Evidence map›Paper›PMID 42442170›Full record

ArticleJACC. Advances2026

Impact of Coronary Microvascular Dysfunction on Patient-Reported Symptoms After PCI.

Frédéric Bouisset, Kazumasa Ikeda, Takuya Mizukami, Daniel Munhoz, Jeroen Sonck, Koshiro Sakai, Hitoshi Matsuo, Hirohiko Ando, Brian Ko, Simone Biscaglia and 17 more

Abstract read
In one paragraph

Article in JACC. Advances, 2026. 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. 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

27 authors.

Frédéric BouissetDepartment of Cardiology Toulouse University Hospital, France.
Kazumasa IkedaDepartment of Cardiology, Tokyo Medical University Hachioji Medical Center, Tokyo, Japan.
Takuya MizukamiDivision of Clinical Pharmacology, Department of Pharmacology, Showa University, Tokyo, Japan; Cardiovascular Center Aalst, OLV Clinic, Aalst, Belgium.
Daniel MunhozCardiovascular Center Aalst, OLV Clinic, Aalst, Belgium.
Jeroen SonckCardiovascular Center Aalst, OLV Clinic, Aalst, Belgium.
Koshiro SakaiDepartment of Medicine, Division of Cardiology, Showa University School of Medicine, Tokyo, Japan.
Hitoshi MatsuoDepartment of Cardiovascular Medicine, Gifu Heart Center, Gifu, Japan.
Hirohiko AndoDepartment of Cardiology, Aichi Medical University, Aichi, Japan.
Brian KoMonash Cardiovascular Research Centre, Monash University and Monash Heart, Monash Health, Clayton, Victoria, Australia.
Simone BiscagliaCardiology Unit, Azienda Ospedaliera Universitaria di Ferrara, Ferrara, Italy.
Fernando RiveroCardiac Department, Hospital Universitario de La Princesa, IIS-IP, Madrid, Spain.
Antonio Maria LeoneCenter of Excellence in Cardiovascular Sciences, Ospedale Isola Tiberina Gemelli Isola, Rome, Italy; Catholic University of the Sacred Heart, Rome, Italy.
Andy YongConcord Repatriation General Hospital, University of Sydney, New South Wales, Australia.
Javier EscanedInstituto de Investigacion Sanitaria del Hospital Clinico San Carlos and Complutense University, Madrid, Spain.
Damien CollisonSchool Cardiovascular and Metabolic Health, University of Glasgow, Glasgow, United Kingdom; NHS Golden Jubilee Hospital, Clydebank, United Kingdom.
Gianluca CampoCardiology Unit, Azienda Ospedaliera Universitaria di Ferrara, Ferrara, Italy.
Liyew DestaDepartment of Cardiology, Karolinska University Hospital, Solna, Stockholm, Sweden.
Tetsuya AmanoDepartment of Cardiovascular Medicine, Gifu Heart Center, Gifu, Japan.
Toshiro ShinkeCardiovascular Center Aalst, OLV Clinic, Aalst, Belgium.
William F FearonDivision of Cardiovascular Medicine and Stanford Cardiovascular Institute, Stanford University School of Medicine and VA Palo Alto Health Care System, Palo Alto, California, USA.
Ethan KorngoldAbbott Vascular.
Evald Høj ChristiansenDepartment of Cardiology, Aarhus University Hospital, Skejby, Aarhus, Denmark.
Colin BerrySchool Cardiovascular and Metabolic Health, University of Glasgow, Glasgow, United Kingdom; NHS Golden Jubilee Hospital, Clydebank, United Kingdom.
Divaka PereraSchool of Cardiovascular Medicine and Sciences, St Thomas' Hospital Campus, King's College London, London, United Kingdom.
Bernard De BruyneDivision of Clinical Pharmacology, Department of Pharmacology, Showa University, Tokyo, Japan.
Nils P JohnsonWeatherhead PET Center, Division of Cardiology, Department of Medicine, McGovern Medical School at UTHealth and Memorial Hermann Hospital, Houston, Texas, USA.
Carlos ColletClinical Trial Center, Cardiovascular Research Foundation, New York, New York, USA. Electronic address: carloscollet@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCoronary microvascular dysfunction (CMD) has been proposed as a mechanism underlying residual angina after percutaneous coronary intervention (PCI).

objectivesThe objective of the study was to investigate the impact of CMD on symptoms in patients undergoing PCI.

methodsPatients with hemodynamically significant coronary artery disease (CAD) (fractional flow reserve ≤0.80) were included. CAD was classified as focal or diffuse using the pull back pressure gradient (PPG) (diffuse CAD defined as PPG <0.62). CMD was defined as microvascular resistance reserve <3.0. The Seattle Angina Questionnaire (SAQ) was administered at baseline and 1 year.

resultsAmong 201 patients (mean age 68.5 ± 10.1 years; 71% male), CMD was present in 75 (37.3%), with no difference between focal and diffuse CAD (41% vs 34%; P = 0.35). At baseline, CMD was associated with more severe symptoms without reaching statistical significance (SAQ summary score 64.0 ± 25.3 vs 69.6 ± 21.0; P = 0.09). At 1 year, symptoms were similar between groups (SAQ summary score 87.6 ± 16.0 vs 89.4 ± 16.4; P = 0.47). A significant interaction between PPG and microvascular resistance reserve was observed for residual angina (P for interaction = 0.015); patients with focal CAD and concomitant CMD had the highest burden of residual symptoms.

conclusionsCMD is present in approximately one-third of patients undergoing PCI and occurs with similar frequency in focal and diffuse CAD. CMD alone was not associated with residual angina. However, its clinical relevance varied according to the epicardial disease pattern: in focal CAD, concomitant CMD was associated with less symptomatic improvement after PCI, whereas in diffuse CAD, residual symptoms appeared to be driven predominantly by persistent epicardial disease.

Indexed as

coronary microvascular functionfractional flow reservemicrovascular resistance reservePer-cutaneous coronary interventionpull back pressure gradient

Identifiers

PMID42442170
PMCPMC13382258

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.