Rupture of a Non-Obstructive Plaque.
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ABSTRACT:
SUBMITTER: Alaiti MA
PROVIDER: S-EPMC8167421 | biostudies-literature | 2018 Apr
REPOSITORIES: biostudies-literature
Publications
Rupture of a Non-Obstructive Plaque.
Alaiti Mohamad Amer MA Fares Anas A Bezerra Hiram G HG
The Journal of invasive cardiology 20180401 4
An invasive and non-invasive imaging series representing a classic rupture of a non-obstructive plaque with thin-cap fibroatheroma. ...[more]
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| S-EPMC4311011 | biostudies-literature
Project description:RationalePlaque rupture is the proximate cause of most myocardial infarctions and many strokes. However, the molecular mechanisms that precipitate plaque rupture are unknown.ObjectiveBy applying proteomic and bioinformatic approaches in mouse models of protease-induced plaque rupture and in ruptured human plaques, we aimed to illuminate biochemical pathways through which proteolysis causes plaque rupture and identify substrates that are cleaved in ruptured plaques.Methods and resultsWe performed shotgun proteomics analyses of aortas of transgenic mice with macrophage-specific overexpression of urokinase (SR-uPA+/0 mice) and of SR-uPA+/0 bone marrow transplant recipients, and we used bioinformatic tools to evaluate protein abundance and functional category enrichment in these aortas. In parallel, we performed shotgun proteomics and bioinformatics studies on extracts of ruptured and stable areas of freshly harvested human carotid plaques. We also applied a separate protein-analysis method (protein topography and migration analysis platform) to attempt to identify substrates and proteolytic fragments in mouse and human plaque extracts. Approximately 10% of extracted aortic proteins were reproducibly altered in SR-uPA+/0 aortas. Proteases, inflammatory signaling molecules, as well as proteins involved with cell adhesion, the cytoskeleton, and apoptosis, were increased. ECM (Extracellular matrix) proteins, including basement-membrane proteins, were decreased. Approximately 40% of proteins were altered in ruptured versus stable areas of human carotid plaques, including many of the same functional categories that were altered in SR-uPA+/0 aortas. Collagens were minimally altered in SR-uPA+/0 aortas and ruptured human plaques; however, several basement-membrane proteins were reduced in both SR-uPA+/0 aortas and ruptured human plaques. Protein topography and migration analysis platform did not detect robust increases in proteolytic fragments of ECM proteins in either setting.ConclusionsParallel studies of SR-uPA+/0 mouse aortas and human plaques identify mechanisms that connect proteolysis with plaque rupture, including inflammation, basement-membrane protein loss, and apoptosis. Basement-membrane protein loss is a prominent feature of ruptured human plaques, suggesting a major role for basement-membrane proteins in maintaining plaque stability.
| S-EPMC7508285 | biostudies-literature
Project description:A significant proportion of patients evaluated for chest pain have ischemia with non-obstructive coronary artery disease (INOCA). Studies have shown INOCA is associated with increased risk of major adverse cardiac events and significant burden on the health care system. While there is scarce scientific evidence on management of INOCA, the CorMicA trial showed that stratified medical therapy based on the type of INOCA improved patients' symptoms and quality of life. There are multiple ongoing trials, including Women's IschemiA Trial to Reduce Events in Non-ObstRuctIve CORonary Artery Disease (WARRIOR trial), assessing the benefit of intensive medical therapy versus usual care for this increasingly recognized clinical entity. In this review, we discuss the definition of INOCA, epidemiology and risk factors, pathophysiology, and management as well as the current knowledge gaps and ongoing clinical trials in this arena.
