Evidence map›Paper›PMID 41019904›Full record

ArticleJournal of the Society for Cardiovascular Angiography & Interventions2025

Smoking and Coronary Atherosclerosis: Disproportionate Impact on the Right Coronary Artery.

Axel Dahlgren, David Erlinge, Ryo Torii, Enhui Yong, Göran Bergström, Tomas Jernberg, Ole Fröbert, Pernille G Thrane, Michael Mæng, Gregg W Stone and 1 more

Abstract read
In one paragraph

Article in Journal of the Society for Cardiovascular Angiography & Interventions, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Suspected Cannabis-Induced Acute Coronary Syndrome and Advanced Heart block.Journal of investigative medicine high impact case reports
    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

11 authors.

Axel DahlgrenDepartment of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden.
David ErlingeDepartment of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden.
Ryo ToriiDepartment of Mechanical Engineering, Faculty of Engineering Science, University College London, London, United Kingdom.
Enhui YongDepartment of Mechanical Engineering, Faculty of Engineering Science, University College London, London, United Kingdom.
Göran BergströmDepartment of Molecular and Clinical Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Tomas JernbergDivision of Cardiovascular Medicine, Department of Clinical Sciences, Karolinska Institutet, Danderyd University Hospital, Stockholm, Sweden.
Ole FröbertDepartment of Cardiology, Faculty of Health, Örebro University, Örebro, Sweden.
Pernille G ThraneDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Michael MængDepartment of Cardiology, Aarhus University Hospital, Aarhus, Denmark.
Gregg W StoneIcahn School of Medicine at Mount Sinai, New York, New York.
Moman A MohammadDepartment of Cardiology, Clinical Sciences, Lund University, Skåne University Hospital, Lund, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: We aimed to study the long-term effect of smoking on coronary atherosclerosis progression at the segmental level. Methods: Angiographic data (1989-2017) on current, former, and nonsmokers were collected from the Swedish Coronary Angiography and Angioplasty Registry. The Western Denmark Heart Registry was used to validate the results. Patients with clinically indicated angiography with ≥2 coronary arteries without obstructive coronary artery disease were included. The main outcome was segmental plaque progression, percutaneous coronary intervention, or coronary artery bypass grafting within 15 years. Results: In total, 215,364 Swedish patients with 993,405 coronary arteries (left anterior descending artery [LAD], left circumflex artery [LCX], and right coronary artery [RCA]) were included. The validation cohort consisted of 19,613 patients. Per 1000 patient-years, plaque progression incidence rate was 11.3 (95% CI, 10.9-11.7) for smokers, 10.2 (95% CI, 9.9-10.5) for former smokers, and 7.7 (95% CI, 7.5-7.9) for nonsmokers. Smokers demonstrated higher relative risk of plaque progression in RCA (hazard ratio, 1.87; 95% CI, 1.73-2.03) vs LAD (hazard ratio, 1.21; 95% CI, 1.12-1.30). Swedish and Danish smokers with ST-segment elevation myocardial infarction had higher proportion of RCA as the culprit artery compared to nonsmokers (smokers: RCA, 42.4%; LAD, 42.0%; LCX, 15.6%; nonsmokers: RCA, 33.1%; LAD, 51.4%; LCX, 15.5%). Conclusions: This observational cohort study identifies distinct differences in plaque progression patterns between smokers and nonsmokers, with smoking linked to increased plaque progression in the RCA, in contrast to the LAD in nonsmokers. These findings reemphasize the need for targeted smoking prevention and warrant further investigation into RCA-specific mechanisms of plaque progression and MI.

Indexed as

coronary artery atherosclerosisnatural progressionsmoking

Identifiers

PMID41019904
PMCPMC12462097

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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.