Non-culprit Sites Research Articles

Frequency of Very Large Lipid-Rich Plaques Identified by NIRS at Non-Culprit Sites

Frequency of Very Large Lipid-Rich Plaques Identified by NIRS at Non-Culprit Sites

CRT-100.22 Frequency of Very Large Lipid-Rich Plaques Identified by NIRS at Non-Culprit Sites

CRT-100.22 Frequency of Very Large Lipid-Rich Plaques Identified by NIRS at Non-Culprit Sites

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 PElipid-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.

Frequency, Predictors, Distribution, and Morphological Characteristics of Layered Culprit and Nonculprit Plaques of Patients With Acute Myocardial Infarction: In Vivo 3-Vessel Optical Coherence Tomography Study.

Subclinical atherothrombosis and plaque healing may lead to rapid plaque progression. The histopathologic healed plaque has a layered appearance when imaged using optical coherence tomography. We assessed the frequency, predictors, distribution, and morphological characteristics of optical coherence tomography layered culprit and nonculprit plaques in patients with acute myocardial infarction. A prospective series of 325 patients with acute myocardial infarction underwent optical coherence tomography imaging of all 3 native coronary arteries. Layered plaque phenotype had heterogeneous signal-rich layered tissue located close to the luminal surface that was clearly demarcated from the underlying plaque. Layered plaques were detected in 74.5% of patients with acute myocardial infarction. Patients with layered culprit plaques had more layered nonculprit plaques; and they more often had preinfarction angina, ST-segment-elevation myocardial infarction, higher low-density lipoprotein cholesterol, and absence of antiplatelet therapy. Layered plaques tended to cluster in the proximal segment of the left anterior descending artery and left circumflex artery but were more uniformly distributed in the right coronary artery. As compared with nonlayered plaques, layered plaques had greater optical coherence tomography lumen area stenosis at both culprit and nonculprit sites. The frequency of layered plaque phenotype (P=0.038) and maximum area of layered tissue (P<0.001) increased from nonculprit thin-cap fibroatheromas to nonculprit ruptures to culprit ruptures. Layered plaques were identified in 3-quarters of patients with acute myocardial infarction, especially in the culprit plaques of patients with ST-segment-elevation myocardial infarction. Layered plaques had a limited, focal distribution in the left anterior descending artery, and left circumflex artery but were more evenly distributed in the right coronary artery and were characterized by greater lumen narrowing at both culprit and nonculprit sites. Graphic Abstract: A graphic abstract is available for this article.

Preliminary Pilot Study of Combined Effects of Physical Activity and Achievement of LDL-Cholesterol Target on Coronary Plaque Volume Changes in Patients with Acute Coronary Syndrome.

Background: We investigated the combined effects of physical activity (PA) and aggressive low-density lipoprotein cholesterol (LDL-C) reduction on the changes in coronary plaque volume (PV) in patients with acute coronary syndrome (ACS) using volumetric intravascular ultrasound (IVUS) analysis. Methods: We retrospectively analyzed data from two different prospective clinical trials that involved 101 ACS patients who underwent percutaneous coronary intervention (PCI) and assessed the non-culprit sites of PCI lesions using IVUS at baseline and at the follow-up. After PCI, all the patients participated in early phase II comprehensive cardiac rehabilitation. Patients were divided into four groups based on whether the average daily step count, measured using a pedometer, was 7000 steps of more and whether the follow-up LDL-C level was <70 mg/dL. At the time of follow-up, we examined the correlation of changes in the PV with LDL-C and PA. Results: The baseline characteristics of the four study groups were comparable. At the follow-up, plaque regression in both the achievement group (PA and LDL-C reduction) was higher than that in the other three groups. In addition, plaque reduction independently correlated with increased PA and reduction in LDL-C level. Conclusions: Combined therapy of intensive PA and achievement of LDL-C target retarded coronary PV in patients with ACS.

Characteristics of non-culprit plaques in acute coronary syndrome patients with layered culprit plaque

Layered plaques represent signs of previous plaque destabilization. A recent study showed that acute coronary syndrome (ACS) patients with layered culprit plaque have more vulnerability at the culprit lesion and systemic inflammation. We aimed to compare the characteristics of non-culprit plaques between patients with or without layered plaque at the culprit lesion. We also evaluated the characteristics of layered non-culprit plaques, irrespective of culprit plaque phenotype. We studied ACS patients who had undergone pre-intervention optical coherence tomography (OCT) imaging. The number of non-culprit lesions was evaluated on coronary angiogram and morphological characteristics of plaques were studied by OCT. In 349 patients, 99 (28.4%) had layered culprit plaque. The number of non-culprit plaques in patients with or without layered culprit plaque was similar (3.2 ± 0.8 and 2.8 ± 0.8, P = 0.23). Among 465 non-culprit plaques, 145 from patients with layered culprit plaque showed a higher prevalence of macrophage infiltration (71.0% vs. 60.9%, P = 0.050). When analysed irrespective of culprit plaque phenotype, layered non-culprit plaques showed higher prevalence of lipid (93.3% vs. 86.0%, P = 0.028), thin cap fibroatheroma (29.7% vs. 13.7%, P < 0.001), and macrophage infiltration (82.4% vs. 54.0%, P < 0.001) than non-layered plaques. Plaques with layered phenotype at both culprit and non-culprit lesions had the highest vulnerability. In ACS patients, those with layered phenotype at the culprit lesion demonstrated greater macrophage infiltration at the non-culprit sites. Layered plaque at the non-culprit lesions was associated with more features of plaque vulnerability, particularly when the culprit lesion also had a layered pattern.

