Evidence mapPaperPMID 42438588Full record

ArticleJournal of molecular and cellular cardiology plus2026

Coronary artery disease in smokers with low traditional risk burden: An exploratory analysis of potential genetic susceptibility.

Francisco Sousa, Maria Isabel Mendonça, João Adriano Sousa, Débora Sá, Gonçalo Abreu, Matilde Ferreira, Sónia Freitas, Sofia Borges, Eva Henriques, Mariana Rodrigues and 3 more

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology plus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Francisco SousaResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
Maria Isabel MendonçaResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
João Adriano SousaResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
Débora SáResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
Gonçalo AbreuResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
Matilde FerreiraResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
Sónia FreitasResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
Sofia BorgesResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
Eva HenriquesResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
Mariana RodriguesResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
António DrumondCardiology Department, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
Ana Célia SousaResearch Centre Dra. Maria Isabel Mendonça, Dr Nélio Mendonça Hospital, SESARAM EPERAM, Portugal.
Roberto Palma Dos ReisFaculty of Medical Sciences of Lisbon/NOVA Medical School, Portugal.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background/objectives: Coronary arterial disease (CAD) poses a significant public health challenge, with tobacco as the most predominant modifiable risk factor in young individuals. Despite a strong correlation between tobacco use and CAD, many smokers remain CAD-free. This fact raises questions about the complex interplay between environmental and genetic factors that contribute to CAD. Objective: Identify genetic polymorphisms that may be responsible for CAD in smokers without the main cardiovascular risk factors. Methods: A small retrospective case-control association study included current smokers aged 35-50 with low-density lipoprotein (LDL) levels <100 mg/dL who were non-diabetic and non-hypertensive. A total of 134 individuals (83% male; mean age of 48.9 ± 8.4 years) were selected from the GENEMACOR population: 97 CAD patients defined as having at least 70% stenosis in one major coronary artery, and 37 controls without CAD. Nine genetic variants from 8 genes previously associated with CAD but not with traditional risk factors (TRFs) were genotyped using TaqMan real-time PCR: Results: The intronic Conclusions: Our findings show that the

Indexed as

Coronary artery diseaseGenetic variantsSmoking

Identifiers

PMID42438588
PMCPMC13356738

What Socratic 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 Socratic graph.