Evidence map›Paper›PMID 37979122›Full record

ReviewCurrent cardiology reports2023

Advancements in the Genetics of Spontaneous Coronary Artery Dissection.

Alexander E Katz, Santhi K Ganesh

Open access · hybridAbstract readReview
In one paragraph

Review in Current cardiology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. 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

2 authors at 2 institutions in 1 country.

Alexander E KatzDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, USA.
Santhi K GaneshDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, USA. sganesh@umich.edu.
Regional West Medical Center · USUniversity of Michigan–Ann Arbor · US

Funding

Genomic and Functional Studies of Dysplasia-Associated Arterial DiseasesR35HL161016 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SANTHI K GANESH · 2022 to 2026
$4.6M
NHLBI NIH HHS R35 HL161016
6 · The paper itself

Abstract

purpose of reviewSpontaneous coronary artery dissection (SCAD) is a significant cause of acute myocardial infarction that is increasingly recognized in young and middle-aged women. The etiology of SCAD is likely multifactorial and may include the interaction of environmental and individual factors. Here, we summarize the current understanding of the genetic factors contributing to the development of SCAD. RECENT

findingsThe molecular findings underlying SCAD have been demonstrated to include a combination of rare DNA sequence variants with large effects, common variants contributing to a complex genetic architecture, and variants with intermediate impact. The genes associated with SCAD highlight the role of arterial cells and their extracellular matrix in the pathogenesis of the disease and shed light on the relationship between SCAD and other disorders, including fibromuscular dysplasia and connective tissue diseases. While up to 10% of affected individuals may harbor a rare variant with large effect, SCAD most often presents as a complex genetic condition. Analyses of larger and more diverse cohorts will continue to improve our understanding of risk susceptibility loci and will also enable consideration of the clinical utility of genetic testing strategies in the management of SCAD.

Indexed as

Coronary Vessel AnomaliesMyocardial InfarctionVascular DiseasesCoronary AngiographyCoronary VesselsFemaleHumansMiddle AgedRisk FactorsAssociation studiesComplex geneticsGeneticsMendelian geneticsSpontaneous coronary artery dissectionSystemic arteriopathy

Identifiers

PMID37979122
PMCPMC10810930
OpenAlexW4388796881

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.