Evidence map›Paper›PMID 33958774›Full record

ReviewNature reviews. Cardiology2021

Interplay between inflammation and thrombosis in cardiovascular pathology.

Konstantin Stark, Steffen Massberg

Abstract readReview
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 582 papers.

0numbers the graph read from it
0cells of the map it votes in
582citing 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

582 citing papers in PubMed.

  1. Platelet count polygenic scores may modify the effect of aspirin in primary prevention of dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Trial
  2. Inflammation and day-to-day occurrence of atrial fibrillation.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    Trial
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  4. Plasma chemokines indicate enhanced bleeding in patients with chronic coronary syndrome undergoing percutaneous coronary stenting.Clinical research in cardiology : official journal of the German Cardiac Society · 2025
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522 more citing papers are in PubMed but not listed here.

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

2 authors.

Konstantin StarkMedizinische Klinik und Poliklinik I, University Hospital, LMU Munich, Munich, Germany. konstantin.stark@med.uni-muenchen.de.ORCID http://orcid.org/0000-0002-5369-8399
Steffen MassbergMedizinische Klinik und Poliklinik I, University Hospital, LMU Munich, Munich, Germany. steffen.massberg@med.uni-muenchen.de.ORCID http://orcid.org/0000-0001-7387-3986

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thrombosis is the most feared complication of cardiovascular diseases and a main cause of death worldwide, making it a major health-care challenge. Platelets and the coagulation cascade are effectively targeted by antithrombotic approaches, which carry an inherent risk of bleeding. Moreover, antithrombotics cannot completely prevent thrombotic events, implicating a therapeutic gap due to a third, not yet adequately addressed mechanism, namely inflammation. In this Review, we discuss how the synergy between inflammation and thrombosis drives thrombotic diseases. We focus on the huge potential of anti-inflammatory strategies to target cardiovascular pathologies. Findings in the past decade have uncovered a sophisticated connection between innate immunity, platelet activation and coagulation, termed immunothrombosis. Immunothrombosis is an important host defence mechanism to limit systemic spreading of pathogens through the bloodstream. However, the aberrant activation of immunothrombosis in cardiovascular diseases causes myocardial infarction, stroke and venous thromboembolism. The clinical relevance of aberrant immunothrombosis, referred to as thromboinflammation, is supported by the increased risk of cardiovascular events in patients with inflammatory diseases but also during infections, including in COVID-19. Clinical trials in the past 4 years have confirmed the anti-ischaemic effects of anti-inflammatory strategies, backing the concept of a prothrombotic function of inflammation. Targeting inflammation to prevent thrombosis leaves haemostasis mainly unaffected, circumventing the risk of bleeding associated with current approaches. Considering the growing number of anti-inflammatory therapies, it is crucial to appreciate their potential in covering therapeutic gaps in cardiovascular diseases.

Indexed as

Anti-Inflammatory AgentsBlood CoagulationCOVID-19Fibrinolytic AgentsHumansImmune SystemInflammationInflammation MediatorsRisk AssessmentRisk FactorsSignal TransductionThrombosisAnti-Inflammatory AgentsFibrinolytic AgentsInflammation Mediators

Identifiers

PMID33958774
PMCPMC8100938

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.