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Cardiovascular diseases are the leading cause of death in the modern world. Atherosclerosis underlies the majority of these pathologies and may result in sudden life-threatening events such as myocardial infarction or stroke. Current concepts consider a rupture (resp. erosion) of "unstable/vulnerable" atherosclerotic plaques as a primary cause leading to thrombus formation and subsequent occlusion of the artery lumen finally triggering an acute clinical event. We and others described SR-B1-/-ApoE-R61h/h mice mimicking clinical coronary heart disease in all major aspects: from coronary atherosclerosis through vulnerable plaque ruptures leading to thrombus formation/coronary artery occlusion, finally resulting in myocardial infarction/ischemia. SR-B1-/-ApoE-R61h/h mouse provides a valuable model to study vulnerable/occlusive plaques, to evaluate bioactive compounds as well as new anti-inflammatory and "anti-rupture" drugs, and to test new technologies in experimental cardiovascular medicine. This review summarizes and discuss our knowledge about SR-B1-/-ApoE-R61h/h mouse model based on recent publications and experimental observations from the lab., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background A previous coronary computed tomography (CT) angiographic study failed to discriminate optical coherence tomography-defined intact fibrous cap culprit lesions (IFC group) from those with ruptured fibrous caps (RFC group) in patients with coronary artery disease. This study aimed to evaluate the diagnostic efficacy of preprocedural coronary CT imaging in identifying subsequently performed optical coherence tomography-defined plaque rupture or erosion at culprit lesions in patients with non-ST-segment-elevation acute myocardial infarction. Methods and Results This study used data from 2 recently published studies that tested the hypothesis that coronary CT angiography (CCTA) before percutaneous coronary intervention may provide diagnostic information on the high-risk atherosclerotic burden in patients with non-ST-segment-elevation acute myocardial infarction. In the analysis of 186 patients, optical coherence tomography identified 106 RFC plaques and 80 IFC plaques as the culprit lesions. On CT, the prevalence of low-attenuation plaque, positive remodeling, napkin-ring sign, and spotty calcification were all significantly lower in the IFC group. The culprit vessel pericoronary adipose tissue inflammation and coronary artery calcium scores were significantly lower in the IFC group than in the RFC group. The absence of low-attenuation plaque, napkin-ring sign, zero coronary artery calcium, and low pericoronary adipose tissue inflammation were independent predictors of IFC. When stratified into 5 subgroups according to the number of these 4 CT factors, the prevalence of IFC was 8.3%, 20.8%, 44.6%, 75.6%, and 100% ( P <0.001), respectively. Conclusions Preprocedural comprehensive coronary CT imaging, including coronary artery calcium and pericoronary adipose tissue inflammation assessment, can accurately and noninvasively identify optical coherence tomography-defined IFC or RFC culprit lesions.

The relationship between high wall shear stress (WSS) and plaque rupture (PR) in longitudinal and circumferential locations remains uncertain. Overall, 100 acute coronary syndrome patients whose culprit lesions had PR, documented by optical coherence tomography (OCT), were enrolled. Lesion-specific three-dimensional coronary artery models were created using OCT data. WSS was computed with computational fluid dynamics analysis. PR was classified into upstream-PR, minimum lumen area-PR, and downstream-PR according to the PR's longitudinal location, and into central-PR and lateral-PR according to the disrupted fibrous cap circumferential location. In the longitudinal 3-mm segmental analysis, multivariate analysis demonstrated that higher WSS in the upstream segment was independently associated with upstream-PR, and thinner fibrous cap was independently associated with downstream-PR. In the PR cross-sections, the PR region had a significantly higher average WSS than non-PR region. In the cross-sectional analysis, the in-lesion peak WSS was frequently observed in the lateral (66.7%) and central regions (70%) in lateral-PR and central-PR, respectively. Multivariate analysis demonstrated that the presence of in-lesion peak WSS at the lateral region, thinner broken fibrous cap, and larger lumen area were independently associated with lateral-PR, while the presence of in-lesion peak WSS at the central region and thicker broken fibrous cap were independently associated with central-PR. In conclusion, OCT-based WSS simulation revealed that high WSS might be related to the longitudinal and circumferential locations of PR., (© 2023. Springer Japan KK, part of Springer Nature.)

