary syndromes occur from coronary thrombosis based on PR, PE, or CN. In vivo differentiation among PR, PE, and CN is a major challenge for intravascular imaging.MethodsThe study enrolled 244 patients with AMI who had a de novo culprit lesion in a native coronary artery. The culprit lesions were assessed by both NIRS-IVUS and optical coherence tomography (OCT). Maximum lipid core burden index in 4 mm (maxLCBI_4mm) was measured by NIRS. Plaque cavity and convex calcium was detected by IVUS. The OCT diagnosis of PR (n = 175), PE (n = 44), and CN (n = 25) was used as a reference standard.ResultsIn the development cohort, IVUS-detected plaque cavity showed a high specificity (100%) and intermediate sensitivity (62%) for identifying OCT-PR. IVUS-detected convex calcium showed a high sensitivity (93%) and specificity (100%) for identifying OCT-CN. NIRS-measured maxLCBI_4mm was largest in OCT-PR (705 [interquartile range (IQR): 545 to 854]), followed by OCT-CN (355 [IQR: 303 to 478]) and OCT-PE (300 [IQR: 126 to 357]) (p < 0.001). The optimal cutoff value of maxLCBI_4mm was 426 for differentiating between OCT-PR and -PE; 328 for differentiating between OCT-PE and -CN; and 579 for differentiating between OCT-PR and -CN. In the validation cohort, the NIRS-IVUS classification algorithm using plaque cavity, convex calcium, and maxLCBI_4mm showed a sensitivity and specificity of 97% and 96% for identifying OCT-PR, 93% and 99% for OCT-PE, and 100% and 99% for OCT-CN, respectively.ConclusionsBy evaluating plaque cavity, convex calcium, and maxLCBI_4mm, NIRS-IVUS can accurately differentiate PR, PE, and CN.     

Sex-Related Differences in Thrombus Burden in STEMI Patients Undergoing Primary Percutaneous Coronary Intervention

BackgroundWomen have a worse prognosis after ST-segment elevation myocardial infarction (STEMI) than men. The prognostic role of thrombus burden (TB) in influencing the sex-related differences in clinical outcomes after STEMI has not been clearly investigated.ObjectivesThe aim of this study was to assess the sex-related differences in TB and its clinical implications in patients with STEMI.MethodsIndividual patient data from the 3 major randomized clinical trials of manual thrombus aspiration were analyzed, encompassing a total of 19,047 patients with STEMI, of whom 13,885 (76.1%) were men and 4,371 (23.9%) were women. The primary outcome of interest was 1-year cardiovascular (CV) death. The secondary outcomes of interest were recurrent myocardial infarction, heart failure, all-cause mortality, stroke, stent thrombosis (ST), and target vessel revascularization at 1 year.ResultsPatients with high TB (HTB) had worse 1-year outcomes compared with those presenting with low TB (adjusted HR for CV death: 1.52; 95% CI: 1.10-2.12; P = 0.01). In unadjusted analyses, female sex was associated with an increased risk for 1-year CV death regardless of TB. After adjustment, the risk for 1-year CV death was higher only in women with HTB (HR: 1.23; 95% CI: 1.18-1.28; P < 0.001), who also had an increased risk for all-cause death and ST than men.ConclusionsIn patients with STEMI, angiographic evidence of HTB negatively affected prognosis. Among patients with HTB, women had an excess risk for ST, CV, and all-cause mortality than men. Further investigations are warranted to better understand the pathophysiological mechanisms leading to excess mortality in women with STEMI and HTB.     

Incidence and Outcomes of Acute Coronary Syndrome After Transcatheter Aortic Valve Replacement

ObjectivesThis study sought to address a knowledge gap by examining the incidence, timing, and predictors of acute coronary syndrome (ACS) after transcatheter aortic valve replacement (TAVR) in Medicare beneficiaries.BackgroundEvidence about incidence and outcomes of ACS after TAVR is scarce.MethodsWe identified Medicare patients who underwent TAVR from 2012 to 2017 and were admitted with ACS during follow-up. We compared outcomes based on the type of ACS: ST-segment elevation myocardial infarction (STEMI), non-STEMI (NSTEMI), and unstable angina. In patients with non–ST-segment elevation ACS, we compared outcomes based on the treatment strategy (invasive vs. conservative) using inverse probability weighting analysis.ResultsOut of 142,845 patients with TAVR, 6,741 patients (4.7%) were admitted with ACS after a median time of 297 days (interquartile range: 85 to 662 days), with 48% of admissions occurring within 6 months. The most common presentation was NSTEMI. Predictors of ACS were history of coronary artery disease, prior revascularization, diabetes, valve-in-TAVR, and acute kidney injury. STEMI was associated with higher 30-day and 1-year mortality compared with NSTEMI (31.4% vs. 15.5% and 51.2% vs. 41.3%, respectively; p < 0.01). Overall, 30.3% of patients with non–ST-segment elevation ACS were treated with invasive approach. On inverse probability weighting analysis, invasive approach was associated with lower adjusted long-term mortality (adjusted hazard ratio: 0.69; 95% confidence interval: 0.66 to 0.73; p < 0.01) and higher risk of repeat revascularization (adjusted hazard ratio: 1.29; 95% confidence interval: 1.16 to 1.43; p < 0.001).ConclusionsAfter TAVR, ACS is infrequent (<5%), and the most common presentation is NSTEMI. Occurrence of STEMI after TAVR is associated with a high mortality with nearly one-third of patients dying within 30 days. Optimization of care is needed for post-TAVR ACS patients and if feasible, invasive approach should be considered in these high-risk patients.     

