Quantification and Characterization of Atherosclerotic Lesions in Mice

Author(s):  
Abhinav Agarwal ◽  
Millicent G. Winner ◽  
Srinivas D. Sithu ◽  
Sanjay Srivastava
2018 ◽  
Vol 99 (3) ◽  
pp. 290-304 ◽  
Author(s):  
Jessica Davis-Knowlton ◽  
Jacqueline E. Turner ◽  
Anna Turner ◽  
Sydney Damian-Loring ◽  
Nicholas Hagler ◽  
...  

1986 ◽  
Vol 14 (5) ◽  
pp. 1061-1063
Author(s):  
Michitaka NAITO ◽  
Masafumi KUZUYA ◽  
Chiaki FUNAKI ◽  
Kazuaki SHIBATA ◽  
Yasukazu NAKAYAMA ◽  
...  

Blood ◽  
1987 ◽  
Vol 69 (4) ◽  
pp. 1038-1045 ◽  
Author(s):  
A Bini ◽  
J Jr Fenoglio ◽  
J Sobel ◽  
J Owen ◽  
M Fejgl ◽  
...  

Abstract Arterial thrombi and atherosclerotic lesions were analyzed immunochemically and examined histologically. The extent of in vivo proteolytic cleavage of the amino-terminal end of fibrinogen by thrombin and plasmin was determined and quantitated by specific radioimmunoassays. The samples were treated with cyanogen bromide (CNBr), and the total amount of fibrinogen and fibrin-derived protein was determined as NDSK, the NH2-terminal disulfide knot of fibrinogen. Thrombin-releasable fibrinopeptides A and B were used to quantitate fibrinogen and fibrin I. Previous plasmin cleavage of the B beta chain was inferred from the amount of B beta 1–42 and B beta 15–42 in undigested NDSK. The results obtained in both acute and organized thrombi indicate that approximately 60% of the total protein (as determined by amino acid analysis) was fibrinogen-derived and that 70% to 80% of the fibrinogen-derived material was fibrin II. These findings support the hypothesis that fibrin II as distinct from fibrin I is the predominant component in a thrombus. In samples from normal and atherosclerotic aortas, fibrinogen-derived protein comprised less than 10% of the total protein. Samples from grossly normal aortas contained only fibrinogen and fibrin I. Fibrinogen concentration decreased and fibrin II concentration increased with increasing severity of the lesions, suggesting that increased fibrin II formation is associated with progression of atheromas.


Author(s):  
Daniel E. Venegas-Pino ◽  
Nicole Banko ◽  
Mohammed I. Khan ◽  
Yuanyuan Shi ◽  
Geoff H. Werstuck

Author(s):  
Rosemarie Romeo ◽  
Joan M. Augustyn ◽  
Gretchen Mandel ◽  
Assaad S. Daoud

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Mohamed Laimoud ◽  
Farouk Faris ◽  
Helmy Elghawaby

Background. Non-ST elevation acute coronary syndromes (NSTE-ACS) may arise from moderately stenosed atherosclerotic lesions that suddenly undergo transformation to vulnerable plaques complicated by rupture and thrombosis. Objective. Assessment and tissue characterization of the coronary atherosclerotic lesions among NSTE-ACS patients compared to those with stable angina. Methodology. Evaluation of IVUS studies of 312 coronary lesions was done by 2 different experienced IVUS readers, 216 lesions in 66 patients with NSTE-ACS (group I) versus 96 lesions in 50 patients with stable angina (group II). Characterization of coronary plaques structure was done using colored-coded iMap technique. Results. The Syntax score was significantly higher in group I compared to group II (18.7 ± 7.8 vs. 8.07 ± 2.5, p=0.001). Body mass index (BMI) was significantly higher in group II while triglycerides levels were higher in group I (P=0.01 & P=0.04, respectively). History of previous MI and PCI was significantly higher in group I (P=0.016 & P=0.001, respectively). The coronary lesions of NSTE-ACS patients had less vessel area (9.86 ± 3.8 vs 11.36 ± 2.9, p=0.001), stenosis percentage (54.7 ± 14.9% vs 68.6 ± 8.7%, p=0.001), and plaque burden (54.4 ± 14.7 vs 67.8 ± 9.8, p=0.001) with negative remodeling index (0.95 ± 20 vs 1.02 ± 0.14, p=0.008) compared to the stable angina group. On the other hand, they had more lipid content (21.8 ± 7.03% vs 7.26 ± 3.47%, p=0.001), necrotic core (18.08 ± 10.19% vs 15.83 ± 4.9%, p=0.02), and calcifications (10.4 ± 5.2% vs 4.19 ± 3.29%, p=0.001) while less fibrosis (51.67 ± 7.07% vs 70.37 ± 11.7%, p=0.001) compared to the stable angina patients. Syntax score and core composition especially calcification and lipid content were significant predictors to NSTE-ACS. Conclusions. The vulnerability rather than the stenotic severity is the most important factor that predisposes to non-ST segment elevation acute coronary syndromes. The vulnerability is related to the lesion characteristics especially lipidic core and calcification while lesion fibrosis favours lesion stability.


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