Evidence map›Paper›PMID 24337500›Full record

Trial reportHeart and vessels2015

Comparison of the effects of pitavastatin versus pravastatin on coronary artery plaque phenotype assessed by tissue characterization using serial virtual histology intravascular ultrasound.

Tsuyoshi Nozue, Shingo Yamamoto, Shinichi Tohyama, Kazuki Fukui, Shigeo Umezawa, Yuko Onishi, Tomoyuki Kunishima, Akira Sato, Toshihiro Nozato, Shogo Miyake and 7 more

Abstract readComparative StudyMulticenter StudyRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in Heart and vessels, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Pitavastatin: Coronary Atherosclerotic Plaques Changes and Cardiovascular Prevention.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2022
    Review
  3. Article
  4. Article
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 15 institutions in 1 country.

Tsuyoshi NozueDivision of Cardiology, Department of Internal Medicine, Yokohama Sakae Kyosai Hospital, Federation of National Public Service Personnel Mutual Associations, 132 Katsura-cho, Sakae-ku, Yokohama, 247-8581, Japan, nozue2493@yahoo.co.jp.
Shingo Yamamoto
Shinichi Tohyama
Kazuki Fukui
Shigeo Umezawa
Yuko Onishi
Tomoyuki Kunishima
Akira Sato
Toshihiro Nozato
Shogo Miyake
Youichi Takeyama
Yoshihiro Morino
Takao Yamauchi
Toshiya Muramatsu
Kiyoshi Hibi
Mitsuyasu Terashima
Ichiro Michishita
Hiratsuka Kyosai Hospital · JPYokohama Sakae Kyosai Hospital · JPEbina General Hospital · JPKanagawa Cardiovascular and Respiratory Center · JPNational Hospital Organization · JPNoguchi Hospital · JPSaiseikai Yokohama Eastern Hospital · JPShowa University Fujigaoka Rehabilitation HospitalSocial Insurance Yokohama Central Hospital · JPTeikyo University · JPTokai University · JPTokyo Women's Medical University · JPToyohashi Heart Center · JPYokohama City University · JPYokosuka Kyosai Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thin-cap fibroatheroma (TCFA) is the most common type of vulnerable plaque and is the precursor of plaque rupture. However, rupture of a TCFA is not the only mechanism underlying thrombus formation or acute coronary syndrome. Although statin therapy changes the composition of coronary artery plaques, the effects of statins, particularly different types of statins, on plaque phenotype have not been fully examined. This study compared the effects of pitavastatin versus pravastatin on coronary artery plaque phenotype assessed by virtual histology (VH) intravascular ultrasound (IVUS) in patients with angina pectoris (AP). Coronary atherosclerosis in nonculprit lesions was evaluated using VH-IVUS at baseline and 8 months after statin therapy; analyzable IVUS data were obtained from 83 patients with stable AP (39 patients treated with pitavastatin and 44 with pravastatin) and 36 patients with unstable AP (19 patients treated with pitavastatin and 17 with pravastatin). Pitavastatin had a strong effect on reducing pathologic intimal thickening (PIT), especially in patients with unstable AP, but had no impact on VH-TCFA or fibroatheroma (FA). By contrast, pravastatin had weak effects on reducing PIT, VH-TCFA, or FA. Increases in the number of calcified plaques were observed for both statins. In conclusion, pitavastatin and pravastatin changed coronary artery plaque phenotype as assessed by VH-IVUS in patients with AP. However, the effects of these statins on coronary artery plaque phenotype were different.

Indexed as

Acute Coronary SyndromeAgedCoronary Artery DiseaseFemaleHumansMaleMiddle AgedNecrosisPhenotypePlaque, AtheroscleroticPravastatinProspective StudiesQuinolinesUltrasonography, InterventionalpitavastatinPravastatinQuinolines

Identifiers

PMID24337500
OpenAlexW2117093946

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.