Evidence map›Paper›PMID 26872673›Full record

ReviewHeart failure reviews2016

The role of inflammation and cell death in the pathogenesis, progression and treatment of heart failure.

Alexandros Briasoulis, Emmanuel Androulakis, Theodoros Christophides, Dimitris Tousoulis

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 5 pooled it
13.5field-weighted citation impact, top 1% 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

90 citing papers in PubMed, 5 syntheses or guidelines pooled it, 169 citations in OpenAlex.

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30 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

4 authors at 2 institutions in 1 country.

Alexandros BriasoulisDivision of Cardiology, Detroit Medical Center, Wayne State University, Detroit, MI, USA. alexbriasoulis@gmail.com.
Emmanuel AndroulakisDivision of Cardiology, Detroit Medical Center, Wayne State University, Detroit, MI, USA.
Theodoros ChristophidesDivision of Cardiology, Detroit Medical Center, Wayne State University, Detroit, MI, USA.
Dimitris TousoulisDivision of Cardiology, Detroit Medical Center, Wayne State University, Detroit, MI, USA.
Wayne State University · USDetroit Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation underlies a variety of seemingly unrelated conditions including coronary artery disease. The interest in exploring the role of inflammation in heart failure (CHF) arises from earlier observations that circulating pro-inflammatory biomarker levels are elevated in patients with both ischaemic and non-ischaemic cardiomyopathies and correlate with severity of disease and prognosis (McMurray et al. in Eur Heart J 33:1787-1847, 2012; Mosterd and Hoes in Heart 93:1137-1146, 2007; Owan et al. in New Engl J Med 355:251-259, 2006). In acute decompensated HF, pro-inflammatory biomarker levels have been associated with mortality and readmission rates (Cowie et al. in Heart 83:505-510, 2000). Similar to neurohormonal activation and inflammation, production of pro-inflammatory cytokines is a response to stress in an attempt to restore cellular function. However, sustained expression and exposure to cytokines can lead to left ventricular dysfunction, negative inotropic effects, altered cardiac metabolism, myocardial remodelling and HF progression. However, it is unclear whether elevated levels of pro-inflammatory biomarkers, such as high-sensitivity C-reactive protein, signify an ongoing inflammatory process that leads to HF progression, or are merely markers of advanced disease. Beta-blockers, renin-angiotensin-aldosterone axis antagonists, statins and immunosuppressants have been found to decrease the levels of cytokines in small clinical studies of patients with HF (Hobbs et al. in Heart J 28:1128-1134, 2007). However, 'immunomodulatory' approaches applied in the RECOVER, RENAISSANCE, ATTACH, IMAC and ACCLAIM double-blind, placebo-controlled studies had neutral or negative effects on outcomes of patients with HF. In the present review, we focus on the role of inflammation in pathogenesis and progression of the HF, the value of pro-inflammatory cytokines as biomarkers and the potential therapeutic applications of immunomodulation in HF patients.

Indexed as

Cell DeathBiomarkersChronic DiseaseC-Reactive ProteinCytokinesDisease ProgressionHeart FailureHumansInflammationPrognosisRandomized Controlled Trials as TopicVentricular Dysfunction, LeftBiomarkersC-Reactive ProteinCytokinesCell deathHeart failure pathogenesis and treatmentImmuneInflammation

Identifiers

PMID26872673
OpenAlexW2261174620

What OpenQuestion 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 OpenQuestion graph.