Circulation: Cardiovascular Imaging Editors’ Picks

<i>Circulation: Cardiovascular Imaging</i> Editors’ Picks

Decreased circulating lipoprotein-associated phospholipase A2 levels are associated with coronary plaque regression in patients with acute coronary syndrome

ObjectiveLipoprotein-associated phospholipase A2 (Lp-PLA2) is a vascular-specific inflammatory enzyme, of which increases are associated with cardiovascular events. However, the relationship between circulating Lp-PLA2 levels and coronary plaque volume has not been clarified in patients with acute coronary syndrome (ACS). MethodsWe studied 40 patients with ACS (age, 61.4±8.0 years; male, 87.5%; statin use, 45.0%) who had undergone successful percutaneous coronary intervention (PCI). Plaque volume (PV) in non-culprit sites of PCI lesions was precisely determined using grayscale intravascular ultrasound (IVUS) at onset and at six months later. We then analyzed associations among PV, lipid profiles and Lp-PLA2 levels. ResultsCirculating Lp-PLA2 levels and PV significantly decreased between baseline and six months of follow-up (458.6±166.7IU/L vs. 378.4±158.5IU/L, p<0.001 and 82.2±34.8mm3 vs. 77.3±33.1mm3, p<0.001, respectively). The % change in PV positively and significantly correlated with % change in LDL-C and in the LDL-C/HDL-C ratio (r=0.444, p=0.004 and r=0.462, p=0.003, respectively). Furthermore, % changes in Lp-PLA2 and in PV correlated even more closely (r=0.496, p=0.001). The absolute change in PV also significantly correlated with the change in Lp-PLA2 levels (r=0.404, p=0.009). ConclusionsCirculating Lp-PLA2 levels are associated with changes in coronary plaque determined by IVUS in patients with ACS.

Detection of very early stent healing after primary angioplasty: an optical coherence tomographic observational study of chromium cobaltum and first-generation drug-eluting stents. The DETECTIVE Study

BackgroundLack of stent coverage appears to be associated with stent thrombosis, a problem of particular concern in patients with ST elevation myocardial infarction (STEMI).MethodsThe DETECTIVE European Multicenter Registry was set...

Plaque Regression Determined by Intravascular Ultrasound Predicts Long-Term Outcomes of Patients with Acute Coronary Syndrome

The usefulness of drugs to treat plaque regression is assessed by intravascular ultrasound (IVUS); however, the impact of plaque regression on clinical outcomes in patients with acute coronary syndrome (ACS) has not been established; therefore, we investigated the relationship between coronary plaque regression and long-term clinical outcomes. We analyzed data from 86 patients who underwent percutaneous coronary intervention (PCI) and who were assessed in detail at baseline and at 6 months of follow-up by measuring proximal non-culprit sites of PCI lesions using volumetric IVUS. Patients were divided according to changes in plaque volume over 6 months into one group with plaque regression (n =55; 64.0%) and another with progression (n =31; 36.0%). They were followed up observationally for a mean of 1,736 days. Baseline characteristics at the time of ACS were similar between the groups. The probability of event-free survival was significantly higher in the regression group than in the progression group as estimated by the Kaplan-Meier method (Log-rank test, p =0.032). Furthermore, the Cox hazards model revealed the relative contribution of plaque regression as a predictor of cardiovascular events (hazard ratio: 0.26; 95% CI, 0.07 to 0.83; p =0.023). Plaque regression determined by volumetric IVUS over a period of 6 months was associated with a lower rate of cardiovascular events among patients with ACS. This study also demonstrated that plaque regression could be a surrogate marker of future cardiovascular events.

