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Acute stress concentration plays an important role in plaque rupture and may cause stroke or myocardial infarction. Quantitative evaluation of the relation between in vivo plaque stress and variations in blood pressure and flow rates is valuable to optimize daily monitoring of the cardiovascular system for high-risk patients as well as to set a safe physical exercise intensity for better quality of life. In this study, we constructed an in vivo stress model for a human carotid bifurcation with atherosclerotic plaque, and analyzed the effects of blood pressure, flow rates, plaque stiffness, and stenosis on the elastic stress and fluid viscous stress around the plaque. According to the maximum values of the mechanical stress, we define a risk index to predict the risk level of plaque rupture under different exercise intensities. For a carotid bifurcation where the blood flow divides, the results suggest that the stenosis ratio determines the ratio of the contributions of elastic shear stress and viscous shear stress to plaque rupture. An increase of the plaque stiffness enhances the maximum elastic shear stress in the plaque, indicating that a high-stiffness plaque is more prone to rupture for given stenosis ratio. High stress co-localization at the shoulder of plaques agrees with the region of plaque injury in clinical observations. It is demonstrated that, due to the stress-shield effect, the rupture risk of a high-stiffness plaque tends to decrease under high-stenosis conditions, suggesting the existence of a specific stenosis corresponding to the maximum risk. This study may help to complement risk stratification of vulnerable plaques in clinical practice and provides a stenosis mechanical property-specific guide for blood pressure control in cardiovascular health management. [ABSTRACT FROM AUTHOR]

Atherosclerosis is a leading cause of cardiovascular and neurological ischemic events. Plaque rupture leads to the exposure of highly thrombogenic material with blood and results in the activation of the coagulation cascade, thrombus formation, and embolic events. Although antiplatelets and anticoagulants are used to prevent thromboembolic episodes, bleeding episodes remain the major adverse effect. Decreased ischemic events have been reported while comparing oral rivaroxaban and apixaban with aspirin to improve the therapeutic outcome in several clinical trials, including Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary Syndrome-Thrombolysis in Myocardial Infarction 51, Apixaban for Prevention of Acute Ischemic and Safety Events, and GEMINI-ACS-1 phase II clinical trials. However, there were bleeding episodes. Thus, there is an unmet need for better therapeutic strategies. Therefore, the current focus is to target Factors IX, XI, and XII to develop safer and efficient strategies. In this article, we critically reviewed and discussed the limitations of current therapies and the potential of targeting Factors IX, XI, and XII for anticoagulant therapy in atherothrombosis. [ABSTRACT FROM AUTHOR]

Dual quantitative coronary angiography (QCA) has been recently tested for assessment of intracoronary thrombus volume in experimental models. The present study aimed to validate dual QCA in vivo for the assessment of thrombus burden by exploring the correlations between dual QCA-thrombus volume and optical coherence tomography (OCT)-derived indices of thrombotic burden. Fifty-one patients with ACS and angiographic evidence of thrombus undergoing OCT of the culprit lesion before stenting were included. Dual QCA-thrombus volume was calculated as difference between edge-detection and video-densitometry area functions along the target segment. Culprit lesion was categorized using the Ambrose's and AHA/ACC angiographic classifications. Thrombus volume (mean thrombus area × thrombus length), thrombus burden [(mean thrombus area/mean lumen area) x100] and Prati thrombus score (number of quadrants with thrombus) were measured by OCT, and the presence of plaque rupture (PR) or intact fibrous cap (IFC) was assessed. Dual QCA-thrombus volume correlated significantly with OCT-thrombus volume (R = 0.791), thrombus burden (R = 0.767) and Prati thrombus score (R = 0.600) (all p < 0.001). Dual-QCA thrombus volume was significantly higher in patients with PR compared with those with IFC (3.48 mm3 [1.45–11.26] vs. 1.69 mm3 [0.09–5.02], p = 0.013). Compared with IFC, PR showed higher prevalence of eccentric type II Ambrose lesion (41.7% vs. 7.4%, p = 0.004), complex B2/C lesion (87.5% vs. 55.6%, p = 0.012), and heavy calcification (29.2% vs. 3.7%, p = 0.013). Dual QCA analysis appears to be a promising tool for quantification of intracoronary thrombus in vivo. This novel methodology may be useful to guide intracoronary thrombus removal during percutaneous coronary intervention and to aid prognostic stratification in patients with ACS. Unlabelled Image • Dual quantitative coronary angiography (QCA) has been tested for the assessment of thrombus volume in experimental models. • In this in vivo study, dual QCA-thrombus volume was correlated with optical coherence tomography indices of thrombus burden. • A combination of angiographic features may enable the discrimination of patients with plaque rupture and intact fibrous cap. • Dual QCA may be useful to guide thrombus removal and aid prognostic stratification in patients with acute coronary syndrome. [ABSTRACT FROM AUTHOR]

