Statin treatment for coronary artery plaque composition based on intravascular ultrasound radiofrequency data analysis

Nozue, Tsuyoshi; Yamamoto, Shingo; Tohyama, Shugo; Umezawa, Shigeo; Kunishima, Tomoyuki; Sato, Akira; Miyake, Shogo; Takeyama, Youichi; Morino, Yoshihiro; Takao, Yoshinori; Muramatsu, Toshiya; Hibi, Kiyoshi; Sozu, Takashi; Terashima, Mitsuyasu; Michishita, Ichiro

doi:10.1016/j.ahj.2011.11.004

Cited by 77 publications

(82 citation statements)

References 31 publications

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“…Serum lipid levels were measured before treatment (at baseline) and at the 8-month follow-up 22) . Serum total cholesterol, LDL cholesterol, high-density lipoprotein cholesterol, and triglycerides levels were measured using standard enzymatic methods (AU2700; Beckman Coulter, CA, USA) and commercial enzymatic kits (Kyowa Medex, Tokyo, Japan).…”

Section: Laboratory Analysismentioning

confidence: 99%

“…Recent genome-wide association studies have identified that a genetic variant at a locus on chromosome 1p13.3 is strongly associated with LDL cholesterol levels and the risk of myocardial infarction [8][9][10] . This locus contains the following four genes: SORT1, study, which was a prospective, open-labeled, randomized, multicenter trial performed at 11 Japanese centers to compare the effects of 8-month treatment with pitavastatin versus pravastatin on coronary atherosclerosis using virtual histology intravascular ultrasound 22) . In brief, 164 patients with angina pectoris who were not receiving lipid-lowering therapy were randomly treated with either pitavastatin (4 mg/day, intensive lipid-lowering group) or pravastatin (20 mg/ day, moderate lipid-lowering group).…”

Section: Introductionmentioning

confidence: 99%

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Effects of Statin Therapy on Plasma Proprotein Convertase Subtilisin/kexin Type 9 and Sortilin Levels in Statin-Naive Patients with Coronary Artery Disease

Nozue

Hashimoto

Ogawa

et al. 2016

JAT

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Aim: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key regulator of serum low-density lipoprotein (LDL) cholesterol levels, and sortilin is linked to lipoprotein metabolism. Although statin therapy increases PCSK9 levels, effects of this therapy on plasma sortilin levels have not been evaluated. The purpose of the present study was to examine the effects of statins on plasma PCSK9 and sortilin levels, and association of statin-induced increase in PCSK9 levels with sortilin. Methods: Serum lipid levels and plasma PCSK9 and sortilin levels were measured at baseline and 8 months after statin therapy in 90 statin-naive patients with coronary artery disease (CAD). Pitavastatin 4 mg/day was used to treat 44 patients and pravastatin 20 mg/day to treat the remaining 46 patients. Results: For both statin groups, significant increases in hetero-dimer PCSK9 levels (pitavastatin: 31%, p 0.0001; pravastatin: 34%, p 0.03) and decreases in sortilin levels (pitavastatin: 8%, p 0.02; pravastatin: 16%, p 0.002) were observed. Although a reduction in LDL cholesterol was greater in the pitavastatin group than in the pravastatin group, no significant differences were observed in percentage changes in hetero-dimer PCSK9 and sortilin levels. A significant positive correlation was observed between percentage changes in hetero-dimer PCSK9 levels and those in sortilin levels (pitavastatin: r 0.359, p 0.02; pravastatin: r 0.276, p 0.06). Conclusions: Use of pitavastatin and pravastatin increased plasma PCSK9 and decreased sortilin levels. Statin-induced increases in PCSK9 were associated with changes in sortilin in statin-naive patients with CAD. J Atheroscler Thromb, 2016; 23: 848-856.