Objectives: This study aimed to assess discordance between results of instantaneous wave-free ratio (iFR), fractional flow reserve (FFR), and intravascular ultrasound (IVUS) in intermediate left main coronary (LM) lesions, and its impact on clinical decision making and outcome., Methods: We enrolled 250 patients with a 40%-80% LM stenosis in a prospective, multicenter registry. These patients underwent both iFR and FFR measurements. Of these, 86 underwent IVUS and assessment of the minimal lumen area (MLA), with a 6 mm2 cutoff for significance., Results: Isolated LM disease was recognized in 95 patients (38.0%), while 155 patients (62.0%) had both LM disease and downstream disease. In 53.2% of iFR+ and 56.7% of FFR+ LM lesions, the measurement was positive in only one daughter vessel. iFR/FFR discordance occurred in 25.0% of patients with isolated LM disease and 36.2% of patients with concomitant downstream disease (P=.049). In patients with isolated LM disease, discordance was significantly more common in the left anterior descending artery and younger age was an independent predictor of iFR-/FFR+ discordance. iFR/MLA and FFR/MLA discordance occurred in 37.0% and 29.4%, respectively. Within 1 year of follow-up, major cardiac adverse events (MACE) occurred in 8.5% and 9.7% (P=.763) of patients whose LM lesion was deferred or revascularized, respectively. Discordance was not an independent predictor of MACE., Conclusions: Current methods of estimating LM lesion significance often yield discrepant findings, complicating therapeutic decision-making.

Acute coronary syndrome (ACS) is the most severe form of ischemic heart disease. Although it is caused by atherosclerotic plaque thrombosis or nonatherosclerotic causes, its pathophysiological mechanism of ACS is not fully understood, and its concept is constantly updated and developed. At present, the main pathophysiological mechanisms include plaque rupture, plaque erosion, calcified nodules (CN) and non-atherosclerotic causes such as coronary vasospasm and myocardial bridging (MB). These mechanisms may overlap and coexist in some ACS patients. Therefore, the pathophysiological mechanism of ACS is complex, and is of great significance for the diagnosis and treatment of ACS. This review will discuss the pathophysiological mechanisms of ACS to provide new thoughts on the pathogenesis, diagnosis and treatment of ACS., Competing Interests: The authors declare no conflict of interest., (Copyright: © 2023 The Author(s). Published by IMR Press.)

Optical coherence tomography (OCT) is an intravascular imaging technique that uses near-infrared light. OCT provides high-resolution cross-sectional images of coronary arteries and enables tissue characterization of atherosclerotic plaques. OCT can identify plaque rupture, plaque erosion, and calcified nodule in culprit lesions of acute coronary syndrome. OCT can also detect important morphologic features of vulnerable plaques such as thin fibrous caps, large lipid cores, macrophages accumulation, intraplaque microvasculature, cholesterol crystals, healed plaques, and intraplaque hemorrhage., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Aim: The actual occurrence of spontaneous plaque rupture in mice has been a matter of debate. We report on an in vivo observation of the actual event of possible plaque disruption in a living ApoE-/- mouse. Methods and Results: During live contrast-enhanced ultrasonography of a 50-week-old ApoE-/- male mouse, symptoms suggesting plaque disruption in the brachiocephalic artery were observed. Histological analysis confirmed the presence of advanced atherosclerotic lesions with dissections and intraplaque hemorrhage in the affected brachiocephalic trunk, pointing towards plaque rupture as the cause of the observed event. However, we did not detect a luminal thrombus or cap rupture, which is a key criterion for plaque rupture in human atherosclerosis. Conclusion: This study reports the real-time occurrence of a possible plaque rupture in a living ApoE-/- mouse.