Objective: To investigate morphological features of plaque lesion in patients under 50 with unstable angina pectoris(UAP) using optical coherence tomography(OCT). Methods: This retrospective study included 147 UAP patients who were all under 50 years old. All of them were given both angiographic and OCT test on culprit lesions of each before percutaneous coronary intervention(PCI) treatment. According to morphological features of culprit lesions to distinguish whether there is a plaque erosion(PE), plaque rupture(PR), and the control group. Results: We got 35(23.8%) patients/culprit lesions were only with erosion, 42(28.6%) patients/culprit lesions were with rupture. In demographic and laboratory findings, PE was more often found in female(60.0%)and PR was more often found in male patients(69.0%). Compared with PR group and control group, PE group was significantly older(P < 0.001). In addition,the patients with PE were more frequently with hyperlipidemia(P = 0.007) and smoking history(P = 0.005). In OCT findings, compared with PE group and control group, the patients with PR were with longer lipid core length(P = 0.002), larger mean lipid arc(P = 0.001)and thinner fibrous-cap thickness(P = 0.013). In multivariable logistic regression model for erosion, we found hyperlipidemia and smoking might be two major factors of incidence of PE. Conclusions: PE and PR contribute to over half of patients under 50 with UAP using OCT. More PE occurred in hyperlipidemia and smoking in patients with UAP. PE became another characteristics of the culprit lesion which could lead cardiac events like PR did. [ABSTRACT FROM AUTHOR]

• Possible rupture sites are identified depending on the most important parameters. • Stenosis severity and plaque core stiffness greatly affect the stress distribution. • The midpoints of the upstream and downstream regions are potential rupture sites. • A mild stenosis with positive remodelling may rupture at the middle of the stenosis. • Shorter lipid cores resulted in higher maximum stresses than longer cores. Numerical simulations of blood flow through a partially-blocked axisymmetric artery are performed to investigate the stress distributions in the plaque. We show that the combined effect of stenosis severity and the stiffness of the lipid core can drastically change the axial stress distribution, strongly affecting the potential sites of plaque rupture. The core stiffness is also an important factor when assessing plaque vulnerability, where a mild stenosis with a lipid-filled core presents higher stress levels than a severe stenosis with a calcified plaque. A shorter lipid core gives rise to an increase in the stress levels. However, the fibrous cap stiffness does not influence the stress distributions for the range of values considered in this work. Based on these mechanical analyses, we identify potential sites of rupture in the axial direction for each case: the midpoints of the upstream and downstream regions of the stenosis (for severe, lipid-filled plaques), the ends of the lipid core (for short cores), and the middle of the stenosis (for mild stenoses with positive remodelling of the arterial wall). [ABSTRACT FROM AUTHOR]

