Evidence map›Paper›PMID 37089884›Full record

ArticleFrontiers in cardiovascular medicine2023

Long QTc in hypertrophic cardiomyopathy: A consequence of structural myocardial damage or a distinct genetic disease?

Francesco Cava, Caterina Micolonghi, Maria Beatrice Musumeci, Simona Petrucci, Camilla Savio, Marco Fabiani, Giacomo Tini, Aldo Germani, Fabio Libi, Carla Rossi and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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  4. Characterization of a NovelInternational journal of molecular sciences · 2025
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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

16 authors at 3 institutions in 1 country.

Francesco CavaDepartment of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Caterina MicolonghiDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Maria Beatrice MusumeciDepartment of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Simona PetrucciDepartment of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Camilla SavioSant'Andrea University Hospital, Rome, Italy.
Marco FabianiDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Giacomo TiniDepartment of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Aldo GermaniDepartment of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Fabio LibiSant'Andrea University Hospital, Rome, Italy.
Carla RossiSant'Andrea University Hospital, Rome, Italy.
Vincenzo ViscoDepartment of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Antonio PizzutiDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Massimo VolpeDepartment of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Camillo AutoreIRCCS S.Raffaele, Cassino, Italy.
Speranza RubattuDepartment of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Maria PianeDepartment of Clinical and Molecular Medicine, Sapienza University, Rome, Italy.
Sapienza University of Rome · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversità degli studi di Cassino e del Lazio Meridionale · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disease, characterized by the presence of unexplained left ventricular hypertrophy. This condition is often associated with electrocardiographic abnormalities including QTc prolongation occurring in 13% of patients. The main explanation for prolonged QTc in HCM is myocardial hypertrophy and the related structural damage. However, other mechanisms, including long QT syndrome (LQTS) genes mutations, may be involved. In the present study we explored the hypothesis of a distinct genetic basis underlying QTc prolongation in HCM by investigating the potential co-inheritance of pathogenic gene variants associated with LQTS and HCM. For this purpose, starting from a cohort of 150 HCM patients carrying pathogenic variants in sarcomere genes, we selected 25 patients carrying a QTc prolongation unexplained by any other cause. The QTc was considered prolonged if greater than 450 ms in males and greater than 470 ms in females. The NGS analysis was performed with Illumina TrueSight Cardio panel genes on Illumina MiniSeq platform. We identified pathogenic/likely pathogenic variants in the

Indexed as

gene muatationhypertrophic cardiomyopathyLQTSQTcQTc abnormalities

Identifiers

PMID37089884
PMCPMC10113437
OpenAlexW4362626735

What OpenQuestion holds

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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 OpenQuestion graph.