Evidence map›Paper›PMID 31050669›Full record

ArticlePloS one2019

Synergistic protective effects of a statin and an angiotensin receptor blocker for initiation and progression of atherosclerosis.

Seul-Gee Lee, Seung-Jun Lee, Nguyen Viet Phuong Thuy, Jung-Sun Kim, Jung-Jae Lee, Oh-Hyun Lee, Choong-Ki Kim, Jaewon Oh, Seil Park, Ok-Hee Lee and 10 more

Full text read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
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  9. Review
  10. Article
  11. Guidelines for animal exercise and training protocols for cardiovascular studies.American journal of physiology. Heart and circulatory physiology · 2020
    Review
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

20 authors.

Seul-Gee LeeCardiovascular Research Institute, Yonsei University College of Medicine, Seoul, Korea.
Seung-Jun LeeCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Nguyen Viet Phuong ThuyCho Ray Hospital, HCMC, Ho Chi Minh, Vietnam.
Jung-Sun KimCardiovascular Research Institute, Yonsei University College of Medicine, Seoul, Korea.ORCID 0000-0003-2263-3274
Jung-Jae LeeGraduate Program in Science for Aging, Yonsei University, Seoul, Korea.
Oh-Hyun LeeCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Choong-Ki KimCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Jaewon OhCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Seil ParkCardiovascular Product Evaluation Center, Yonsei University College of Medicine, Seoul, Korea.
Ok-Hee LeeCardiovascular Product Evaluation Center, Yonsei University College of Medicine, Seoul, Korea.
Se Hoon KimDepartment of Pathology, Yonsei University College of Medicine, Seoul, Korea.
Sungha ParkCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Sang-Hak LeeCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Sung-Jin HongCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Chul-Min AhnCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Byeong-Keuk KimCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Young-Guk KoCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Donghoon ChoiCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Myeong-Ki HongCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.
Yangsoo JangCardiology Division, Severance Cardiovascular Hospital, Yonsei University College of Medicine, Seoul, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimAlthough the atheroprotective effects of statins and angiotensin II receptor blockers (ARBs) are well-established, little is known about their additive effects, especially during the early period of atherosclerosis. The aim of this study was to investigate whether combination of a statin and an ARB exerts synergistic anti-atherosclerotic effects, and to elucidate the mechanisms of combined effects.

methodsAtherosclerotic plaques were developed in arteries of 23 rabbits using a high-cholesterol diet (HCD) and intra-arterial balloon inflation. Rabbits received one of five different treatment strategies for 4 weeks: positive control [n = 5, HCD]; negative control [n = 3, regular chow diet]; statin [n = 5, HCD and rosuvastatin 10 mg]; ARB [n = 5, HCD and olmesartan 20 mg]; and combination [n = 5, HCD and statin+ARB].

resultsHistological analysis demonstrated that development of atherosclerotic plaques was inhibited more in combination group than in statin group (P = 0.001). Although macrophage infiltration identified by RAM11 staining was not significantly different between combination and individual treatment groups (31.76±4.84% [combination] vs. 38.11±6.53% [statin; P = 0.35] or 35.14±2.87% [ARB; P = 0.62]), the relative proportion of pro-inflammatory M1-macrophages was significantly lower in combination group than in ARB group (3.20±0.47% vs. 5.20±0.78%, P = 0.02). Furthermore, M2-macrophage polarization was higher in combination group than in statin group (17.70±3.04% vs. 7.86±0.68%, P = 0.001).

conclusionCombination treatment with a statin and an ARB produced synergistic protective effects for atherosclerosis initiation and progression, which may be attributed to modulation of macrophage characteristics in the early period of atherosclerosis.

Indexed as

Angiotensin Receptor AntagonistsAnimalsAtherosclerosisCell PolarityDisease Models, AnimalDrug SynergismImidazolesMacrophagesMaleMiceRabbitsRAW 264.7 CellsRosuvastatin CalciumTetrazolesTreatment OutcomeAngiotensin Receptor AntagonistsImidazolesolmesartanRosuvastatin CalciumTetrazoles

Identifiers

PMID31050669
PMCPMC6499436

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Registered trials

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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.