| S-EPMC10125006 | biostudies-literature
Project description:BackgroundCoronary atherosclerosis can lead to acute clinical events upon atherosclerotic plaque rupture (PR) or erosion and arterial thrombus formation. Identifying the effect of distinct plaque characteristics on clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI) is critical for clinical therapy. Our goal was to ascertain the correlation between clinical outcome, long-term prognosis, and morphological plaque characteristics in STEMI.MethodsThe data used in this prospective cohort research came from a prior multicenter prospective cohort study (ChiCTR1800019923). One hundred and thirteen consecutive STEMI patients were involved in our cohort study. Patients with STEMI who received primary percutaneous coronary intervention (pPCI) within 24 hours of symptom onset were included in the study and divided into two groups according to plaque characteristics derived from intravascular ultrasound (IVUS): a PR group and a non-PR group. The primary outcome was the incidence of no reflow or slow flow, the secondary outcome was major adverse cardiac events (MACEs) at 1-year follow-up.ResultsThis study enrolled 113 consecutive patients with STEMI [mean age 56 (range, 49-65.5) years; males 90.27%]. Of the 113 patients, PR was found in 93 (82.3%), while non-PR was found in 20 (17.7%). The PR group had a higher rates of plaque eccentricity index (64.28%±22.69% vs. 60.08%±15.54%; P=0.045), higher rates of lipid pool-like images (62.37% vs. 30.00%; P=0.008), and higher rates of tissue prolapse (22.95% vs. 13.33%; P=0.01). Compared with that in the non-PR group, the incidence of no reflow or slow flow was higher in the PR group after pPCI (26.88% vs. 5.00%; P=0.04). Multivariable logistic regression showed that PR [odds ratio (OR) =8.188; 95% confidence interval (CI): 1.020-65.734; P=0.048] was an independent predictor of no reflow or slow flow. Survival analysis revealed no significant differences in MACE incidence between the two groups at 1-year follow-up (7.61% vs. 10.00%; P=0.66). Furthermore, 29 patients with PR were treated without stenting, most of them were free of MACEs (27/29). MACE between subgroups of stenting and non-stenting had no significant differences (7.94% vs. 6.90%; P=0.86) in the PR group.ConclusionsIn comparison to patients with non-PR, PR were not associated with the risk of recurrent myocardial infarction (MI), revascularization, heart failure, or cardiac death at 1-year follow-up, while associated with an increased incidence of no reflow or slow flow during pPCI. This observation would be considered while risk stratification and dealing with patients who have STEMI. Most patients with PR who were treated without stenting were MACE free. Further research should be conducted to determine whether interventional treatment without stenting is feasible for patients with STEMI and PR.
| S-EPMC11635223 | biostudies-literature
Project description:ObjectivesThe aim of this study was to identify the determinants of plaque structural stress (PSS) and the relationship between PSS and plaques with rupture.BackgroundPlaque rupture is the most common cause of myocardial infarction, occurring particularly in higher risk lesions such as fibroatheromas. However, prospective intravascular ultrasound-virtual histology studies indicate that <10% higher risk plaques cause clinical events over 3 years, indicating that other factors also determine plaque rupture. Plaque rupture occurs when PSS exceeds its mechanical strength; however, the determinants of PSS and its association with plaques with proven rupture are not known.MethodsWe analyzed plaque structure and composition in 4,053 virtual histology intravascular ultrasound frames from 32 fibroatheromas with rupture from the intravascular ultrasound-virtual histology in Vulnerable Atherosclerosis study and 32 fibroatheromas without rupture on optical coherence tomography from a stable angina cohort. Mechanical loading in the periluminal region was estimated by calculating maximum principal PSS by finite element analysis.ResultsPSS increased with increasing lumen area (r = 0.46; p = 0.001), lumen eccentricity (r = 0.32; p = 0.001), and necrotic core ≥10% (r = 0.12; p = 0.001), but reduced when dense calcium was ≥10% (r = -0.12; p = 0.001). Ruptured fibroatheromas showed higher PSS (133 kPa [quartiles 1 to 3: 90 to 191 kPa] vs. 104 kPa [quartiles 1 to 3: 75 to 142 kPa]; p = 0.002) and variation in PSS (55 kPa [quartiles 1 to 3: 37 to 75 kPa] vs. 43 kPa [quartiles 1 to 3: 34 to 59 kPa]; p = 0.002) than nonruptured fibroatheromas, with rupture primarily occurring either proximal or immediately adjacent to the minimal luminal area (87.5% vs. 12.5%; p = 0.001). PSS was higher in segments proximal to the rupture site (143 kPa [quartiles 1 to 3: 101 to 200 kPa] vs. 120 kPa [quartiles 1 to 3: 78 to 180 kPa]; p = 0.001) versus distal segments, associated with increased necrotic core (19.1% [quartiles 1 to 3: 11% to 29%] vs. 14.3% [quartiles 1 to 3: 8% to 23%]; p = 0.001) but reduced fibrous/fibrofatty tissue (63.6% [quartiles 1 to 3: 46% to 78%] vs. 72.7% [quartiles 1 to 3: 54% to 86%]; p = 0.001). PSS >135 kPa was a good predictor of rupture in higher risk regions.ConclusionsPSS is determined by plaque composition, plaque architecture, and lumen geometry. PSS and PSS variability are increased in plaques with rupture, particularly at proximal segments. Incorporating PSS into plaque assessment may improve identification of rupture-prone plaques.