Background: Atherosclerosis progression is modulated by interactions with the adaptive immune system. Humoral immunity can help protect against atherosclerosis formation; however, the existence, origin, and function of putative atherogenic antibodies are controversial. How such atherosclerosis-promoting antibodies could affect the specific composition and stability of plaques, as well as the vasculature generally, remains unknown.Methods: We addressed the overall contribution of antibodies to atherosclerosis plaque formation, composition, and stability in vivo (1) with mice that displayed a general loss of antibodies, (2) with mice that had selectively ablated germinal center-derived IgG production, or (3) through interruption of T-B-cell interactions and further studied the effects of antibody deficiency on the aorta by transcriptomics.Results: Here, we demonstrate that atherosclerosis-prone mice with attenuated plasma cell function manifest reduced plaque burden, indicating that antibodies promote atherosclerotic lesion size. However, the composition of the plaque was altered in antibody-deficient mice, with an increase in lipid content and decreases in smooth muscle cells and macrophages, resulting in an experimentally validated vulnerable plaque phenotype. Furthermore, IgG antibodies enhanced smooth muscle cell proliferation in vitro in an Fc receptor-dependent manner, and antibody-deficient mice had decreased neointimal hyperplasia formation in vivo. These IgG antibodies were shown to be derived from germinal centers, and mice genetically deficient for germinal center formation had strongly reduced atherosclerosis plaque formation. mRNA sequencing of aortas revealed that antibodies are required for the sufficient expression of multiple signal-induced and growth-promoting transcription factors and that aortas undergo large-scale metabolic reprograming in their absence. Using an elastase model, we demonstrated that absence of IgG results in an increased severity of aneurysm formation.Conclusions: We propose that germinal center-derived IgG antibodies promote the size and stability of atherosclerosis plaques, through promoting arterial smooth muscle cell proliferation and maintaining the molecular identity of the aorta. These results could have implications for therapies that target B cells or B-T-cell interactions because the loss of humoral immunity leads to a smaller but less stable plaque phenotype. [ABSTRACT FROM AUTHOR]

Atherothrombotic events such as myocardial infarction and ischemic stroke are a major cause of morbidity and mortality worldwide. Understanding the molecular and cellular mechanisms of atherosclerotic plaque destabilization or erosion, and developing new therapeutics to prevent acute cardiovascular events is important for vascular biology research and clinical cardiovascular medicine. However, basic research on plaque destabilization, rupture and erosion is hampered by the lack of appropriate animal models of atherothrombosis. Unprovoked atherothrombosis is very scarce in commonly used mouse models for atherosclerosis, the low-density lipoprotein receptor knockout and apolipoprotein E knockout mice. Therefore, specific interventions are required to induce atherothrombosis in these models. Two strategies can be employed to induce atherothrombosis: 1) plaque destabilization and 2) induction of blood hypercoagulability. Although the individual strategies yield atherothrombosis at low incidence, it appears that the combination of both plaque destabilization and an increase in blood coagulability is the most promising strategy to induce atherothrombosis on a larger scale. In this review, we summarize the recent developments on mouse models for the investigation of atherothrombosis. • Preclinical atherothrombosis research is hampered by a lack of mouse models. • A combined approach is a promising strategy to induce atherothrombosis in mice. • Caution is warranted in the interpretation of plaque vulnerability in mice. [ABSTRACT FROM AUTHOR]

Abstract The catastrophic mechanical rupture of an atherosclerotic plaque is the underlying cause of the majority of cardiovascular events. The infestation of vascular calcification in the plaques creates a mechanically complex tissue composite. Local stress concentrations and plaque tissue strength properties are the governing parameters required to predict plaque ruptures. Advanced imaging techniques have permitted insight into fundamental mechanisms driving the initiating inflammatory-driven vascular calcification of the diseased intima at the (sub-) micron scale and up to the macroscale. Clinical studies have potentiated the biomechanical relevance of calcification through the derivation of links between local plaque rupture and specific macrocalcification geometrical features. The clinical implications of the data presented in this review indicate that the combination of imaging, experimental testing, and computational modelling efforts are crucial to predict the rupture risk for atherosclerotic plaques. Specialised experimental tests and modelling efforts have further enhanced the knowledge base for calcified plaque tissue mechanical properties. However, capturing the temporal instability and rupture causality in the plaque fibrous caps remains elusive. Is it necessary to move our experimental efforts down in scale towards the fundamental (sub-) micron scales in order to interpret the true mechanical behaviour of calcified plaque tissue interactions that is presented on a macroscale in the clinic and to further optimally assess calcified plaques in the context of biomechanical modelling. [ABSTRACT FROM AUTHOR]

