Residual thrombus following plaque disruption contributes to rapid plaque progression

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Osamu Kurihara ◽  
Masamichi Takano ◽  
Makoto Araki ◽  
Akihiro Nakajima ◽  
Kyoichi Mizuno ◽  
...  
Keyword(s):  
Plaque Progression ◽  
Plaque Disruption ◽  
Residual Thrombus

Predictors of rapid plaque progression: an optical coherence tomography study

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Araki ◽  
T Yonetsu ◽  
O Kurihara ◽  
A Nakajima ◽  
H Lee ◽  
...  
Keyword(s):  
Morphological Changes ◽  
Multivariable Analysis ◽  
Morphological Characteristics ◽  
Critical Threshold ◽  
Rapid Progression ◽  
Plaque Progression ◽  
Plaque Disruption ◽  
Lipid Rich Plaque ◽  
Oct Imaging

Abstract Background Two patterns of plaque progression have been described: slow linear progression and rapid step-wise progression. The former will cause stable angina when the narrowing reaches a critical threshold, while the latter may lead to acute coronary syndromes or sudden cardiac death. Purpose The aim of the study was to identify morphologic predictors for rapid plaque progression. Methods Patients who had OCT imaging during the index procedure and follow-up angiography with a minimum of 6-month interval were selected. Non-culprit lesion was defined as a plaque with a diameter stenosis ≥30% on index angiogram. Lesion progression was defined as the decrease of angiographic minimum lumen diameter ≥0.4 mm at follow-up (mean, 7.1 months). Baseline morphological characteristics of the plaques with rapid progression were evaluated by OCT. In a subgroup with follow-up OCT imaging for plaques with progression, morphological changes from baseline to follow-up were assessed. Results Among 517 lesions, 50 lesions showed progression. These lesions had a significantly higher prevalence of lipid-rich plaque (76.0% vs. 50.5%), thin-cap fibroatheroma (TCFA) (20.0% vs. 5.8%), layered plaque (60.0% vs. 34.0%), macrophage accumulation (62.0% vs. 42.4%), microvessel (46.0% vs. 29.1%), plaque rupture (12.0% vs. 4.7%), and thrombus (6.0% vs. 1.1%), compared to those without progression. The multivariable analysis identified lipid-rich plaque [odds ratio (OR) 2.17, 95% confidence interval (CI) 1.02–4.62, p=0.045], TCFA (OR 5.85, 95% CI 2.01–17.03, p=0.001), and layered plaque (OR 2.19, 95% CI 1.03–4.17, p=0.040) as predictors of subsequent lesion progression. In a subgroup with follow-up OCT, a new layer was detected in 14/41 (34.1%) plaques. Conclusions Lipid-rich plaque, TCFA, and layered plaque were predictors of subsequent rapid plaque progression. A new layer, a signature of rapid progression through plaque disruption and healing, was detected in 1/3 of the cases. Funding Acknowledgement Type of funding source: None

Less Plaque Progression in TNF Inhibitor Users

2011 ◽  
Vol 44 (15) ◽  
pp. 26-27
Author(s):  
MICHELE G. SULLIVAN
Keyword(s):  
Tnf Inhibitor ◽  
Plaque Progression

scholarly journals OCT Findings in MINOCA

2021 ◽  
Vol 10 (13) ◽  
pp. 2759
Author(s):  
Krzysztof Bryniarski ◽  
Pawel Gasior ◽  
Jacek Legutko ◽  
Dawid Makowicz ◽  
Anna Kedziora ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Imaging Modality ◽  
Obstructive Coronary Artery Disease ◽  
Coronary Artery Spasm ◽  
Morphological Characteristics ◽  
Artery Dissection ◽  
Plaque Disruption ◽  
Artery Disease