Although recent optical coherence tomography (OCT) studies have focused on spotty calcification, whether there were any characteristics in the concomitant existence of calcification and plaque rupture remains unknown. The aim of the present study was to investigate the characteristics of spotty calcification in acute coronary syndrome (ACS) patients with or without plaque rupture, using OCT. This study enrolled 98 consecutive patients with ACS. OCT image acquisitions were performed in the culprit lesions, and patients were divided into the plaque rupture group ( n = 38) and the non-rupture group ( n = 60). The frequency of spotty calcification ( p = 0.006), thin-capped fibroatheroma ( p = 0.012), macrophage infiltration ( p = 0.022), and the number of spotty calcification per patient ( p < 0.001) were significantly higher and the largest arc and the minimum depth of spotty calcification from the luminal surface were significantly smaller in the rupture group. Moreover, in the rupture group, most of the spotty calcifications in the site nearest to the minimum lumen area were observed in the proximal portion of that site, and tended to be located near the plaque rupture. Multivariate analysis revealed that the presence of spotty calcification (OR 3.19, 95 % CI 1.12-9.76, p = 0.030) and age (OR 1.08, 95 % CI 1.02-1.14, p = 0.008) were independent predictive factors for plaque rupture. This study demonstrates the characteristics of spotty calcification in ACS patients with plaque rupture and the positional relationship between spotty calcification and plaque rupture. These detailed observations could impact on treatment strategies for the prevention of ACS. [ABSTRACT FROM AUTHOR]

Background: Few studies have evaluated the distinct ability of contrast-enhanced ultrasonography for detecting carotid plaque rupture versus histological observations. Aims: The aim of this study was to quantitatively assess the ability of contrast-enhanced ultrasonography to detect plaque rupture compared to ultrasonographic and histological images in terms of geometric accordance. Methods: Carotid plaque morphology was classified as "smooth," "irregular," or "ulcerated" on 45 conventional ultrasonography and contrast-enhanced ultrasonography images from consecutive patients undergoing endarterectomy, and 55 regions of interests were captured on contrast-enhanced ultrasonography. A comparative study with a receiver operating characteristic analysis was performed using histological findings for reference. Results: Contrast-enhanced ultrasonography exhibited a higher percentage of "ulcerated" findings in patients with plaque rupture compared to conventional ultrasonography (P1/40.002) as well as an association with thrombus formation (P1/40.048) and fibrous cap disruption (P<0.0001). On contrast-enhanced ultrasonography, "ulcerated" were significantly more likely than "smooth" findings when the fibrous cap was disrupted (odds ratio (OR), 41.5). The receiver operating characteristic areas under the curve for the orifice, depth, and width of the concavities on contrast-enhanced ultrasonography were significantly greater than 0.5, while their optimal cut-off values were 1.40 mm, 1.30 mm, and 1.88 mm, respectively. When one of these variables was greater than the optimal cut-off value, the sensitivity, negative hit rate, and odds ratio for detecting fibrous cap disruption were 91.3%, 91.6%, and 23.1, respectively. Conclusions: In our study, contrast-enhanced ultrasonography has high sensitivity for identifying histological plaque rupture, and the measurement of concavity on contrast-enhanced ultrasonography may enable the accurate detection of fibrous cap disruption. [ABSTRACT FROM AUTHOR]

The prevalence of atherosclerotic disease continues to increase, and despite significant reductions in major cardiovascular events with current medical interventions, an additional therapeutic window exists. Atherosclerotic plaque growth is a complex integration of cholesterol penetration, inflammatory cell infiltration, vascular smooth muscle cell (VSMC) migration, and neovascular invasion. A family of matrix-degrading proteases, the matrix metalloproteinases (MMPs), contributes to all phases of vascular remodeling. The contribution of specific MMPs to endothelial cell integrity and VSMC migration in atherosclerotic lesion initiation and progression has been confirmed by the increased expression of these proteases in plasma and plaque specimens. Endogenous blockade of MMPs by the tissue inhibitors of metalloproteinases (TIMPs) may attenuate proteo-lysis in some regions, but the progression of matrix degeneration suggests that MMPs predominate in atherosclerotic plaque, precipitating vulnerability. Plaque neovascularization also contributes to instability and, coupling the known role of MMPs in angiogenesis to that of atherosclerotic plaque growth, interest in targeting MMPs to facilitate plaque stabilization continues to accumulate. This article aims to review the contributions of MMPs and TIMPs to atherosclerotic plaque expansion, neovascularization, and rupture vulnerability with an interest in promoting targeted therapies to improve plaque stabilization and decrease the risk of major cardiovascular events. [ABSTRACT FROM AUTHOR]

