Atherosclerosis T1-weighted characterization (CATCH): evaluation of the accuracy for identifying intraplaque hemorrhage with histological validation in carotid and coronary artery specimens

Abstract Introduction Intraplaque hemorrhage (IPH) is known to play an important role in plaque vulnerability in coronary artery. However, the biological reaction in IPH and clinical features of patients with IPH remain unknown, since most histological studies of IPH in coronary artery were performed on autopsy cases. Directional coronary atherectomy (DCA) enables the direct pathological evaluation of collected tissue from “living” patients. Purpose We aimed to clarify the clinical presentations and histopathologic features of IPH using specimens obtained by DCA. Method This multicentral prospective observational study included consecutive patients who underwent percutaneous coronary intervention for de novo lesions using DCA from June 2015 to February 2018. Histopathological sections that were collected from coronary plaques by DCA were evaluated and classified by the presence of IPH. IPH in DCA specimens was defined as clusters of hemosiderin (Figure A, arrows), erythrocytes (Figure B, arrow heads) and fibrin (Figure C, arrows) within the coronary plaque. A total of 154 de novo lesions from 154 patients were ultimately analyzed, and were divided into IPH group (n=37) and non-IPH group (n=117). Result Clinical profiles of patients in the two groups were comparable, except that unstable angina rather than chronic coronary syndrome was significantly more prevalent in the IPH group (32.4% vs. 16.2%, P=0.04). Histopathological analysis showed a significantly higher incidence of cellular-rich plaque (46.0% vs. 25.6%, P=0.02) and spindle-shaped cells (18.9% vs. 6.0%, P=0.02), which indicate active cell proliferations, in the IPH group. The prevalence of necrotic core was also higher in IPH group compared to non-IPH group (48.7% vs. 13.7%, P<0.01). Conclusion Pathohistological analysis revealed that coronary plaques with IPH had an active cell proliferation, and patients with IPH likely to had clinical presentations of unstable angina. Figure 1 Funding Acknowledgement Type of funding source: None

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Expression of Cyclophilin A in Coronary Artery Plaque with Intraplaque Hemorrhage Is More Frequent in Deceased Patients Who Had Impaired Kidney Function

International Heart Journal ◽

10.1536/ihj.20-283 ◽

2020 ◽

Vol 61 (6) ◽

pp. 1129-1134

Author(s):

Mai Nakai ◽

Aiko Shimokado ◽

Takashi Kubo ◽

Yosuke Katayama ◽

Tsuyoshi Nishiguchi ◽

...

Keyword(s):

Coronary Artery ◽

Kidney Function ◽

Cyclophilin A ◽

Intraplaque Hemorrhage ◽

Coronary Artery Plaque

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The Role of Angiogenesis in Coronary Artery Disease: A Double-Edged Sword: Intraplaque Angiogenesis in Physiopathology and Therapeutic Angiogenesis for Treatment

Current Pharmaceutical Design ◽

10.2174/1381612824666171227220815 ◽

2018 ◽

Vol 24 (4) ◽

pp. 451-464 ◽

Cited By ~ 5

Author(s):

Wen Wu ◽

Xiaobo Li ◽

Guangfeng Zuo ◽

Jiangqin Pu ◽

Xinlei Wu ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Plaque Rupture ◽

Therapeutic Angiogenesis ◽

Intraplaque Hemorrhage ◽

Protein Therapy ◽

Angiogenic Growth Factors ◽

Coronary Syndrome ◽

Artery Disease

Angiogenesis is described as a sprouting and growth process of new blood vessels from pre-existing vasculature. The relationship between angiogenesis and coronary artery disease (CAD) is double-sided. On one hand, angiogenesis within plaques is responsible for facilitating the growth and vulnerability of plaques by causing intraplaque hemorrhage and inflammatory cell influx, and overabundance of erythrocytes and inflammatory cells within a plaque probably causes plaque rupture, further leading to acute coronary syndrome. Therefore, inhibiting intraplaque angiogenesis has been considered as a potential therapeutic target for CAD. On the other hand, aiming at improving reperfusion to the ischemic myocardium in patients with CAD, angiogenesis promoting has been utilized as a therapeutic approach to expand myocardial microvascular network. Current strategies include direct administration of angiogenic growth factors (protein therapy), promoting angiogenic genes expression in vivo (gene therapy), and delivering stem cells (cell therapy) or exosomes (cell free therapy). This article will start by clarifying the basic concept of angiogenesis, interpret the mechanism of excessive intraplaque angiogenesis in atherosclerosis, and discuss its role in the growth and vulnerability of plaques. Then we will focus on the four distinct strategies of therapeutic angiogenesis. Despite promising animal studies and smallscale clinical trials of therapeutic angiogenesis in patients with ischemic heart disease, investigations have far not shown definite evidence of clinical efficacy. Hence, while acknowledging future work that remains to be done to validate the clinical results, we reviewed the critical challenges in this arena and highlighted the exciting progress that has occurred recently.

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Histological validation of simultaneous non-contrast angiography and intraplaque hemorrhage imaging (SNAP) for characterizing carotid intraplaque hemorrhage

European Radiology ◽

10.1007/s00330-020-07352-0 ◽

2020 ◽

Author(s):

Dongye Li ◽

Huiyu Qiao ◽

Yongjun Han ◽

Hualu Han ◽

Dandan Yang ◽

...

Keyword(s):

Intraplaque Hemorrhage ◽

Contrast Angiography ◽

Histological Validation

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Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

Clinical Science ◽

10.1042/cs20190999 ◽

2019 ◽

Vol 133 (22) ◽

pp. 2283-2299

Author(s):

Apabrita Ayan Das ◽

Devasmita Chakravarty ◽

Debmalya Bhunia ◽

Surajit Ghosh ◽

Prakash C. Mandal ◽

...

Keyword(s):

Risk Factors ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Chronic Inflammation ◽

Ex Vivo ◽

Human Subjects ◽

Critical Role ◽

Atherosclerotic Cardiovascular Disease ◽

Tnf Α ◽

Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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