Evidence map›Paper›PMID 38519897›Full record

ArticleBMC cardiovascular disorders2024

Low HDL cholesterol and the eNOS Glu298Asp polymorphism are associated with inducible myocardial ischemia in patients with suspected stable coronary artery disease.

Cecilia Vecoli, Chiara Caselli, Martina Modena, Giancarlo Todiere, Rosa Poddighe, Serafina Valente, Fabrizio Bandini, Andrea Natali, Lorenzo Ghiadoni, Aldo Clerico and 5 more

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024
    Review
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

15 authors at 7 institutions in 1 country.

Cecilia VecoliInstitute of Clinical Physiology-CNR, Via G. Moruzzi 1, Pisa, Italy. cecilia.vecoli@cnr.it.
Chiara CaselliInstitute of Clinical Physiology-CNR, Via G. Moruzzi 1, Pisa, Italy.
Martina ModenaSant'Anna School of Advanced Studies, Pisa, Italy.
Giancarlo TodiereCardiovascular Department, Gabriele Monasterio Foundation, Via G. Moruzzi 1, Pisa, Italy.
Rosa PoddigheOspedale Della Versilia, Lido Di Camaiore, Lucca, Italy.
Serafina ValenteCareggi University Hospital (AOUC), Florence, Italy.
Fabrizio BandiniAz. Sanitaria Di Firenze, Florence, Italy.
Andrea NataliDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Lorenzo GhiadoniDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Aldo ClericoCardiovascular Department, Gabriele Monasterio Foundation, Via G. Moruzzi 1, Pisa, Italy.
Concetta PronteraCardiovascular Department, Gabriele Monasterio Foundation, Via G. Moruzzi 1, Pisa, Italy.
Simona VittoriniCardiovascular Department, Gabriele Monasterio Foundation, Via G. Moruzzi 1, Pisa, Italy.
Nicoletta BottoCardiovascular Department, Gabriele Monasterio Foundation, Via G. Moruzzi 1, Pisa, Italy.
Michele EmdinCardiovascular Department, Gabriele Monasterio Foundation, Via G. Moruzzi 1, Pisa, Italy.
Danilo NegliaCardiovascular Department, Gabriele Monasterio Foundation, Via G. Moruzzi 1, Pisa, Italy. dneglia@ftgm.it.
Fondazione Toscana Gabriele Monasterio · ITScuola Superiore Sant'Anna · ITUniversity of Pisa · ITAzienda Ospedaliero-Universitaria Careggi · ITAzienda Sanitaria di Firenze · ITIstituto di Fisiologia Clinica · ITOspedale Versilia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe endothelial nitric oxide synthase (eNOS) gene deficiency is known to cause impaired coronary vasodilating capability in animal models. In the general clinical population, the eNOS gene polymorphisms, able to affect eNOS activity, were associated with cardiometabolic risk features and prevalence of coronary artery disease (CAD).

aimTo investigate the association of eNOS Glu298Asp gene polymorphism, cardiometabolic profile, obstructive CAD and inducible myocardial ischemia in patients with suspected stable CAD.

methodsA total of 506 patients (314 males; mean age 62 ± 9 years) referred for suspected CAD was enrolled. Among these, 325 patients underwent stress ECG or cardiac imaging to assess the presence of inducible myocardial ischemia and 436 patients underwent non-invasive computerized tomography or invasive coronary angiography to assess the presence of obstructive CAD. Clinical characteristics and blood samples were collected for each patient.

resultsIn the whole population, 49.6% of patients were homozygous for the Glu298 genotype (Glu/Glu), 40.9% heterozygotes (Glu/Asp) and 9.5% homozygous for the 298Asp genotype (Asp/Asp). Obstructive CAD was documented in 178/436 (40.8%) patients undergoing coronary angiography while myocardial ischemia in 160/325 (49.2%) patients undergoing stress testing. Patients with eNOS Asp genotype (Glu/Asp + Asp/Asp) had no significant differences in clinical risk factors and in circulating markers. Independent predictors of obstructive CAD were age, gender, obesity, and low HDL-C. Independent predictors of myocardial ischemia were gender, obesity, low HDL-C and Asp genotype. In the subpopulation in which both stress tests and coronary angiography were performed, the Asp genotype remained associated with increased myocardial ischemia risk after adjustment for obstructive CAD.

conclusionIn this population, low-HDL cholesterol was the only cardiometabolic risk determinant of obstructive CAD. The eNOS Glu298Asp gene polymorphism was significantly associated with inducible myocardial ischemia independently of other risk factors and presence of obstructive CAD.

Indexed as

Coronary Artery DiseaseMyocardial IschemiaAgedArteriesCholesterol, HDLGenotypeHumansMaleMiddle AgedNitric Oxide Synthase Type IIIObesityPolymorphism, GeneticRisk FactorsCholesterol, HDLNitric Oxide Synthase Type IIINOS3 protein, humanEndothelial dysfunctionEndothelial nitric oxide synthaseeNOSInducible myocardial ischemiaObstructive coronary artery diseaseSingle nucleotide polymorphism

Identifiers

PMID38519897
PMCPMC10958845
OpenAlexW4393090086

What OpenQuestion holds

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LicenceCC BY
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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.