| S-EPMC5725311 | biostudies-literature
Project description:The leading cause of heart disease in developed countries is coronary atherosclerosis, which is not simply a result of ageing but a chronic inflammatory process that can lead to acute clinical events upon atherosclerotic plaque rupture or erosion and arterial thrombus formation. The composition and location of atherosclerotic plaques determine the phenotype of the lesion and whether it is more likely to rupture or to erode. Although plaque rupture and erosion both initiate platelet activation on the exposed vascular surface, the contribution of platelets to thrombus formation differs between the two phenotypes. In this review, plaque phenotype is discussed in relation to thrombus composition, and an overview of important mediators (haemodynamics, matrix components, and soluble factors) in plaque-induced platelet activation is given. As thrombus formation on disrupted plaques does not necessarily result in complete vessel occlusion, plaque healing can occur. Therefore, the latest findings on plaque healing and the potential role of platelets in this process are summarized. Finally, the clinical need for more effective antithrombotic agents is highlighted.
| S-EPMC10757869 | biostudies-literature
Project description:BackgroundIn coronary artery disease (CAD), plaque progression and plaque composition are associated with cardiovascular risk. Whether compositional plaque progression in non-obstructive CAD differs between women and men is less studied.MethodsWe included 31 patients (42% women) with chronic non-obstructive CAD from the Norwegian Registry of Invasive Cardiology, undergoing serial coronary computed tomography angiography (CCTA) on clinical indication (median inter-scan interval 1.8 [1.5-2.2] years). We performed quantitative and qualitative plaque analysis of all coronary artery segments.ResultsWomen were older compared to men (65 ± 8 years vs. 55 ± 12 years, p = 0.019), while there was no difference in the prevalence of hypertension, diabetes, smoking or statin treatment between groups. At baseline, women had a higher total plaque burden, more calcified plaques, and less fibro-fatty and necrotic core plaques compared to men (all p < 0.05). During follow-up, men showed faster progression of fibro-fatty plaques (4.0 ± 5.4 % per year vs. -0.6 ± 3.1 % per year, p = 0.019) and a greater reduction of fibrous plaques (-7.3 ± 6.1 % per year vs. 2.1 ± 7.2 % per year, p = 0.003) compared to women even after age adjustment. At follow-up, total plaque burden remained higher in women compared to men (24.9 ± 3.3 % vs. 21.1 ± 2.6 %, p = 0.001), while men had an increase in fibro-fatty (21.2 ± 9.3 % vs. 28.6 ± 9.8 %, p = 0.004) and necrotic core plaques (5.6 ± 3.6 % vs. 10.8 ± 7.2 %, p = 0.006), and a decrease in fibrous plaques (69.0 ± 11.9 % vs. 54.7 ± 13.7 %, p < 0.001). Women's plaque composition remained unaltered.ConclusionIn non-obstructive CAD, serial CCTA demonstrated a higher total plaque burden and a stable plaque composition in women, while men had a faster progression of unstable low-attenuating fibro-fatty plaques.Clinical trial registration: ClinicalTrials.gov: Identifier NCT04009421.