Myocardial infarction with non-obstructive coronary artery disease (MINOCA) is a working diagnosis for patients presenting with acute myocardial infarction without obstructive coronary artery disease on coronary angiography. It is a heterogenous entity with a number of possible etiologies that can be determined through the use of appropriate diagnostic algorithms. Common causes of a MINOCA may include plaque disruption, spontaneous coronary artery dissection, coronary artery spasm, and coronary thromboembolism. Optical coherence tomography (OCT) is an intravascular imaging modality which allows the differentiation of coronary tissue morphological characteristics including the identification of thin cap fibroatheroma and the differentiation between plaque rupture or erosion, due to its high resolution. In this narrative review we will discuss the role of OCT in patients presenting with MINOCA. In this group of patients OCT has been shown to reveal abnormal findings in almost half of the cases. Moreover, combining OCT with cardiac magnetic resonance (CMR) was shown to allow the identification of most of the underlying mechanisms of MINOCA. Hence, it is recommended that both OCT and CMR can be used in patients with a working diagnosis of MINOCA. Well-designed prospective studies are needed in order to gain a better understanding of this condition and to provide optimal management while reducing morbidity and mortality in that subset patients.

scholarly journals Bone marrow-derived NGFR+ cells regulate arterial remodeling and those poor mobilizations in peripheral blood in acute coronary syndrome predicts plaque progression at the non-targeted lesion

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Takashima ◽  
S Usui ◽  
S Matsuura ◽  
C Goten ◽  
O Inoue ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Coronary Syndrome ◽  
Peripheral Blood ◽  
Funding Source ◽  
Arterial Remodeling ◽  
Plaque Progression ◽  
Wild Type ◽  
Plaque Volume ◽  
Coronary Syndrome

Abstract Background In our previous 5-year cohort study, we demonstrated that low gene expression of nerve growth factor receptor (NGFR) in peripheral leucocytes in acute coronary syndrome (ACS) predicted repetitive coronary interventions at the de novo lesions. An NGFR-positive cell has been demonstrated to reside in bone marrow (BM) stromal fraction and to be increased in peripheral blood mononuclear cell (MNCs) fraction in patients with ischemic heart disease. Purpose To investigate whether the BM-NGFR+ cell is associated with arterial remodeling and the relationship between the levels of peripheral NGFR+ cells after ACS and coronary plaque progression in an experimental and prospective clinical study. Methods and results In an experimental study, 8-week-old C57B6/J wild type male mice were subjected to irradiation with 9.6 Gy and transplantation with BM (BMT) isolated from GFP-transgenic NGFR wild type (WT) or knock-out (KO) mice at day 1. Four weeks after BMT, the right carotid artery was ligated for 4 weeks. Induced neointimal area was increased (p<0.05), where cells under apoptosis were decreased (p<0.05) in NGFR-KO-BMT group compared to WT-BMT group (n=4). NGFR+ cells were not detected in wild type sham-operated artery, whereas in the ligated artery in WT-BMT group NGFR+ cells assembled in the developed neointima and exclusively presented double positive with GFP, but absent in NGFR-KO-BMT group (p<0.05, n=4). In a clinical study, thirty patients with ACS who underwent primary percutaneous coronary intervention (PCI) were enrolled. The peripheral blood sample was collected on days 0, 3 and 7, and 9 months follow-up and the number of NGFR+MNCs were measured by flowcytometric analysis. The plaque volume at non-targeted coronary lesion (non-TL:>5 mm proximal or distal to the implanted stents) were quantitatively analysed using gray-scale intravascular ultrasound (IVUS) and Q-IVUS™ software at the acute phase and 9 months follow-up. The number of NGFR+MNCs in peripheral blood was 1.5-fold increased at day 3 (0.064±0.056%) compared to day 0 (0.042±0.030%) (p<0.05). The change in normalized total plaque volume (TAVN) at non-TL at 9 months was negatively correlated with the number of NGFR+MNCs at day 0 (r=−0.51), day 3 (r=−0.51) and 9 months (r=−0.59) after ACS (p<0.05). Multiple regression analysis showed that NGFR+MNCs at day 0 (β=−0.48, p=0.01) and CRP (β=−0.53, P<0.01) are independent factors associating with TAVN change at non-TL at 9 months, regardless of LDL-cholesterol control level. ROC analysis revealed that NGFR+MNCs <0.049 at day 0 predicted the increase of TAVN with AUC 0.78; sensitivity 0.82 and specificity 0.67. Conclusions Bone marrow-derived peripheral NGFR+ cells negatively regulate arterial remodeling through appropriate apoptosis of neointimal cells and the peripheral level of NGFR+ cells in ACS predicts plaque progression at the non-targeted lesion. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): KAKENHI