Abstract Background and aims Intraplaque cholesterol crystal (CC) is recognized as a component of vulnerable plaques. However, the clinical characteristics of patients with CC and the impact of CC on clinical events remain unknown. Methods A total of 340 consecutive patients who underwent optical coherence tomography (OCT) imaging of culprit lesions were included in the study. CC was defined as a thin linear structure with high reflectivity and low signal attenuation on OCT images. The incidence of major adverse cardiovascular events (MACE) at 1-year was compared between patients with CC (CC group) and those without CC (non-CC group). MACE included cardiac death, non-fatal myocardial infarction, target vessel revascularization (TVR), and non-TVR (NTVR). Results CC was observed in 29% (n = 98) of the patients. There was no significant difference in baseline clinical characteristics between the CC and non-CC groups, other than in eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio (0.39 ± 0.29 vs. 0.47 ± 0.33, p = 0.047) and hemoglobin A1c (HbA1c) levels (6.51 ± 0.97 vs. 6.25 ± 0.87%, p = 0.016). The incidence of MACE and NTVR at 1-year was significantly higher in the CC group than in the non-CC group (15.3 vs. 7.9%, P = 0.038; 8.1 vs. 2.5%, p = 0.017). The presence of CC was significantly associated with a higher rate of 1-year MACE (odds ratio 4.78, confidential interval 2.02–10.10, p < 0.001). Conclusions Patients with CC in the culprit lesion had higher HbA1c and lower EPA/AA than patients without CC. The 1-year clinical outcomes in patients with CC in the culprit lesion were worse than in those without CC. Graphical abstract Image 1 Highlights • The incidence of cholesterol crystals in culprit lesions requiring PCI was 29%. • Lower EPA/AA was associated with the presence of cholesterol crystals. • The presence of cholesterol crystals was associated with worse clinical outcomes. [ABSTRACT FROM AUTHOR]

Intracoronary thrombus burden affects the quality of myocardial reperfusion in the setting of ST-elevation myocardial infarction (STEMI). We aimed to study the characteristics of the plaque and thrombus assessed by intracoronary optical frequency domain imaging (OFDI) according to the presence of plaque rupture or erosion in STEMI patients treated with successful fibrinolysis. Pre-stenting thrombus and post-stenting atherothrombotic burden were compared between plaque rupture and erosion. Twenty-seven consecutive patients were included: 17 (63%) had OFDI-plaque rupture and 10 (37%) had OFDI-erosion. Thrombus volume and burden were significantly higher in case of rupture compared to erosion at baseline (13.4 ± 18.4 vs 2.8 ± 2.3 mm3; p = 0.03 and 33.8 ± 17.5 vs 17.5 ± 9.9%; p = 0.007, respectively). In the rupture group, the core of the thrombus consisted dominantly of red thrombus evenly distributed along the entire culprit plaque. In the erosion group, it consisted dominantly of white thrombus with a focal distribution near the minimal lumen area zone. After stenting, the atherothrombotic volume, burden and its distribution, as well as angiographic estimators of myocardial reperfusion were similar between groups. Our study showed that pre-PCI thrombus amount, typesetting and distribution are mainly linked to the underlying mechanism of STEMI. After stenting, the atherothrombotic burden and its distribution were similar between the groups. [ABSTRACT FROM AUTHOR]

Tortuosity is an abnormality that may occur in some arteries such as carotid. It disrupts blood flow to the brain and, even in severe cases, causes ischemia and stroke. Tortuosity can be congenital or occurs due to hypertension and reduced axial pre-stretch of the artery that is buckling. Since atherosclerotic plaques disrupt the normal pattern of blood flow, and, thus, make the artery more susceptible to buckling, in this study, the effect of atherosclerotic plaques on arterial stability has been investigated, using a computational simulation of fluidstructure interaction under pulsatile flow and large deformation. Ideal and 3D geometry of normal and atherosclerotic carotid artery with different plaques (symmetric or asymmetric and in different percentage of stenosis) were constructed and used to simulate normal (1.5) and reduced (1.3) axial stretch ratio by ADINA Finite Element Analysis Software. The blood flow was assumed to be Newtonian and laminar. Arterial wall was considered as an anisotropic and hyperelastic material based on the Ogden’s model. The results show that stenosis reduces the critical buckling pressure and arteries with asymmetric plaque have lower critical buckling pressure compared to the arteries with symmetric plaque. By reducing the axial stretch ratio from 1.5 to 1.3, the critical buckling pressure is reduced by 33-39%. Buckling increases the peak stress in the plaque and, thus, increases the risk of plaque rupture. [ABSTRACT FROM AUTHOR]

