Topological recovery for non-rigid 2D/3D registration of coronary artery models

2021 ◽  
pp. 105922
Author(s):  
Siyeop Yoon ◽  
Chang Hwan Yoon ◽  
Deukhee Lee
Keyword(s):  
Coronary Artery ◽  
3D Registration

Accurate Extraction of Coronary Vascular Structures in 2D X-ray Angiogram Using Vascular Topology Information in 3D Computed Tomography Angiography

2019 ◽  
Vol 9 (2) ◽  
pp. 242-250
Author(s):  
Taeyong Park ◽  
Sunhye Lim ◽  
Heeryeol Jeong ◽  
Juneseuk Shin ◽  
Jeongjin Lee
Keyword(s):  
Computed Tomography ◽  
Coronary Artery ◽  
Computed Tomography Angiography ◽  
Coronary Intervention ◽  
Depth Information ◽  
Vascular Structure ◽  
3D Registration ◽  
X Ray ◽  
3D Computed Tomography ◽  
Topology Information

Since the 2D X-ray angiogram enables the detection of vascular stenosis in real-time, it is essential for percutaneous coronary intervention (PCI). However, the accurate vascular structure is very difficult to determine due to background clutter and loss of depth information of 2D projection. To cope with these difficulties, we propose a fast and accurate extraction method of a vascular structure in 2D X-ray angiogram (XA) based on the vascular topology information of 3D computed tomography angiography (CTA) of the same patient. First, an initial vascular structure is robustly extracted based on vessel enhancement filtering. Then, 2D XA and 3D CTA are spatially aligned by 2D–3D registration. Finally, the 2D vascular structure is accurately reconstructed based on 3D vascular topology information by measuring the similarity of 2D and 3D vascular segments. Experimental results showed the fast and accurate extraction of a vascular structure using 10 images each of the left coronary artery (LCA) and right coronary artery (RCA). Our method can be used as a computer-aided technology for PCI. Our method can be applied to the study of other various types of vessels.

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

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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