One well-established cause of ischemic stroke is atherosclerotic plaque rupture in the carotid artery. Rupture occurs when a tear in the fibrous cap exposes highly thrombogenic material in the lipid core. Though some fibrous cap material properties have been measured, such as ultimate tensile strength and stress-strain responses, there has been very little, if any, data published regarding the fracture behavior of atherosclerotic fibrous caps. This study aims to characterize the qualitative and quantitative fracture behavior of human atherosclerotic plaque tissue obtained from carotid endarterectomy samples using two different metrics. Uniaxial tensile experiments along with miniature single edge notched tensile (MSENT) experiments were performed on strips of isolated fibrous cap. Crack tip opening displacement (CTOD) and stress in the un-cracked segment (UCS) were measured at failure in fibrous cap MSENT specimens subjected to uniaxial tensile loading. Both CTOD and the degree of crack blunting, measured as the radius of curvature of the crack tip, increased as tearing propagated through the tissue. Higher initial stress in the UCS is significantly correlated with higher collagen content and lower macrophage content in the fibrous cap (ρ = 0.77, P = 0.009; ρ = −0.64, P = 0.047; respectively). Trends in the data show that higher CTOD is inversely related to collagen content, though the sample size in this study is insufficient to statistically substantiate this relationship. To the authors’ knowledge, this is the pioneering study examining the fracture behavior of fibrous caps and the first use of the CTOD metric in vascular tissue. Statement of Significance A tear in the fibrous cap of atherosclerotic plaque can lead to ischemic stroke or myocardial infarction. While there is some information in the literature regarding quantitative measures of fibrous cap failure, there is little information regarding the behavior of the tissue during failure. This study examines the failure behavior of fibrous caps both qualitatively, by examining how and where the tissue fails, and quantitatively, by measuring (a) crack tip opening displacement (CTOD) in vascular tissue for the first time and (b) uniaxial stress in the un-cracked segment (UCS). This study shows that both metrics should be evaluated when assessing plaque vulnerability. [ABSTRACT FROM AUTHOR]

Aims The prevalence of plaque rupture at the culprit lesion identified by optical coherence tomography (OCT) in different clinical subset of patients undergoing coronary angiography and its clinical predictors remain to be defined. Methods All studies including patients with OCT evaluation of the culprit coronary plaque were included. The prevalence of culprit plaque rupture (CPR) and thin-cap fibro-atheroma (TCFA) were the primary endpoints. The factors associated with these findings were studied in a subset of patients with different clinical presentations [ST-elevation myocardial (STEMI) vs. nonST-elevation myocardial infarction (NSTEMI) vs. unstable angina (UA) vs. stable angina pectoris (SAP)]. Results One hundred and fifty citations were initially appraised at the abstract level and 23 full-text studies were assessed. The mean prevalence of CPR and TCFA was 48.1% (40.5-55.8) and 48.7% (37.4-60.1), respectively. The prevalence of CPR and TCFA were higher in STEMI (70.4 and 76.6%) than in NSTEMI (55.6 and 56.3%) and UA (39.1 and 52.9%) or SAP (6.2 and 22.8%). In the overall population at meta-regression analysis, TCFA and current smoking were the only predictors of CPR (B 3.6:2.0-5.1, P < 0.001 and 0.06:0.02-0.1, P = 0.002, respectively). The factors associated with CPR were different depending on clinical presentation. Hypertension was the only clinical predictor for STEMI (B 3.3: 1.2.-5.3 P = 0.001), while advanced age (B 0.12: 0.02-0.22, P = 0.021), diabetes mellitus (B 0.04: 0.01-0.08, P = 0.012), and hyperlipidaemia (B 0.07:0.02-0.11, P = 0.005) were the predictors in NSTEMI and UA. No clinical predictor was found in SA. Conclusions Our analysis showed high rates of CPR and TCFA detected by OCT in CAD patients, especially in those with ACS, although their prevalence is not negligible in stable patients. TCFA seems to be a strong predictor of CPR in all the ACS scenarios. [ABSTRACT FROM AUTHOR]