Abstract Background A sizeable proportion of patients with Acute Coronary Syndromes (ACS) shows a unique adaptive immune system profile, associated to a worse outcome, characterized by higher CD4+CD28null T-cells, lower regulatory T-cells (Treg) and increased CD4+CD28null/Treg ratio. We sought to investigate the correlation between CD4+CD28null T-cells, Treg, CD4+CD28null/Treg ratio and plaque phenotype as assessed by Optical Coherence Tomography (OCT). Methods Peripheral blood mononuclear cells (PBMC) were collected from 30 Non-ST Elevation Myocardial Infarction (NSTEMI) patients, sub-grouped according to OCT analysis of culprit lesions into two cohorts: Ruptured Fibrous Cap (NSTEMI-RFC, n = 12) and Intact Fibrous Cap (NSTEMI-IFC, n = 18). Stable Angina patients (SA, n = 18) were used as controls. We examined the frequency of CD4+CD28null and Treg (defined as CD4+CD25highCD127lowFoxp3+ T-cells) by flow-cytometry. Results CD4+CD28null frequency (median, range) was significantly higher in NSTEMI-RFC patients (17.3%, 12.5–33.8) as compared with NSTEMI-IFC (3.8%, 0.3–14.1) and SA (3%, 0.6–17.7) (P < 0.001 for all comparisons). We also found a higher CD4+CD28null/Treg ratio in NSTEMI-RFC patients (6.6%, 3.7–13.9) than in NSTEMI-IFC (1.6%, 0.3–5.2) and SA (1.2%, 0.3–8.7) (P < 0.001 for all comparisons). Finally, there was an inverse correlation between CD4+CD28null/Treg ratio and cap-thickness (R = −0.44; P = 0.002). Conclusion Patients with NSTEMI presenting with RFC as culprit lesion at OCT evaluation have a specific perturbation of adaptive immunity, mostly involving CD4+CD28null T- cells and Tregs, as compared with patients with IFC and SA. This specific imbalance of T-cells might play a key role in fibrous cap thinning, predisposing atherosclerotic plaque to rupture. Highlights • Plaque rupture at OCT evaluation is associated to a specific adaptive immune system signature. • A deeper perturbation of adaptive immunity might be involved in fibrous cap thinning. • Molecular and morphological plaque phenotyping might be a new frontier for personalized medicine. [ABSTRACT FROM AUTHOR]

This case documents the finding of a spontaneous plaque rupture with thrombus formation in the left main coronary artery of a patient who presented with an infarction of the circumflex artery. This serendipitous observation supports the hypothesis that spontaneous plaque ruptures occur sporadically and do not necessarily lead to occlusion.

This case documents the finding of a spontaneous plaque rupture with thrombus formation in the left main coronary artery of a patient who presented with an infarction of the circumflex artery. This serendipitous observation supports the hypothesis that spontaneous plaque ruptures occur sporadically and do not necessarily lead to occlusion.

Plaque erosion (PE) and plaque rupture (PR) are the main subtypes of ST-segment elevation myocardial infarction (STEMI), the differences of metabolic patterns between PE and PR remain largely unknown. 132 STEMI patients were divided into training set (PR, n = 36; PE, n = 36) and test set (PR, n = 30; PE, n = 30), the plasma from patients were analyzed by liquid chromatography quadruple time-of-flight mass spectrometry. We identified 56 and 28 differences in training and test set, respectively. Among these metabolites, it was found that docosahexaenoic acid (DHA), salicylic acid and proline were recognized in both tests. Receiver Operating Characteristic (ROC) analysis showed that the area under curve of docosahexaenoic acid (DHA) was 0.81 and 0.75 in training and test samples, respectively; proline was 0.67 and 0.74 in training and test samples, respectively; salicylic acid was 0.70 and 0.73 in training and test samples, respectively. DHA, salicylic acid, and proline could be used as non-invasive biomarkers to differentiate PE and PR. [Display omitted] • The metabolic patterns of plaque erosion (PE) and plaque rupture (PR) were significantly different. • DHA, proline and salicylic acid were detected in training set and test set, DHA and proline were increased in PR group; salicylic acid was increased in PE group. • DHA, proline and salicylic acid could be used as a stable diagnosis marker to predict PE and PR. [ABSTRACT FROM AUTHOR]