scholarly journals Erythrocytes: Central Actors in Multiple Scenes of Atherosclerosis

2021 ◽  
Vol 22 (11) ◽  
pp. 5843
Author(s):  
Chloé Turpin ◽  
Aurélie Catan ◽  
Olivier Meilhac ◽  
Emmanuel Bourdon ◽  
François Canonne-Hergaux ◽  
...  
Keyword(s):  
Iron Homeostasis ◽  
The Body ◽  
Diabetic Patients ◽  
Special Focus ◽  
Plaque Progression ◽  
Cell Dysfunction ◽  
Circulating Cells ◽  
The Impact ◽  
Progression Of Atherosclerosis

The development and progression of atherosclerosis (ATH) involves lipid accumulation, oxidative stress and both vascular and blood cell dysfunction. Erythrocytes, the main circulating cells in the body, exert determinant roles in the gas transport between tissues. Erythrocytes have long been considered as simple bystanders in cardiovascular diseases, including ATH. This review highlights recent knowledge concerning the role of erythrocytes being more than just passive gas carriers, as potent contributors to atherosclerotic plaque progression. Erythrocyte physiology and ATH pathology is first described. Then, a specific chapter delineates the numerous links between erythrocytes and atherogenesis. In particular, we discuss the impact of extravasated erythrocytes in plaque iron homeostasis with potential pathological consequences. Hyperglycaemia is recognised as a significant aggravating contributor to the development of ATH. Then, a special focus is made on glycoxidative modifications of erythrocytes and their role in ATH. This chapter includes recent data proposing glycoxidised erythrocytes as putative contributors to enhanced atherothrombosis in diabetic patients.

scholarly journals Therapies Targeted at Non-Coding RNAs in Prevention and Limitation of Myocardial Infarction and Subsequent Cardiac Remodeling—Current Experience and Perspectives

2021 ◽  
Vol 22 (11) ◽  
pp. 5718
Author(s):  
Michal Kowara ◽  
Sonia Borodzicz-Jazdzyk ◽  
Karolina Rybak ◽  
Maciej Kubik ◽  
Agnieszka Cudnoch-Jedrzejewska
Keyword(s):  
Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Cardiac Remodeling ◽  
Therapeutic Option ◽  
Circular Rna ◽  
Plaque Progression ◽  
Cardiac Damage ◽  
Non Coding Rna ◽  
Causes Of Mortality ◽  
Long Non Coding Rna

Myocardial infarction is one of the major causes of mortality worldwide and is a main cause of heart failure. This disease appears as a final point of atherosclerotic plaque progression, destabilization, and rupture. As a consequence of cardiomyocytes death during the infarction, the heart undergoes unfavorable cardiac remodeling, which results in its failure. Therefore, therapies aimed to limit the processes of atherosclerotic plaque progression, cardiac damage during the infarction, and subsequent remodeling are urgently warranted. A hopeful therapeutic option for the future medicine is targeting and regulating non-coding RNA (ncRNA), like microRNA, circular RNA (circRNA), or long non-coding RNA (lncRNA). In this review, the approaches targeted at ncRNAs participating in the aforementioned pathophysiological processes involved in myocardial infarction and their outcomes in preclinical studies have been concisely presented.

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