The morphologic features of familial coronary artery disease (CAD) resulting in sudden coronary death (SCD) are poorly studied. The presence and type of culprit lesions may have important implications in the genetic basis for familial heart disease. Autopsies of SCD victims over a 5-year period from a statewide medical examiner's office were studied. Premature familial disease was defined as sudden death at ≤50 years in women and ≤45 years in men, with premature SCD or acute coronary syndrome in a first-degree relative. Culprit lesion was defined as acute plaque rupture, plaque erosion, and severe narrowing without thrombus (stable plaque). There were 174 acute plaque ruptures (age 49±10 years, 9% women), 49 plaque erosions (age 45±8 years, 37% women), and 213 stable plaques (age 53±11 years, 22% women). There were 8 plaque rupture with family history. There were 9 plaque erosions with family history. There were 7 stable plaques with family history. The rate of familial history in premature coronary disease was 18.4% in erosions, 4.6% in ruptures (p=.02 vs. erosion), and 3.3% in stable plaque (p=.002 vs. erosion). We concluded that the frequency of family history of premature sudden death due to CAD may be higher in plaque erosion as compared to patients dying with acute plaque rupture or stable plaque. [ABSTRACT FROM AUTHOR]

The pathogenesis of the acute coronary syndrome (ACS) is very complex and not fully clarified, bringing in front the questions regarding the differences between acute coronary syndrome with ST segment elevation (STEMI) and the one without ST segment elevation (UA/NSTEMI), because there isn't always a ruptured plaque beneath all coronary thrombi. Indeed, plaque rupture declines as a cause of ACS, while superficial erosion appears on the rise, and STEMI wanes as NSTEMI waxes. There is a change in the character of human plaques in the statin era: they are getting less fatty and less "inflamed". The plaques prone to erosion: have a poor lipid content, are rich in proteoglycan and glycosaminoglycan, with non-fibrillar collagen breakdown, few inflammatory cells, endothelial cells apoptosis and secondary neutrophil involvement, they appear more frequently in patients with diabetes, with high triglycerides and have a female predominance. Understanding the pathogenesis is essential regarding the potential effective treatment: in patients with plaque erosion, as inflammation represents an intense local thrombogenic stimulus, a potent antithrombotic treatment might be one of the treatment choice, so the treatment choice expands beyond the traditional focus on reducing stenoses. [ABSTRACT FROM AUTHOR]

Persistent inflammation and mechanical injury associated with cholesterol crystal accretion within atherosclerotic plaques typically precedes plaque disruption (rupture and/or erosion) and thrombosis-often the terminal events of atherosclerotic cardiovascular disease. To elucidate the mechanisms of these events, the atherosclerotic rabbit model provides a unique and powerful tool that facilitates studies of atherogenesis starting with plaque buildup to eventual disruption. Examination of human coronary arteries obtained from patients who died with myocardial infarction demonstrates evidence of cholesterol crystals perforating the plaque cap and intimal surface of the arterial wall that can lead to rupture. These observations were made possible by omitting ethanol, an avid lipid solvent, from the tissue processing steps. Importantly, the atherosclerotic rabbit model exhibits a similar pathology of cholesterol crystals perforating the intimal surface as seen in ruptured human plaques. Local and systemic inflammatory responses in the model are also similar to those observed in humans. The strong parallel between the rabbit and human pathology validates the atherosclerotic rabbit model as a predictor of human pathophysiology of atherosclerosis. Thus, the atherosclerotic rabbit model can be used with confidence to evaluate diagnostic imaging and efficacy of novel anti-atherosclerotic therapy. [ABSTRACT FROM AUTHOR]