EROSION III: A Multicenter RCT of OCT-Guided Reperfusion in STEMI With Early Infarct Artery Patency

ObjectivesThe aim of this study was to test whether optical coherence tomographic (OCT) guidance would provide additional useful information beyond that obtained by angiography and lead to a shift in reperfusion strategy and improved clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI) with early infarct artery patency.BackgroundAngiography is limited in assessing the underlying pathophysiological mechanisms of the culprit lesion.MethodsEROSION III (Optical Coherence Tomography–Guided Reperfusion in ST-Segment Elevation Myocardial Infarction With Early Infarct Artery Patency) is an open-label, prospective, multicenter, randomized, controlled study approved by the ethics committees of participating centers. Patients with STEMI who had angiographic diameter stenosis ≤ 70% and TIMI (Thrombolysis In Myocardial Infarction) flow grade 3 at presentation or after antegrade blood flow restoration were recruited and randomized to either OCT guidance or angiographic guidance. The primary efficacy endpoint was the rate of stent implantation.ResultsAmong 246 randomized patients, 226 (91.9%) constituted the per protocol set (112 with OCT guidance and 114 with angiographic guidance). The median diameter stenosis was 54.0% (IQR: 48.0%-61.0%) in the OCT guidance group and 53.5% (IQR: 43.8%-64.0%) in the angiographic guidance group (P = 0.57) before randomization. Stent implantation was performed in 49 of 112 patients (43.8%) in the OCT group and 67 of 114 patients (58.8%) in the angiographic group (P = 0.024), demonstrating a 15% reduction in stent implantation with OCT guidance. In patients treated with stent implantation, OCT guidance was associated with a favorable result with lower residual angiographic diameter stenosis (8.7% ± 3.7% vs 11.8% ± 4.6% in the angiographic guidance group; P < 0.001). Two patients (1 cardiac death, 1 stable angina) met the primary safety endpoint in the OCT guidance group, as did 3 patients (3 cardiac deaths) in the angiographic guidance group (1.8% vs 2.6%; P = 0.67). Reinfarction was not observed in either group. At 1 year, the rates of predefined cardiocerebrovascular events were comparable between the groups (11.6% after OCT guidance vs 9.6% after angiographic guidance; P = 0.66).ConclusionsIn patients with STEMI with early infarct artery patency, OCT guidance compared with angiographic guidance of reperfusion was associated with less stent implantation during primary percutaneous coronary intervention. These favorable results indicate the value of OCT imaging in optimizing the reperfusion strategy of patients with STEMI. (EROSION III: OCT- vs Angio-Based Reperfusion Strategy for STEMI; NCT03571269)     

2-Year Outcomes After Stenting of Lipid-Rich and Nonrich Coronary Plaques

BackgroundAutopsy studies suggest that implanting stents in lipid-rich plaque (LRP) may be associated with adverse outcomes.ObjectivesThe purpose of this study was to evaluate the association between LRP detected by near-infrared spectroscopy (NIRS) and clinical outcomes in patients with coronary artery disease treated with contemporary drug-eluting stents.MethodsIn this prospective, multicenter registry, NIRS was performed in patients undergoing coronary angiography and possible percutaneous coronary intervention (PCI). Lipid core burden index (LCBI) was calculated as the fraction of pixels with the probability of LRP >0.6 within a region of interest. MaxLCBI_4mm was defined as the maximum LCBI within any 4-mm-long segment. Major adverse cardiac events (MACE) included cardiac death, myocardial infarction, definite or probable stent thrombosis, or unplanned revascularization or rehospitalization for progressive angina or unstable angina. Events were subcategorized as culprit (treated) lesion–related, nonculprit (untreated) lesion–related, or indeterminate.ResultsAmong 1,999 patients who were enrolled in the COLOR (Chemometric Observations of Lipid Core Plaques of Interest in Native Coronary Arteries Registry), PCI was performed in 1,621 patients and MACE occurred in 18.0% of patients, of which 8.3% were culprit lesion–related, 10.7% were nonculprit lesion–related, and 3.1% were indeterminate during 2-year follow-up. Complications from NIRS imaging occurred in 9 patients (0.45%), which resulted in 1 peri-procedural myocardial infarction and 1 emergent coronary bypass. Pre-PCI NIRS imaging was obtained in 1,189 patients, and the 2-year rate of culprit lesion–related MACE was not significantly associated with maxLCBI_4mm (hazard ratio of maxLCBI_4mm per 100: 1.06; 95% confidence interval: 0.96 to 1.17; p = 0.28) after adjusting clinical and procedural factors.ConclusionsFollowing PCI with contemporary drug-eluting stents, stent implantation in NIRS-defined LRPs was not associated with increased periprocedural or late adverse outcomes compared with those without significant lipid.     

