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Coronary artery disease in smokers with low traditional risk burden

2026-09Artigo científico Acesso aberto
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dc.contributor.authorSousa, Francisco
dc.contributor.authorMendonça, Maria Isabel
dc.contributor.authorSousa, João Adriano
dc.contributor.authorSá, Débora
dc.contributor.authorAbreu, Gonçalo
dc.contributor.authorFerreira, Matilde
dc.contributor.authorFreitas, Sónia
dc.contributor.authorBorges, Sofia
dc.contributor.authorHenriques, Eva
dc.contributor.authorRodrigues, Mariana
dc.contributor.authorDrumond, António
dc.contributor.authorSousa, Ana Célia
dc.contributor.authorReis, Roberto Palma Dos
dc.contributor.institutionNOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM)
dc.contributor.pblElsevier BV
dc.date.accessioned2026-07-14T10:49:02Z
dc.date.available2026-07-14T10:49:02Z
dc.date.issued2026-09
dc.descriptionPublisher Copyright: © 2026
dc.description.abstractBackground/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: CDKN2B-AS1, TCF21, PHACTR1, MIA3, ADAMTS7, ZC3HC1, SMAD3, and GJA4. Bivariate analyses compared genotypic proportions between CAD and non-CAD groups, reporting odds ratios (ORs) and confidence intervals (CIs). Multivariate logistic regression evaluates variables independently associated with CAD. The Hardy-Weinberg equilibrium was tested. Results: The intronic PHACTR1 polymorphism rs12526453 C > T was significantly more prevalent in cases, with the dominant model presenting 86.6% in CAD smokers and 70.3% in non-CAD smokers (OR = 2.73; p = 0.028). After logistic regression, which included significant variables in the bivariate analysis, PHACTR1 rs12526453 remained in the model (OR = 3.02; p = 0.038), along with dyslipidemia (OR = 3.58; p = 0.004), obesity (OR = 4.39; p = 0.031), and a family history of CAD (OR = 5.56; p = 0.031). Conclusions: Our findings show that the PHACTR1 T allele is associated with an increased risk of CAD in smokers with a family history, dyslipidemia and obesity, in the absence of other major cardiovascular risk factors. These results support the concept that genetic susceptibility may modulate the vascular response to chronic inflammatory and oxidative stress. Further prospective and functional studies are warranted to clarify the underlying biological mechanisms and the potential clinical value of integrating genetic profiling into personalised cardiovascular risk stratification.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent1003029
dc.identifier.doi10.1016/j.jmccpl.2026.100855
dc.identifier.issn2772-9761
dc.identifier.otherPURE: 168296447
dc.identifier.otherPURE UUID: 6c1f7c04-b45e-44de-a804-ee23716aed8c
dc.identifier.otherScopus: 105043813999
dc.identifier.urihttp://hdl.handle.net/10362/204491
dc.identifier.urlhttps://www.scopus.com/pages/publications/105043813999
dc.language.isoeng
dc.peerreviewedyes
dc.subjectCoronary artery disease
dc.subjectGenetic variants
dc.subjectSmoking
dc.subjectDentistry (miscellaneous)
dc.subjectCardiology and Cardiovascular Medicine
dc.subjectSDG 3 - Good Health and Well-being
dc.titleCoronary artery disease in smokers with low traditional risk burdenen
dc.title.subtitleAn exploratory analysis of potential genetic susceptibilityen
dc.typejournal article
degois.publication.titleJournal of Molecular and Cellular Cardiology Plus
degois.publication.volume17
dspace.entity.typePublication
rcaap.rightsopenAccess

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