The types of lesion instability responsible for the majority of acute coronary events frequently include plaque disruption and plaque erosion with superimposed thrombosis. The term 'vulnerable plaque' is used to describe atherosclerotic (ATS) plaques that are particularly prone to rupture and susceptible to thrombus formation, such as the thin-cap fibroatheroma (TCFA). The aim of the present study was to assess the morphological and histological differences between plaques that are unstable and those that are vulnerable to instability. Carotid artery endarterectomy specimens were obtained from 26 patients with carotid artery stenosis, consisting of 20 men and 6 women (age range, 35-80 years). Histological and morphometric methods were used to visualize and characterize the ATS plaques. Among the 26 carotid ATS plaques, 23% were stable, 23% were unstable and 54% were vulnerable. With regard to morphometric characteristics, the following mean values were obtained for the TCFA and unstable plaques, respectively: Fibrous cap thickness, 21.91 and 11.66 µM; proportion of necrotic core area in the total plaque area, 25.90 and 22.03%; and the proportion of inflammatory area in the total plaque area, 8.41 and 3.04%. No plaque calcification was observed in any of them. Since ATS coronary artery disease is considerably widespread and fatal, it is crucial to further study ATS lesions to obtain an improved understanding of the nature of vulnerable and unstable plaques. The methods used to detect plaque size, necrotic core area and fibrous cap thickness are considered to be particularly useful for identifying vulnerable and unstable plaques. [ABSTRACT FROM AUTHOR]

Apoptosis plays an important role in atherogenesis and rupture of vulnerable plaques in coronary artery disease. FAS and FAS ligand (FASL) induce apoptosis when FAS binds to FAS-L. However sFas blocks apoptosis by binding to FAS and FASL or sFasL. The present study is sought to examine the role of extrinsic apoptotic genes (FAS, FASL) polymorphism and serum levels of FAS, FASL in the pathogenesis and susceptibility to CAD in south Indian population. The study included 300 CAD patients and 300 healthy controls. Lipid profiles, sFas, sFasL were estimated by commercially available kits. FAS −670 G>A, FASL −844 T>C genotypes were analyzed by PCR-RFLP. Secondary structures of pre mRNA were analyzed by the Vienna RNA webserver and gene-gene and gene-environment interactions were determined by MDR analysis. Total cholesterol, triglyceride and LDL levels were significantly high in CAD patients compared to the controls. Molecular analysis revealed that the frequency of the AA genotype of FAS (54 % vs 27 %) and CC genotypes of FASL (10.3 % vs 1.3 %) were high in CAD patients compared to controls. Secondary structure analysis of FAS and FASL confirmed our molecular analysis. sFas levels were low while serum sFasL were high in CAD patients. MDR analysis revealed synergistic effects of gene polymorphisms and additive effects of epidemiological factors on risk of CAD. Polymorphisms of FAS (−670 G/A), FASL (−844 T/C) and their circulating levels play an important role in the pathology of CAD. [ABSTRACT FROM AUTHOR]

Optical coherence tomography (OCT) is an intracoronary imaging modality which utilizes near-infrared light to provide high-resolution cross-sectional in-vivo images of the coronary artery. OCT imaging technique enables detailed evaluation of plaque morphology in patients with acute coronary syndrome and helps to understand the underlying mechanisms including plaque rupture, plaque erosion, and calcified nodule. It is useful to optimize percutaneous coronary intervention, and evaluate vascular response to coronary intervention and pharmacological therapy. Advances in intracoronary OCT and further research on clinical applications have the potential to contribute to a better prognosis in acute coronary syndrome. [ABSTRACT FROM AUTHOR]

We investigated the feasibility of using sonography of abnormal plaque motion to diagnose high-risk carotid lesions ranging from plaque rupture to ulcer formation. Fifty consecutive carotid arteries of 49 patients (71 ± 7 y, 37 males) who underwent carotid endarterectomy were investigated by carotid sonography to find a plaque concavity (sonographic ulcer [SU]), fine trembling motion inside the plaque (FTMI) and systolic retractive motion of the plaque surface (SRMS). Plaque rupture or ulcer, necrotic core and intra-plaque hemorrhage were determined at carotid endarterectomy. Twenty-two SUs, 41 cases of FTMI and 20 cases of SRMS were detected by carotid sonography. The sensitivity and specificity of SU in diagnosing plaque rupture or ulcer at carotid endarterectomy were 48% and 90%, and those of FTMI were 93% and 60%. Plaques with SRMS more frequently had both a necrotic core and intra-plaque hemorrhage than those without SRMS (80% vs. 30%, p = 0.0005). Abnormal plaque motion detected by carotid sonography is useful in detecting a ruptured or ulcerated plaque with a necrotic core and/or hemorrhage. [ABSTRACT FROM AUTHOR]

