Evidence map›Paper›PMID 37115472›Full record

ReviewHeart failure reviews2023

Inflammation across the spectrum of hypertrophic cardiac phenotypes.

Rosa Lillo, Francesca Graziani, Francesco Franceschi, Giulia Iannaccone, Massimo Massetti, Iacopo Olivotto, Filippo Crea, Giovanna Liuzzo

Open access · hybridAbstract readReview
In one paragraph

Review in Heart failure reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

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  16. Evidence for chronic inflammation in cats with cardiomyopathies.Journal of feline medicine and surgery · 2025
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  18. Observational
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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

8 authors at 3 institutions in 1 country.

Rosa LilloDepartment of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo A. Gemelli 8, Rome, 00168, Italy.
Francesca GrazianiDepartment of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo A. Gemelli 8, Rome, 00168, Italy. francesca.graziani@policlinicogemelli.it.
Francesco FranceschiDepartment of Emergency Medicine, Fondazione Policlinico Universitario A. Gemelli IRCCS, Catholic University of the Sacred Heart, Rome, Italy.
Giulia IannacconeDepartment of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo A. Gemelli 8, Rome, 00168, Italy.
Massimo MassettiDepartment of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo A. Gemelli 8, Rome, 00168, Italy.
Iacopo OlivottoCardiology Unit, Meyer Children's Hospital IRCCS, Florence, Italy.
Filippo CreaDepartment of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo A. Gemelli 8, Rome, 00168, Italy.
Giovanna LiuzzoDepartment of Cardiovascular Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo A. Gemelli 8, Rome, 00168, Italy.
Istituti di Ricovero e Cura a Carattere Scientifico · ITUniversità Cattolica del Sacro Cuore · ITAgostino Gemelli University Polyclinic · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hypertrophic cardiomyopathy phenotype encompasses a heterogeneous spectrum of genetic and acquired diseases characterized by the presence of left ventricular hypertrophy in the absence of abnormal cardiac loading conditions. This "umbrella diagnosis" includes the "classic" hypertrophic cardiomyopathy (HCM), due to sarcomere protein gene mutations, and its phenocopies caused by intra- or extracellular deposits, such as Fabry disease (FD) and cardiac amyloidosis (CA). All these conditions share a wide phenotypic variability which results from the combination of genetic and environmental factors and whose pathogenic mediators are poorly understood so far. Accumulating evidence suggests that inflammation plays a critical role in a broad spectrum of cardiovascular conditions, including cardiomyopathies. Indeed, inflammation can trigger molecular pathways which contribute to cardiomyocyte hypertrophy and dysfunction, extracellular matrix accumulation, and microvascular dysfunction. Growing evidence suggests that systemic inflammation is a possible key pathophysiologic process potentially involved in the pathogenesis of cardiac disease progression, influencing the severity of the phenotype and clinical outcome, including heart failure. In this review, we summarize current knowledge regarding the prevalence, clinical significance, and potential therapeutic implications of inflammation in HCM and two of its most important phenocopies, FD and CA.

Indexed as

CardiomyopathiesCardiomyopathy, HypertrophicFabry DiseaseHumansHypertrophy, Left VentricularInflammationPhenotypeCardiac amyloidosisCardiomyopathyFabry diseaseHypertrophic cardiomyopathyHypertrophyInflammation

Identifiers

PMID37115472
PMCPMC10403403
OpenAlexW4367299966

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.