Evidence map›Paper›PMID 29226101›Full record

ReviewJournal of clinical and translational hepatology2017

Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review.

Ahmed Babiker, Jean Jeudy, Seth Kligerman, Miriam Khambaty, Anoop Shah, Shashwatee Bagchi

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of clinical and translational hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
5.2field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 104 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Observational
  6. Article
  7. Review
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  14. Review
  15. Review
  16. Article
  17. Cardiovascular Implications of Immune Disorders in Women.Circulation research · 2022 · on this map
    Review
  18. Article
  19. Review
  20. Advanced detection strategies for cardiotropic virus infection in a cohort study of heart failure patients.Laboratory investigation; a journal of technical methods and pathology · 2022
    Article
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

6 authors at 2 institutions in 1 country.

Ahmed BabikerProvidence Hospital, Washington, DC, USA.
Jean JeudyDepartment of Radiology, University of Maryland School of Medicine, Baltimore, MD, USA.
Seth KligermanDepartment of Radiology, University of Maryland School of Medicine, Baltimore, MD, USA.
Miriam KhambatyDivision of Infectious Diseases, University of Maryland School of Medicine, Baltimore, MD, USA.
Anoop ShahDivision of Cardiology, University of Edinburgh, Little France, Edinburgh.
Shashwatee BagchiDivision of Infectious Diseases, University of Maryland School of Medicine, Baltimore, MD, USA.
University of Maryland, Baltimore · USProvidence Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis C (HCV) infection has an estimated global prevalence of 2.5%, causing chronic liver disease in 170 million people worldwide. Recent data has identified HCV infection as a risk factor for subclinical and clinical cardiovascular disease (CVD), but these data have been mixed and whether HCV is an independent risk factor for development of CVD remains controversial. In this review, we present the literature regarding the association of HCV with subclinical and clinical CVD and the possible underlying mechanisms leading to increased CVD among those infected with HCV. HCV infection leads to increased CVD via direct and indirect mechanisms with chronic inflammation, endothelial dysfunction and direct invasion of the arterial wall cited as possible mechanisms. Our review showed that HCV infection, particularly chronic HCV infection, appears to lead to increased subclinical CVD most consistently and potentially also to increased clinical CVD outcomes, leading to increased morbidity and mortality. Furthermore, the majority of studies evaluating the impact of HCV therapy on CVD morbidity and mortality showed an improvement in subclinical and clinical CVD endpoints in patients who were successfully treated and achieved sustained viral suppression. These results are of particular interest following the development of new direct antiviral agents which have made HCV eradication simple and feasible for many more patients globally, and in doing so may possibly reduce CVD morbidity and mortality in those with chronic HCV infection.

Indexed as

AtherosclerosisCardiovascular diseaseCerebrovascular diseaseCoronary heart diseaseHepatitis C

Identifiers

PMID29226101
PMCPMC5719192
OpenAlexW2751961442

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.