scholarly journals The Goal of Achieving Atherosclerotic Plaque Regression with Lipid-Lowering Therapy: Insights from IVUS Trials

2019 ◽  
Vol 26 (7) ◽  
pp. 592-600 ◽  
Author(s):  
Hiroyuki Daida ◽  
Tomotaka Dohi ◽  
Yoshifumi Fukushima ◽  
Hirotoshi Ohmura ◽  
Katsumi Miyauchi
Keyword(s):  
Atherosclerotic Plaque ◽  
Lipid Lowering ◽  
Lipid Lowering Therapy ◽  
Lowering Therapy ◽  
Plaque Regression

scholarly journals The Use of Plaque Score Measurements to Assess Changes in Atherosclerotic Plaque Burden Induced by Lipid-Lowering Therapy Over Time: The METEOR Study

2011 ◽  
Vol 18 (9) ◽  
pp. 784-795 ◽  
Author(s):  
Sanne A.E. Peters ◽  
Soner Dogan ◽  
Rudy Meijer ◽  
Mike K. Palmer ◽  
Diederick E. Grobbee ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Lipid Lowering ◽  
Plaque Burden ◽  
Lipid Lowering Therapy ◽  
Plaque Score ◽  
Lowering Therapy ◽  
Over Time

scholarly journals Raman Spectroscopic Evaluation of the Effects of Diet and Lipid-Lowering Therapy on Atherosclerotic Plaque Development in Mice

2001 ◽  
Vol 21 (10) ◽  
pp. 1630-1635 ◽  
Author(s):  
Sweder W.E. van de Poll ◽  
Tjeerd J. Römer ◽  
Oscar L. Volger ◽  
Dianne J.M. Delsing ◽  
Tom C. Bakker Schut ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Lipid Lowering ◽  
Lipid Lowering Therapy ◽  
Raman Spectroscopic ◽  
Lowering Therapy ◽  
Plaque Development

Abstract 12007: Combination Therapy of Eicosapentaenoic Acid and Pitavastatin for Coronary Plaque Regression Evaluated by Integrated Backscatter Intravascular Ultrasonography: A Randomized Controlled Trial

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Kaoru Ando ◽  
Tetsu Watanabe ◽  
Hyuma Daidoji ◽  
Yoichiro Otaki ◽  
Naoto Hashimoto ◽  
...  
Keyword(s):  
Coronary Plaque ◽  
Lipid Lowering ◽  
High Dose ◽  
Lipid Lowering Therapy ◽  
Intravascular Ultrasonography ◽  
Plaque Volume ◽  
Lowering Therapy ◽  
Plaque Regression ◽  
Coronary Plaque Volume

Introduction: High intensity statin therapy is established for secondary prevention of coronary heart disease (CHD). However, additional therapy is required to reduce residual risk in CHD patients with aggressive lipid-lowering therapy. Eicosapentaenoic acid (EPA) was reported to be beneficial especially in secondary prevention. The aim of this study was to investigate whether coronary plaque regression and stabilization are reinforced by additional administration of EPA to high dose pitavastatin (PTV) therapy. Methods: We enrolled 200 CHD patients who underwent percutaneous coronary intervention in 6 hospitals. Patients were randomly allocated to PTV group (PTV 4 mg/day, n=98) and PTV/EPA group (PTV 4 mg/day and EPA 1800 mg/day, n=102), and prospectively followed for 6 to 8 months. Coronary plaque volume and composition in non-stenting lesion were analyzed by integrated backscatter intravascular ultrasonography at baseline and follow up. Results: EPA / arachidonic acid (AA) ratio was significantly increased in PTV/EPA group compared to PTV group at follow up period. Plaque volume and lipid volume were significantly reduced in PTV/EPA group, but not PTV group. There was a significant inverse correlation between change in EPA/AA ratio and changes in plaque volume (r=-0.332, p<0.001). Plaque regression was defined as percent change in plaque volume more than -14.6% according to previous reports. A multivariate logistic analysis demonstrated that the additional administration of EPA was independently associated with plaque regression after adjustment of confounding factors. The prevalence rate of plaque regression was significantly higher in PTV/EPA group than in PTV group (50% vs. 24%, p<0.001). Conclusions: Additional administration of EPA to high dose PTV therapy significantly reduced coronary plaque volume, suggesting that combination therapy of EPA and PTV might reduce residual risk in CHD patients with aggressive lipid-lowering therapy.

