Evidence mapPaperPMID 34234310Full record

ReviewNature reviews. Cardiology2021

A pathophysiological compass to personalize antianginal drug treatment.

Edoardo Bertero, Gerd Heusch, Thomas Münzel, Christoph Maack

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Guideline for Chronic Coronary Syndrome - 2025.Arquivos brasileiros de cardiologia · 2025
    Article
  5. Article
  6. Article
  7. Association of statins with peak oxygen consumption in 4,941 adults: A cross-sectional study.International journal of cardiology. Heart & vasculature · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Coronary Microvascular Angina: A State-of-the-Art Review.Frontiers in cardiovascular medicine · 2022
    Review
  15. 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

4 authors at 3 institutions in 1 country.

Edoardo BerteroComprehensive Heart Failure Center (CHFC), University Clinic Würzburg, Würzburg, Germany.ORCID http://orcid.org/0000-0002-3175-8151
Gerd HeuschInstitute for Pathophysiology, West German Heart and Vascular Center, University of Duisburg-Essen, Essen, Germany.ORCID http://orcid.org/0000-0001-7078-4160
Thomas MünzelDepartment of Cardiology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany. tmuenzel@uni-mainz.de.ORCID http://orcid.org/0000-0001-5503-4150
Christoph MaackComprehensive Heart Failure Center (CHFC), University Clinic Würzburg, Würzburg, Germany. maack_c@ukw.de.ORCID http://orcid.org/0000-0003-3694-4559
Johannes Gutenberg University Mainz · DEUniversity of Würzburg · DEWest German Heart and Vascular Center Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial ischaemia results from coronary macrovascular or microvascular dysfunction compromising the supply of oxygen and nutrients to the myocardium. The underlying pathophysiological processes are manifold and encompass atherosclerosis of epicardial coronary arteries, vasospasm of large or small vessels and microvascular dysfunction - the clinical relevance of which is increasingly being appreciated. Myocardial ischaemia can have a broad spectrum of clinical manifestations, together denoted as chronic coronary syndromes. The most common antianginal medications relieve symptoms by eliciting coronary vasodilatation and modulating the determinants of myocardial oxygen consumption, that is, heart rate, myocardial wall stress and ventricular contractility. In addition, cardiac substrate metabolism can be altered to alleviate ischaemia by modulating the efficiency of myocardial oxygen use. Although a universal agreement exists on the prognostic importance of lifestyle interventions and event prevention with aspirin and statin therapy, the optimal antianginal treatment for patients with chronic coronary syndromes is less well defined. The 2019 guidelines of the ESC recommend a personalized approach, in which antianginal medications are tailored towards an individual patient's comorbidities and haemodynamic profile. Although no antianginal medication improves survival, their efficacy for reducing symptoms profoundly depends on the underlying mechanism of the angina. In this Review, we provide clinicians with a rationale for when to use which compound or combination of drugs on the basis of the pathophysiology of the angina and the mode of action of antianginal medications.

Indexed as

Angina PectorisCardiovascular AgentsPrecision MedicineHumansCardiovascular Agents

Identifiers

PMID34234310
OpenAlexW3181125992

What Socratic 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 Socratic graph.