Prophylactic Rivaroxaban Therapy for Left Ventricular Thrombus After Anterior ST-Segment Elevation Myocardial Infarction

ObjectivesThe aim of this study was to investigate the effects of rivaroxaban on left ventricle thromboprophylaxis in patients with anterior ST-segment elevation myocardial infarction (STEMI).BackgroundAnterior STEMI is associated with an increased risk of left ventricular thrombus (LVT) formation. The contemporary role of prophylactic rivaroxaban therapy remains unclear.MethodsWe randomly assigned 279 patients with anterior STEMI who had undergone primary percutaneous coronary intervention to receive, in a 1:1 ratio, low-dose rivaroxaban (2.5 mg twice daily for 30 days) and dual antiplatelet therapy (DAPT) or only DAPT. The primary efficacy outcome was the LVT formation within 30 days. Net clinical adverse events were assessed at 30 days and 180 days, including all-cause mortality, LVT, systemic embolism, rehospitalization for cardiovascular events, and bleeding.ResultsThe addition of low-dose rivaroxaban to DAPT reduced LVT formation within 30 days compared with only DAPT (0.7% vs 8.6%; HR: 0.08; 95% CI: 0.01-0.62; P = 0.015; P < 0.001 for superiority). Net clinical adverse events were lower within 30 days in the rivaroxaban group versus those in the only DAPT group and remained relatively low throughout the follow-up period. There were no significant differences in bleeding events between the 2 groups in 30 days and 180 days. However, 1 case of intracranial hemorrhage (major bleeding) occurred in the rivaroxaban group within 30 days.ConclusionsOur results supported that the short-duration addition of low-dose rivaroxaban to DAPT could prevent LVT formation in patients with anterior STEMI following primary percutaneous coronary intervention. A larger multiple-institution study is necessary to determine the generalizability.     

Multivessel Versus Culprit-Vessel Percutaneous Coronary Intervention in Patients With Non–ST-Segment Elevation Myocardial Infarction and Cardiogenic Shock

ObjectivesThe aim of this study was to compare in-hospital outcomes and long-term mortality of multivessel versus culprit vessel–only percutaneous coronary intervention (PCI) in patients with non–ST-segment elevation myocardial infarction (NSTEMI), multivessel disease (MVD) and cardiogenic shock.BackgroundThe clinical benefits of complete revascularization in patients with NSTEMI, MVD, and cardiogenic shock remain uncertain.MethodsAmong 25,324 patients included in the National Cardiovascular Data Registry CathPCI Registry from July 2009 to March 2018, the rates of in-hospital procedural outcomes were compared between those undergoing multivessel PCI and those undergoing culprit vessel–only PCI after 1:1 propensity score matching. Among patients aged ≥65 years matched to the Centers for Medicare and Medicaid Services database, long-term mortality was compared using proportional hazards analysis.ResultsMultivessel PCI was performed in 9,791 patients (38.7%), which increased from 32.2% in 2010 to 44.2% in 2017 (p for trend <0.001). After 1:1 propensity matching (n = 7,864 in each group), those undergoing multivessel PCI had a 3.5% (95% confidence interval [CI]: 2.0% to 5.0%) lower absolute rate of in-hospital mortality (30.9% vs. 34.4%; p < 0.001; odds ratio [OR]: 0.85; 95% CI: 0.80 to 0.91), but a higher risk for bleeding (13.2% vs. 10.8%; p < 0.001; OR: 1.26; 95% CI: 1.15 to 1.40) and new requirement for dialysis (5.7% vs. 4.6%; p = 0.001; OR: 1.26; 95% CI: 1.10 to 1.46). Among those surviving to discharge, all-cause mortality was similar through 7 years (conditional hazard ratio: 0.95; 95% CI: 0.87 to 1.03; p = 0.20).ConclusionsNearly 40% of patients with NSTEMI with MVD and cardiogenic shock underwent multivessel PCI, which was associated with lower in-hospital mortality but greater peri-procedural complications. Among those surviving to discharge, multivessel PCI did not confer additional long-term mortality benefit.     