| S-EPMC10865024 | biostudies-literature
Project description:Despite the recent innovations in cardiovascular care, atherothrombosis is still a major complication of acute coronary syndromes (ACS). We evaluated the involvement of the CD31 molecule in thrombotic risk through the formation of monocyte-platelet (Mo-Plt) aggregates in patients with ACS with no-ST-segment elevation myocardial infarction (NSTEMI) on top of dual anti-platelet therapy (DAPT). We enrolled 19 control (CTRL) subjects, 46 stable angina (SA), and 86 patients with NSTEMI, of which, 16 with Intact Fibrous Cap (IFC) and 19 with Ruptured Fibrous Cap (RFC) as assessed by the Optical Coherence Tomography (OCT). The expression of CD31 on monocytes and platelets was measured. Following the coronary angiography, 52 NSTEMIs were further stratified according to thrombus grade (TG) evaluation. Finally, a series of ex vivo experiments verified whether the CD31 participates in Mo-Plt aggregate formation. In patients with NSTEMI, CD31 was reduced on monocytes and was increased on platelets, especially in NSTEMI presented with RFC plaques compared to those with IFC lesions, and in patients with high TG compared to those with zero/low TG. Ex vivo experiments documented an increase in Mo-Plt aggregates among NSTEMI, which significantly decreased after the CD31 ligation, particularly in patients with RFC plaques. In NSTEMI, CD31 participates in Mo-Plt aggregate formation in spite of optimal therapy and DAPT, suggesting the existence of alternative thrombotic pathways, as predominantly displayed in patients with RFC.
| S-EPMC8821091 | biostudies-literature
Project description:BackgroundNon-anastomotic thoracic aortic graft rupture is extremely rare and difficult to diagnose. Non-obstructive general angioscopy can help monitor the aortic intima and detect the locations of abnormal findings, while aortic angioscopy can detect vulnerable plaques in the aorta, which are difficult to visualize using conventional diagnostic methods. Herein, we report the case of a patient with non-anastomotic thoracic aortic graft rupture diagnosed using non-obstructive aortic angioscopy.Case presentationAn 85-year-old man who had undergone total arch replacement 5 years prior complained of chest pain. Emergent contrast-enhanced computed tomography (CT) revealed an intra-mediastinal hematoma around the vascular graft of the ascending aorta and angiography revealed pooling of contrast medium on the dorsal side of the vascular graft. We suspected extravasation of the thoracic vascular graft. Aortic angioscopic examination revealed a red vascular graft defect that matched extravasation at the contralateral level of the prosthetic left common carotid artery branch. Subsequently, non-anastomotic thoracic aortic graft rupture was diagnosed. The patient underwent a two-debranching thoracic endovascular aortic repair (Zone 0) with a right subclavian artery-left common carotid artery-left subclavian artery bypass. Postoperative angiography revealed disappearance of the extravasation from the graft rupture site, patent grafted vessels with flow, and no endoleak. Follow-up CT at 6 months postoperatively showed no extravasation.ConclusionsTo our knowledge, this is the first report of non-anastomotic thoracic aortic graft rupture detected using non-obstructive aortic angioscopy. Aortic angioscopy can help establish a definitive diagnosis in patients with aortic graft rupture.
| S-EPMC8921450 | biostudies-literature
Project description:Coronary plaque rupture is the most common cause of acute coronary syndrome. However, the timely biomarker-based diagnosis of plaque rupture remains a major unmet clinical challenge. Balloon dilatation and stent implantation during percutaneous coronary intervention (PCI) could cause plaque injury and rupture. Here we aimed to assess the possibility of circulating microRNAs (miRNAs) as biomarkers of acute coronary plaque rupture by virtue of the natural model of PCI-induced plaque rupture. Stable coronary artery disease patients underwent PCI with single stent implantation were recruited and a three-phase approach was conducted in the present study: (i) profiling of plasma miRNAs in a group of patients before (0 h) and after balloon dilatation for 1 h (1 h vs. 0 h), (ii) replication of significant miRNAs in the second group of patients (1 h vs. 0 h), (iii) validation of a multi-miRNAs panel in the third group of patients (0.5 h, 1 h vs. 0 h). Out of 24 miRNAs selected for replication, 6 miRNAs remained significantly associated with plaque rupture. In the validation phase, combinations of miR-483-5p and miR-451a showed the highest area under the receiver-operating-characteristic curve (AUC) (0.982; CI: 0.907-0.999) in patients with plaque rupture for 0.5 h; combinations of miR-483-5p and miR-155-5p showed the highest AUC (0.898; CI: 0.790-0.962) after plaque rupture for 1 h. In conclusion, using a profiling-replication-validation model, we identified 3 miRNAs including miR-155-5p, miR-483-5p and miR-451a, which may be biomarkers for the early identification of plaque rupture.
| S-EPMC5564633 | biostudies-other