Abstract 148: Intensive Lipid Lowering Therapy Using Rosuvastatin Associates with Greater Atherosclerotic Aortic Plaques Regression - A Magnetic Resonance Imaging Study

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Makiko Yogo ◽  
Makoto Ayaori ◽  
Hiroki Sato ◽  
Teruyoshi Kihara ◽  
Sasaki Makoto ◽  
...  
Keyword(s):  
Standard Therapy ◽  
Serum Lipids ◽  
Lipid Lowering ◽  
Standard Group ◽  
Lipid Lowering Therapy ◽  
Lowering Therapy ◽  
Increased Risk ◽  
Plaque Regression ◽  
Aortic Plaques ◽  
Intensive Group

Whether intensive lipid-lowering therapy yields greater regression of atherosclerotic plaques remains inconclusive. We therefore performed a prospective, randomized trial comparing standard (achieving LDL-C levels recommended by the Japanese guideline) and intensive (achieving further 30% lower levels than the former) rosuvastatin therapy for 1 year with primary outcome of aortic plaques evaluated by MRI. Sixty dyslipidemic patients, who were eligible for statins therapy, were randomized to standard or intensive group, and dose of rosuvastatin were titrated to achieve the respective target LDL-C. Average doses of rosuvastatin throughout the study were 2.9±3.1 and 6.5±5.1 mg/day in standard and intensive group, respectively. Although both treatments significantly reduced serum LDL-C and hsCRP levels, reduction of LDL-C levels was greater in intensive group than in standard group (-46 vs. -34%). Intensive therapy improved endothelial function as evaluated by FMD in brachial artery compared to standard therapy (95 vs. 22%). MRI study revealed that both thoracic and abdominal plaques were significantly regressed in both groups with greater regression in thoracic plaques in intensive group compared to standard group (-9.1 vs. -3.2%) (Figure A). Correlation analysis revealed no significant association of plaque regression with the doses of rosuvastatin and the changes in serum lipids/FMD. In contrast, thoracic plaque regression correlated with hsCRP reduction (Figure B). Multivariate analysis demonstrated that this association still remain significant even after adjustment of the doses at flow-up, serum lipids and FMD. In conclusions, the present study demonstrated that intensive lipid-lowering using rosuvastatin led to additive plaques regression compared to standard therapy. Therefore, rosuvastatin may provide long term benefit in patients with increased risk through its LDL-C lowering and anti-inflammatory effects.

scholarly journals Early Effect of Lipid-Lowering Therapy With Pitavastatin on Regression of Coronary Atherosclerotic Plaque

2009 ◽  
Vol 73 (8) ◽  
pp. 1466-1472 ◽  
Author(s):  
Toru Toi ◽  
Isao Taguchi ◽  
Shuichi Yoneda ◽  
Michiya Kageyama ◽  
Akiko Kikuchi ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Lipid Lowering ◽  
Lipid Lowering Therapy ◽  
Early Effect ◽  
Lowering Therapy ◽  
Coronary Atherosclerotic Plaque

scholarly journals The effects of lipid-lowering therapy on coronary plaque regression: a systematic review and meta-analysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yingrui Li ◽  
Songbai Deng ◽  
Bin Liu ◽  
Yulin Yan ◽  
Jianlin Du ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Final Analysis ◽  
Coronary Plaque ◽  
Lipid Lowering ◽  
Lipid Lowering Therapy ◽  
Target Level ◽  
Plaque Volume ◽  
Lowering Therapy ◽  
Plaque Regression