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Section: Laboratory Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Statin Therapy on Plasma Proprotein Convertase Subtilisin/kexin Type 9 and Sortilin Levels in Statin-Naive Patients with Coronary Artery Disease

Nozue

Hashimoto

Ogawa

et al. 2016

JAT

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“…Using virtual histology (VH)-IVUS, the TRUTH study reported that fibrous plaques regressed more in patients in whom statin treatment led to the regression of coronary plaque than in those in whom this increased. 21) Moreover, in an investigation of changes in plaque components using IB-IVUS in patients with stable angina pectoris, Kawasaki, et al 7) reported that the internal administration of atorvastatin (20 mg) could cause plaque lipid components to be replaced by fibrous components. We demonstrated that statin treatment caused reductions in fibrous components, in contrast to findings of previous reports.…”

Section: Discussionmentioning

confidence: 99%

Impact of Water- and Lipid-Soluble Statins on Nonculprit Lesions in Patients with Acute Coronary Syndrome

et al. 2018

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SummaryStatins can be differentiated into two types, based on their solubility, which have potentially differing effects on the coronary artery wall. However, suspected differences in statins' effects on plaque composition have not been systemically investigated.Sixty-seven patients with acute coronary syndrome (ACS) were randomly assigned to either atorvastatin (10 mg/day) or rosuvastatin (2.5 mg/day). Intravascular ultrasound (IVUS) and integrated backscatter (IB)-IVUS, an established tool to quantify each plaque's components, were performed immediately after emergent percutaneous coronary intervention (PCI). Follow-up IVUS was performed between 6 and 12 months after PCI. Serial changes in serum lipid profiles and plaque composition volumes were compared between the two groups.Thirty-five patients were eligible for serial IB-IVUS analyses. The mean low-density lipoprotein-cholesterol level significantly decreased in the atorvastatin and rosuvastatin groups (P < 0.001); plaque volumes were also significantly reduced from 82.0 ± 46.2 to 74.9 ± 41.3 mm 3 (P = 0.01) and from 74.7 ± 35.3 to 67.7 ± 27.0 mm 3 (P = 0.02), respectively. IB-IVUS revealed a significant reduction in fibrous volume from 33.8 ± 20.0 to 27.5 ± 14.9 mm 3 (P < 0.01) and from 29.6 ± 13.6 to 24.8 ± 7.6 mm 3 (P < 0.05), respectively; however, significant changes were not noted in the volume of the lipid pool for the atorvastatin group and the rosuvastatin group, respectively.Water-and lipid-soluble statins may be similarly effective in reducing coronary plaques in patients with ACS as judged qualitatively and quantitatively. Further study is needed to determine whether differences between water-and lipid-soluble statins affect plaque components.(Int Heart J 2018; 59: 27-34)

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“…Studies conducted to analyze the structural variation in the fibrous cap and necrotic core with specific drug treatments (e.g., all statins, angiotensin converting enzyme inhibitors, etc...) revealed an enhancement in plaque stability (Nozue et al 2012). Our group showed (Finet et al 2004) that a very slight increase in the mechanical properties of plaque constituents, namely the hardening of the lipidic necrotic core, can tilt a VP from instability to stability.…”

Section: Conclusion and Clinical Implicationmentioning

confidence: 99%

An intravascular ultrasound anisotropic elasticity-palpography technique for in vivo coronary atherosclerotic plaque detection and characterization

Gómez

Tacheau

Finet

et al. 2017

Computer Methods in Biomechanics and Biomedical Engineering

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Statin treatment for coronary artery plaque composition based on intravascular ultrasound radiofrequency data analysis

Cited by 77 publications

References 31 publications

Effects of Statin Therapy on Plasma Proprotein Convertase Subtilisin/kexin Type 9 and Sortilin Levels in Statin-Naive Patients with Coronary Artery Disease

Effects of Statin Therapy on Plasma Proprotein Convertase Subtilisin/kexin Type 9 and Sortilin Levels in Statin-Naive Patients with Coronary Artery Disease

Impact of Water- and Lipid-Soluble Statins on Nonculprit Lesions in Patients with Acute Coronary Syndrome

An intravascular ultrasound anisotropic elasticity-palpography technique for in vivo coronary atherosclerotic plaque detection and characterization

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