• Histopathology and intravascular imaging show that a stable atheroma undergoes one of several phenotypic changes to become destabilized and at risk for occlusive luminal thrombosis. • An unstable plaque associated with clinical luminal thrombosis manifests one of several phenotypes, including erosion, fibrous cap rupture, nodular calcification and rupture, and cap rupture overlying single or multiple layers of previous cap "rupture-and-repair." • The phenotypes are characterized by altered hemodynamic shear stress, prominent endothelial denudation and dysfunction, smooth muscle cells phenotypic changes, fibrous cap remodeling, expansion, and growth of the vasa vasorum, activation of adventitial and perivascular adipose tissue cells, and alteration in chronic inflammation and lipid deposition. • There are no adequate animal models to study the transition of stable to unstable atheromas to validate the numerous pathogenic steps that have been suggested based on human studies. • Advancement in noninvasive imaging is essential to understand atheroma destabilization and establish plaque burden in vulnerable patients. Data from histopathology studies of human atherosclerotic tissue specimens and from vascular imaging studies support the concept that the local arterial microenvironment of a stable atheroma promotes destabilizing conditions that result in the transition to an unstable atheroma. Destabilization is characterized by several different plaque phenotypes that cause major clinical events such as acute coronary syndrome and cerebrovascular strokes. There are several rupture-associated phenotypes causing thrombotic vascular occlusion including simple fibrous cap rupture of an atheroma, fibrous cap rupture at site of previous rupture-and-repair of an atheroma, and nodular calcification with rupture. Endothelial erosion without rupture has more recently been shown to be a common phenotype to promote thrombosis as well. Microenvironment features that are linked to these phenotypes of plaque instability are neovascularization arising from the vasa vasorum network leading to necrotic core expansion, intraplaque hemorrhage, and cap rupture; activation of adventitial and perivascular adipose tissue cells leading to secretion of cytokines, growth factors, adipokines in the outer artery wall that destabilize plaque structure; and vascular smooth muscle cell phenotypic switching through transdifferentiation and stem/progenitor cell activation resulting in the promotion of inflammation, calcification, and secretion of extracellular matrix, altering fibrous cap structure, and necrotic core growth. As the technology evolves, studies using noninvasive vascular imaging will be able to investigate the transition of stable to unstable atheromas in real time. A limitation in the field, however, is that reliable and predictable experimental models of spontaneous plaque rupture and/or erosion are not currently available to study the cell and molecular mechanisms that regulate the conversion of the stable atheroma to an unstable plaque. [ABSTRACT FROM AUTHOR]

To enhance the antithrombotic properties of recombinant glycoprotein VI fragment crystallizable (GPVI-Fc), the authors incubated GPVI-Fc with anti-human Fc antibodies to cross-link the Fc tails of GPVI-Fc. Cross-linking potentiated the inhibition of human plaque- and collagen-induced platelet aggregation by GPVI-Fc under static and flow conditions without increasing bleeding time in vitro. Cross-linking with anti-human-Fc Fab2 was even superior to anti-human-Fc immunoglobulin G (IgG). Advanced optical imaging revealed a continuous sheath-like coverage of collagen fibers by cross-linked GPVI-Fc complexes. Cross-linking of GPVI into oligomeric complexes provides a new, highly effective, and probably safe antithrombotic treatment as it suppresses platelet GPVI-plaque interaction selectively at the site of acute atherothrombosis.