Delayed Arterial Healing and Increased Late Stent Thrombosis at Culprit Sites After Drug-Eluting Stent Placement for Acute Myocardial Infarction Patients

The long-term safety of drug-eluting stents (DES) for acute myocardial infarction (AMI) remains uncertain. Using autopsy data, we evaluated the pathological responses of the stented segment in patients treated with DES for AMI and compared with patients with stable angina. From the CVPath Registry of 138 DES autopsies, we identified 25 patients who presented with AMI and had an underlying necrotic core with a ruptured fibrous cap. Twenty-six patients who had stable angina with thick-cap fibroatheroma treated by DES were selected as controls. Histomorphometric analysis was performed in patients with >30-day stent duration. We compared the response to stenting at the culprit site in these 2 groups and to nonculprit sites within each stent. Late stent thrombosis was significantly less frequent in stable (11%) than in AMI (41%; P=0.04) patients. Although neointimal thickness in the AMI culprit site was significantly less (median, 0.04 mm; interquartile range [IQR], 0.02 to 0.09 mm), the prevalence of uncovered struts (49%; IQR, 16% to 96%), fibrin deposition (63+/-28%), and inflammation (35%; IQR, 27% to 49%) were significantly greater compared with the culprit site in stable patients (neointimal thickness: 0.11 mm [IQR, 0.07 to 0.21 mm], P=0.008; uncovered struts: 9% [IQR, 0% to 39%], P=0.01; fibrin: 36+/-27%, P=0.008; inflammation, 17% [IQR, 7% to 25%], P=0.003) and the nonculprit site within each stent. Vessel healing at the culprit site in AMI patients treated with DES is substantially delayed compared with the culprit site in patients receiving DES for stable angina, emphasizing the importance of underlying plaque morphology in the arterial response to DES. Our data suggest an increased risk of thrombotic complications in patients treated with DES for AMI.

Abstract 2824: Drug Eluting Stents Implantation In Acute Myocardial Infarction Significantly Delays Healing And Increases Stent Thrombosis

Background Although early clinical results of DES implantation for acute myocardial infarction (AMI) show no significant differences in late thrombosis however, long-term safety is still unclear. We evaluated the pathologic responses following DES implantation in AMI patients and compared to stents implanted in non-AMI lesions. Methods From CVPath DES autopsy registry of 116 cases, we identified 22 who presented with AMI at the time of DES implantation and had underlying plaque rupture (PR) or thin-cap fibroatheroma (TCFA). Morphometric analysis was performed using calibrated software (IPLab, Scanalytics) in patients who died ≥30 days after DES implantation. The percentage of struts with fibrin deposition, inflammation (&gt;10 cells/strut), and uncovered struts were also recorded. We assessed arterial healing, by comparing culprit to non-culprit sites within each stented section. Furthermore, age and stent duration matched non-AMI patients who had underlying fibroatheroma (FA) lesion were selected as controls. Results Of the 22 patients with AMI, 14 died ≥30 days (mean duration: 285±277 days) and stent thrombosis was documented in 7 (50%, mean duration: 333±396 days), whereas in non-AMI patients with underlying FA, thrombosis was significantly less frequent (8%). Morphometric analysis revealed neointimal thickness was significantly less in culprit sites as compared to non-culprit sites in AMI patients. The percentages of uncovered struts, and struts with inflammation were significantly greater in culprit sites as compared to non-culprit sites in AMI lesions. Lesions in non-AMI patients were significantly different from AMI patients with greater neointimal thickness, less fibrin around struts, inflammation and uncovered struts (Table ). Conclusions A higher prevalence of stent thrombosis was observed in patients with AMI than those without AMI and is associated with substantial delayed in arterial healing especially at culprit sites. Pathologic and Morphmetric Analysis, Culprit vs. Non-Culprit and AMI vs. Non-AMI

Pathological Changes in Acute Coronary Syndromes: The Role of Statin Therapy in the Modulation of Inflammation, Endothelial Function and Coagulation

Considerable progress has been made in our understanding of the pathophysiology of coronary artery disease (CAD), their acute presentations as acute coronary syndromes (ACS) and the role of LDL cholesterol. In particular there is clear evidence that atherosclerosis is far from being a process that leads to an amorphous flow limiting lesion on an angiogram, but rather involves a complex interplay between the endothelium, inflammatory cells and the coagulation cascade occurring throughout the coronary vascular bed. While a culprit flow limiting lesion may be effectively treated by a drug eluting stent or coronary bypass surgery, this will have little impact on the global molecular processes that determine recurrent plaque instability at non-culprit sites. The search for systemic long term therapy, which is safe and effective and reduces the changes in inflammation, endothelial function and thrombosis that are the hallmark of ACS, has pushed statins to the forefront. A number of recent clinical trials have shown the benefits of early statin therapy in the treatment of ACS. In addition to their effects on LDL cholesterol, statins have a number of properties collectively referred to as pleiotropic effects, which enable them to modulate the adverse biological changes that are associated with ACS. The purpose of this review is to acquaint the reader with the biological changes that accompany ACS, highlight how these pathways may be modulated for clinical benefit by statins and identify potential novel targets for future therapy.