AbstractTo assess the influence of lipid-lowering therapy on coronary plaque volume, and to identify the LDL and HDL targets for plaque regression to provide a comprehensive overview. The databases searched (from inception to 15 July 2020) to identify prospective studies investigating the impact of lipid-lowering therapy on coronary plaque volume and including quantitative measurement of plaque volume by intravascular ultrasound after treatment. Thirty-one studies that included 4997 patients were selected in the final analysis. Patients had significantly lower TAV (SMD: 0.123 mm3; 95% CI 0.059, 0.187; P = 0.000) and PAV (SMD: 0.123%; 95% CI 0.035, 0.212; P = 0.006) at follow-up. According to the subgroup analyses, TAV was significantly reduced in the LDL < 80 mg/dL and HDL > 45 mg/dL group (SMD: 0.163 mm3; 95% CI 0.092, 0.234; P = 0.000), and PAV was significantly reduced in the LDL < 90 mg/dL and HDL > 45 mg/dL group (SMD: 0.186%; 95% CI 0.081, 0.291; P = 0.001).Thirty-one studies that included 4997 patients were selected in the final analysis. Patients had significantly lower TAV (SMD: 0.123 mm3; 95% CI 0.059, 0.187; P = 0.000) and PAV (SMD: 0.123%; 95% CI 0.035, 0.212; P = 0.006) at follow-up. According to the subgroup analyses, TAV was significantly reduced in the LDL < 80 mg/dL and HDL > 45 mg/dL group (SMD: 0.163 mm3; 95% CI 0.092, 0.234; P = 0.000), and PAV was significantly reduced in the LDL < 90 mg/dL and HDL > 45 mg/dL group (SMD: 0.186%; 95% CI 0.081, 0.291; P = 0.001). Our meta-analysis suggests that not only should LDL be reduced to a target level of < 80 mg/dL, but HDL should be increased to a target level of > 45 mg/dL to regress coronary plaques.Trial Registration PROSPERO identifier: CRD42019146170.

scholarly journals Repurposing the atypical antidepressant trazodone for atherosclerotic cardiovascular disease

2021 ◽  
Author(s):  
Kipp Johnson ◽  
Jagat Narula ◽  
Benjamin Glicksberg ◽  
Khader Shameer ◽  
Farhan Chaudhry ◽  
...  
Keyword(s):  
Gene Expression ◽  
Atherosclerotic Plaque ◽  
Expression Patterns ◽  
Rabbit Model ◽  
Lipid Lowering ◽  
Plaque Burden ◽  
Atherosclerotic Cardiovascular Disease ◽  
Lipid Lowering Therapy ◽  
Cholesterol Levels ◽  
Lowering Therapy

Abstract Background. Current lipid-lowering drugs often leave significant residual risk for adverse outcomes. Identification of previously approved drugs for new indications, drug repurposing, may provide a cost effective alternative to de novo drug developing.Objectives. We combined clinical, transcriptomic, computational, and experimental strategies to explore lipid-lowering and plaque-stabilizing effects of atypical antidepressant trazodone.Methods. First, a connectivity mapping strategy was used to match rosuvastatin gene expression signature derived from a clinical trial of 85 patients with to the expression patterns of 1,309 different small molecules to discover a similarity between the rosuvastatin and trazodone gene expression signatures. Then, we assessed the lipid-lowering ability of trazodone in vitro using HepG2 cells and in vivo using molecular imaging of rabbit atherosclerotic lesions. In addition, we analyzed electronic medical records of patients from three large medical centers who had a prescription for trazodone and lipid laboratory measurements available.Results. Trazodone significantly reduced cholesterol levels in the HepG2 human hepatocyte model, decreased atherosclerotic plaque burden in a rabbit model and lowered low-density lipoprotein (LDL) cholesterol levels in patients.Conclusion. Our results indicate that trazodone may be a promising candidate for adjunctive lipid lowering therapy. It may provide significant benefits to patients with hyperlipidemia, including lipid level reduction and formation of a more favorable atherosclerotic plaque morphology. Patients diagnosed with major depressive disorder requiring better lipid control would benefit the most from the for adjunctive lipid lowering therapy.

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