Background and objectives Endothelial soluble lectin-type oxidized low-density lipoprotein receptor 1 (sLOX-1) recognizes oxidized low-density lipoprotein (LDL) and triggers downstream signaling leading to atherosclerosis. The objective of this study was to demonstrate the utility of sLOX-1 as a biomarker for detecting acute myocardial infarction (MI) and stable angina (SA) and to develop a diagnostic algorithm for distinguishing coronary vasospasm from coronary plaque rupture. Methods We enrolled 62 patients who underwent diagnostic coronary angiography (CAG) and 30 healthy controls (21 men and nine women) and measured sLOX-1, troponin I, and cardiac myosin-binding protein C (c-MyBPC) using commercial kits. Results Patients with MI exhibited higher sLOX-1 levels (301.55 ± 196.16 pg/ml) than patients with stable angina (220.76 ± 103.65 pg/ml) and healthy controls (121.14 ± 77.10, F: 10.55, p<0.001). Although higher troponin I levels were detected in MI patients (263.00 ± 493.00 vs. 3.19 ± 2.15 ng/ml, p=0.0019), no significant elevation was observed in SA patients (1.91 ± 0.79 ng/ml). Plasma sLOX-1 levels showed a positive association with age (r=0.37, p=0.003), but not with gender (r=0.04, p=0.75). Troponin I showed no association with age (r=0.12, p=0.36) or gender (r=0.06, p=0.62). Receiver operating characteristic (ROC) curves revealed that among the three biomarkers, troponin-I showed a higher area under the curve (AUC) (AUC: 0.941), followed by sLOX-1 (AUC: 0.888), while c-MyBPC showed no clinical utility in the detection of MI (AUC: 0.666). Conclusions A marked elevation of sLOX-1 can detect MI and differentiate the presence or absence of plaque rupture, along with diagnosing stable angina., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2023, Narsini et al.)

Aims: Eicosapentaenoic acid (EPA) has shown beneficial effects on coronary plaque stabilization. Based on our previous study, we speculated that EPA might be associated with the development of healed plaques and might limit thrombus size. This study aimed to elucidate the association between EPA and arachidonic acid (AA) ratios and various plaque characteristics in patients with plaque rupture., Methods: A total of 95 patients with acute coronary syndrome (ACS) caused by plaque rupture who did not take lipid-lowering drugs and underwent percutaneous coronary intervention using optical coherence tomography (OCT) were included. Clinical characteristics, lipid profiles, and OCT findings were compared between patients with lower and higher EPA/AA ratios (0.41) according to the levels in the Japanese general population., Results: In the high EPA/AA (n=29, 30.5%) and low EPA/AA (n=66, 69.5 %) groups, the high EPA/AA group was significantly older (76.1 vs. 66.1 years, P＜0.01) and had lower peak creatine kinase (556 vs. 1651 U/L, P=0.03) than those with low EPA/AA. Similarly, patients with high EPA/AA had higher prevalence of layered and calcified plaque (75.9 vs. 39.4 %, P＜0.01; 79.3 vs. 50.0 %, P＜0.01, respectively) than low EPA/AA group. Multivariate logistic regression analysis demonstrated that a high EPA/AA ratio was an independent factor in determining the development of layered and calcified plaques., Conclusion: A high EPA/AA ratio may be associated with the development of layered and calcified plaques in patients with plaque rupture.

Background: The challenge with the stentless strategy is that the method of optimal predilatation, and predictors of success remain unknown. Studies involving the stentless strategy prior to predilatation are limited. This study aimed to evaluate the long-term efficacy and safety of a new stentless strategy for treating acute coronary syndrome (ACS) using gradual, prolonged predilation with a perfusion balloon combined with a drug-coated balloon (DCB)., Methods: This was a single-center, prospective, single-arm study. A total of 30 patients with ACS underwent gradual, prolonged predilation using a perfusion balloon for 10 minutes, followed by additional dilation using a DCB. The primary end point was target vessel failure at 24 months. Secondary end points were a composite of acute end points, including stentless strategy success rate, procedural complications, final grade of coronary dissection, acute coronary occlusion, in-hospital major adverse cardiac events, and a chronic end point of target vessel failure at 24 months., Results: A successful stentless strategy was achieved in 24 patients (80%), and 2 (8.3%) patients required ischemic-driven target lesion revascularization in the chronic phase. Six (20%) patients required stent placement due to type C dissection or acute recoil. No acute occlusion and in-hospital major adverse cardiac events were reported., Conclusions: A novel stentless strategy using predilation with a perfusion balloon and DCB may be helpful for the revascularization of patients with ACS., (© 2023 The Author(s).)

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Copyright of Archives of Cardiovascular Diseases is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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