Background and aims MRI has been validated as a suitable imaging modality for in vivo , non-invasive detection of atherosclerosis and has provided quantitative predictors of high-risk plaque. Here, we apply serial MRI to monitor the natural progression of plaques over a 3-month period in a rabbit model of atherothrombosis to determine differences over time between plaques that ultimately disrupt to form a luminal mural thrombus and plaques that remain stable. Methods Atherosclerotic plaques were induced in 12 male New Zealand White (NZW) rabbits by aortic endothelial injury and a 1% cholesterol diet. The rabbits were imaged 5 times: at baseline, 1, 2, and 3 months, and 48hr after pharmacological triggering for plaque disruption. Results Starting at 2 months, plaques that disrupted after triggering exhibited a higher remodeling ratio (RR, 1.05 ± 0.11 vs 0.97 ± 0.10, p = 0.0002) and a larger vessel wall area (VWA, 6.99 ± 1.54 mm 2 vs 6.30 ± 1.37 mm 2 , p = 0.0072) than the stable non-disrupted plaques. The same trends were observed at 3 months: plaques that disrupted had a higher RR (1.04 ± 0.02 vs 0.99 ± 0.01, p = 0.0209), VWA (8.19 ± 2.69 mm 2 vs 6.81 ± 1.60 mm 2 , p = 0.0001), and increased gadolinium uptake (75.51 ± 13.77% for disrupted vs 31.02 ± 6.45% for non-disrupted, p = 0.0022). Conclusions MR images of plaques that disrupted revealed larger VWAs, RRs, and increased gadolinium uptake at 2 months and continued progression of these vulnerable features between 2 and 3 months. Non-disrupted plaques had an independent history without these hallmarks of vulnerability. Our results show that MRI can provide early detection of plaques at a higher-risk for luminal thrombosis. [ABSTRACT FROM AUTHOR]

Background While ‘plaque rupture’ is the paradigm of type 1 myocardial infarction (T1MI), T2MI is myocardial necrosis secondary to oxygen supply-demand mismatch. Being a heterogeneous and rather newly defined group, data are lacking about T2MI. Methods A retrospective review of medical records of patients diagnosed with T2MI in the Rabin Cardiology Center, Israel between the years 2007 and 2012 was performed. Following a descriptive analysis, we used multivariate time dependent models to estimate the association of T2MI with the risk for 30-day, 1-year, and 5-year all-cause-mortality and major adverse cardiovascular events (MACE), and compared it to a T1MI group matched for age, gender and electrocardiographic changes. Results The study included 107 T2MI (and 107 T1MI) patients. Sepsis, anemia, and atrial fibrillation were the most common etiologies. Triple anti-thrombotic therapy was given to 22% of T2MI patients (vs. 82% of T1MI patients, p < 0.001). Twenty-five percent were managed using urgent percutaneous coronary intervention. Angiography unmasked acute plaque rupture in 29% of T2MI patients group. Compared to T1MI, T2MI was associated with higher all-cause-mortality rate: adjusted-hazard-ratio 7.14 (1.31–38.9) at 30 days, 3.42 (1.51–7.75) at 1 year, and 2.08 (1.14–3.81) at 5 years follow-up. MACE risk was consistent between T2 and T1MI patients. Conclusions The most common T2MI triggers are sepsis, anemia, and atrial fibrillation. Compared to a T1MI population, T2MI is associated with higher short- and long-term mortality rates but equal cardiovascular mortality and MACE risk. As many as 30% may harbor plaque rupture and in fact have T1MI. [ABSTRACT FROM AUTHOR]