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 ◽  
...  
2021 ◽  
Author(s):  
Kipp Johnson ◽  
Jagat Narula ◽  
Benjamin Glicksberg ◽  
Khader Shameer ◽  
Farhan Chaudhry ◽  
...  

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.


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 ◽  
...  

2019 ◽  
Vol 26 (7) ◽  
pp. 592-600 ◽  
Author(s):  
Hiroyuki Daida ◽  
Tomotaka Dohi ◽  
Yoshifumi Fukushima ◽  
Hirotoshi Ohmura ◽  
Katsumi Miyauchi

2009 ◽  
Vol 73 (8) ◽  
pp. 1466-1472 ◽  
Author(s):  
Toru Toi ◽  
Isao Taguchi ◽  
Shuichi Yoneda ◽  
Michiya Kageyama ◽  
Akiko Kikuchi ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jingbo Hou ◽  
Haibo Jia ◽  
Sining Hu ◽  
Lei Xing ◽  
Shuang Yang ◽  
...  

Background: Despite dramatic improvements in clinical outcome, intravascular ultrasound (IVUS) trials have shown minimal improvement of atheroma volume with statin therapy. Changes in plaque composition rather than plaque volume may contribute to the marked clinical benefit. Objectives: To assess the effect of intensive versus moderate lipid-lowering therapy on fibrous cap thickness (FCT) by optical coherence tomography (OCT) and percent atheroma volume (PAV) by IVUS. Methods: The patients with ≥1 non-treated lipid-rich plaque (LRP) with moderate stenosis were randomized to receive atorvastatin 60 mg (AT60), or atorvastatin 20 mg (AT20). OCT and IVUS imaging were performed at baseline, 6 months and 12 months. The primary endpoint was the change in FCT. The secondary endpoints were the change in PAV and the percent change in normalized total atheroma volume (%NTAV). Sixty-six LRP in 46 patients defined by OCT were studied. Results: Low-density lipoprotein cholesterol (LDL-C) was reduced significantly in both groups at 6 months; however, there was no further reduction at 12 months (Fig A, C). OCT demonstrated a continuous increase in FCT over time in both groups, with greater increase in the AT60 group than the AT20 group at 6 months (139.7±160.9% vs. 68.1±83.9%, p=0.021) and 12 months (211.3±125.4% vs. 120.2±136.9%, p<0.0001) (Fig B, D). IVUS showed no significant changes in PAV and NTAV over time in two groups. The changes in PAV were similar between the two groups at 6 months (-0.48±3.4% in AT60 vs. 0.28±5.2% in AT20, p=0.50) and 12 months (-0.26±4.3% vs. 0.11±4.1%, p=0.73). %NTAV were also comparable between the two groups at 6 months and at 12 months. Conclusions: Intensive atorvastatin therapy induces more rapid and effective stabilization of coronary lipid-rich plaques by increasing FCT, as compared with moderate atorvastatin therapy. IVUS analysis did not show significant change in plaque volume over time in both groups.


2021 ◽  
Vol 5 (3) ◽  
Author(s):  
Norihito Takahashi ◽  
Tomotaka Dohi ◽  
Hirohisa Endo ◽  
Shinya Okazaki

Abstract Background Lipid-rich plaques (LRP) in the non-culprit lesions (NCL) in patients with the acute coronary syndrome may trigger lesion-related, adverse cardiovascular events. Aggressive lipid-lowering therapy may stabilize LRP; however, the times of stabilization remain undefined. Case summary A 60-year-old man presented with unstable angina. Coronary angiography revealed a severely stenotic lesion (culprit lesion) in the left descending artery, and another non-obstructive lesion in the distal left main trunk artery. Near-infrared spectroscopy (NIRS) imaging showed LRP with a maximum lipid core burden index (LCBI)4mm of 422. Optical coherence tomographic (OCT) imaging showed the vulnerable plaque as a thin cap fibroatheroma with a thickness of 50 µm. We prescribed aggressive lipid-lowering treatment with a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor, and serially observed this lesion for 24 months. The NIRS imaging showed that the LCBI gradually decreased over time (max LCBI4mm of 422, 417, 318, 265, and 106 conducted at index percutaneous coronary intervention, 3, 8, 12, and 24 months, respectively). As plaque regression and stabilization of high-risk LRP were observed, we promptly discontinued treatment with the PCSK9i inhibitor. Discussion During the long-term, 24-month, follow-up using serial NIRS–IVUS imaging, we observed the gradual decrease in LCBI over time, due to aggressive lipid-lowering therapy. Compared with the lowering of low-density lipoprotein cholesterol, the stabilization of vulnerable plaques may require longer times of about 2 years. Evaluation of NCL-related adverse cardiac events by serial intravascular imaging over time, using NIRS–IVUS or OCT, may be warranted in such cases.


Sign in / Sign up

Export Citation Format

Share Document