FFR- Versus Angiography-Guided Revascularization for Nonculprit Stenosis in STEMI and Multivessel Disease: A Network Meta-Analysis

ObjectivesThe aim of this study was to examine the efficacy and safety of fractional flow reserve (FFR)–guided versus angiography-guided approaches for nonculprit stenosis among patients with acute ST-segment elevation myocardial infarction (STEMI) and multivessel disease.BackgroundThe optimal strategy to guide revascularization of nonculprit stenosis among patients with STEMI and multivessel disease remains uncertain.MethodsElectronic databases were searched for randomized trials evaluating the outcomes of culprit-only revascularization, angiography-guided complete revascularization (CR), or FFR-guided CR. A pairwise meta-analysis comparing CR versus culprit-only revascularization and a network meta-analysis comparing the different revascularization techniques were conducted. The primary outcome was major adverse cardiac events (MACE).ResultsThe analysis included 11 trials with 8,195 patients. CR (ie, angiography-guided or FFR-guided CR) was associated with a lower incidence of MACE (odds ratio [OR]: 0.46; 95% CI: 0.35 to 0.59), cardiovascular mortality (OR: 0.63; 95% CI: 0.41 to 0.98), recurrent myocardial infarction (OR: 0.67; 95% CI: 0.48 to 0.95), and repeat ischemia-driven revascularization (OR: 0.26; 95% CI: 0.19 to 0.35). Network meta-analysis demonstrated that the incidence of MACE was lower with both angiography-guided CR (OR: 0.43; 95% CI: 0.31 to 0.58) and FFR-guided CR (OR: 0.52; 95% CI: 0.35 to 0.78) compared with a culprit-only approach, while there was no difference in risk for MACE between angiography-guided and FFR-guided CR (OR: 0.81; 95% CI: 0.51 to 1.29).ConclusionsAmong patients with STEMI and multivessel disease, CR, with angiographic or FFR guidance for nonculprit stenosis, was associated with lower incidence of adverse events compared with culprit-only revascularization. FFR-guided CR was not superior to angiography-guided CR in reducing the incidence of adverse events. Future studies investigating other tools to risk-stratify nonculprit stenoses are encouraged.     

Revascularization Deferral of Nonculprit Stenoses on the Basis of Fractional Flow Reserve: 1-Year Outcomes of 8,579 Patients

BackgroundIntracoronary physiology is increasingly used in nonculprit stenoses of patients with acute coronary syndromes (ACS). However, evidence regarding the safety of fractional flow reserve-based deferral in patients with ACS, compared with patients with stable angina pectoris (SAP), is scarce.ObjectivesThe aim of this study was to evaluate the safety of revascularization deferral on the basis of fractional flow reserve interrogation of nonculprit lesions in patients with ACS.MethodsA pooled analysis was performed of individual patient data included in 5 large international published studies on physiology-guided revascularization. The primary endpoint was major adverse cardiac events (MACE) (a composite of death, nonfatal myocardial infarction, or unplanned revascularization) at 1-year follow-up. Clinical outcomes of patients with ACS and SAP were compared in both the deferred and the revascularized groups.ResultsA total of 8,579 patients were included in the analysis, 6,461 with SAP and 2,118 with ACS and nonculprit stenoses. Using fractional flow reserve, revascularization was deferred in 5,129 patients (59.8%) and performed in 3,450 patients (40.2%). In the deferred ACS group, a higher MACE rate was observed compared with the deferred SAP group (4.46% vs. 2.83%; adjusted hazard ratio [HR]: 1.72; 95% confidence interval [CI]: 1.17 to 2.53; p < 0.01). In particular, early unplanned revascularization (3.34% and 2.04% in ACS and SAP; adjusted HR: 1.81; 95% CI: 1.09 to 3.00; p = 0.02) contributed to this excess in MACE but the difference between the ACS and SAP groups did not reach statistical significance. On the contrary, no differences in outcomes linked to clinical presentation were found in treated patients (MACE rate 6.51% vs. 6.20%; adjusted HR: 1.21; 95% CI: 0.88 to 1.26; p = 0.24).ConclusionsPatients with ACS in whom revascularization of nonculprit lesions was deferred on the basis of fractional flow reserve have more MACE at 1 year compared with patients with SAP with deferred revascularization. Unplanned revascularization mainly contributed to this excess of MACE.