Exploring the relationship between biomechanical stresses and coronary atherosclerosis

2020 ◽  
Vol 302 ◽  
pp. 43-51
Author(s):  
James N. Cameron ◽  
Ojas H. Mehta ◽  
Michael Michail ◽  
Jasmine Chan ◽  
Stephen J. Nicholls ◽  
...  
2011 ◽  
Vol 144 (1-3) ◽  
pp. 436-444 ◽  
Author(s):  
Yahya Islamoglu ◽  
Osman Evliyaoglu ◽  
Ebru Tekbas ◽  
Habib Cil ◽  
Mehmet Ali Elbey ◽  
...  

2017 ◽  
Vol 49 (5S) ◽  
pp. 156
Author(s):  
Vincent L. Aengevaeren ◽  
Arend Mosterd ◽  
Thijs L. Braber ◽  
Niek HJ Prakken ◽  
Paul D. Thompson ◽  
...  

2016 ◽  
Vol 248 ◽  
pp. 190-195 ◽  
Author(s):  
Se-Jun Park ◽  
Hyoung-Mo Yang ◽  
Kyoung-Woo Seo ◽  
So-Yeon Choi ◽  
Byoung-Joo Choi ◽  
...  

Author(s):  
Taotao Wei ◽  
Junnan Liu ◽  
Demei Zhang ◽  
Xiaomei Wang ◽  
Guangling Li ◽  
...  

Atherosclerosis is the basic pathological process of many diseases, such as coronary atherosclerosis and stroke. Nutrients can affect the occurrence and development of atherosclerosis. At present, in nutrition science, the research on atherosclerosis focuses on which nutrients play an important role in its prevention strategy, and what are the possible mechanisms of its action. In the current study, the process of atherosclerosis can be affected by adjusting the proportion of nutrients in the diet. In this review, we pay attention to the effects of phytosterols, omega-3-polyunsaturated fatty acids, polyphenol, vitamin, and other nutrients on atherosclerosis, pay attention to their current epidemiological status, current nutritional research results, and prevention or a possible mechanism to reduce the risk of development of atherosclerosis. So that more personalized nutritional approaches may be more effective in terms of nutritional intervention responses to atherosclerosis.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Stephen J Nicholls ◽  
Danielle M Brennan ◽  
Kathy Wolski ◽  
Srinivasa R Kalidindi ◽  
Keon-Woong Moon ◽  
...  

Background: Administration of the CETP inhibitor torcetrapib does not slow the rate of progression of coronary atherosclerosis. The reason for the lack of therapeutic efficacy remains unknown. This analysis investigated the relationship between changes in HDL cholesterol (HDL-C) and LDL cholesterol (LDL-C) and atheroma volume in patients treated with torcetrapib. Methods: 910 patients with angiographic coronary artery disease underwent IVUS imaging within a single coronary artery before and during 24 months of treatment with torcetrapib (n = 464) or placebo (n = 446) on a background of atorvastatin therapy. The relationship between changes in levels of HDL-C and LDL-C and both percent atheroma volume (PAV) and total atheroma volume (TAV) was evaluated in patients treated with torcetrapib. Results: Administration of torcetrapib raised HDL-C by 61% and lowered LDL-C by 20% when compared to atorvastatin alone. An inverse relationship was observed between changes in HDL-C and both PAV (r = −0.17, p < 0.001) and TAV (r = −0.17, p < 0.001). Patients with the highest level of HDL-C (> 87 mg/dL) had the lowest rate of progression of PAV (−0.7 v +0.7%, p = 0.0003) and TAV (−9.2 v −4.6 mm 3 , p = 0.09). The greatest elevation in level of HDL-C (> 80%) was associated with the lowest progression of PAV (−0.3 v +0.9%, p = 0.002) and TAV (−12.6 v −3.4 mm 3 , p = 0.0006). Patients undergoing regression (any reduction in PAV) had greater absolute levels (73 v 66 mg/dL, p = 0.02) and changes (59.5 v 48.3%, p = 0.02) of HDL-C. No difference in the impact of torcetrapib on changes in PAV (+0.3 v +0.1%, p = 0.34) and TAV (−9.1 v −9.3 mm 3 , p = 0.95) was observed in patients with baseline levels below or above 40 mg/dL. No relationship was observed between changes in LDL-C and either PAV (r = 0.06, p = 0.20) or TAV (r = 0.07, p = 0.12) in torcetrapib treated patients. On multivariate analysis, changes in levels of HDL-C independently predicted the impact of torcetrapib on progression of PAV (p = 0.007) and TAV (p = 0.004). Conclusion: Increasing levels of HDL-C from torcetrapib treatment were associated with a beneficial impact of torcetrapib on plaque progression. This is consistent with the generation of functional HDL particles and suggests other effects to be responsible for the lack of benefit of torcetrapib.


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