ReviewCurrent cardiology reports2009
Genomic view of factors leading to plaque instability.
Review in Current cardiology reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Heterogeneity of the phenotypic definition of coronary artery disease and its impact on genetic association studies.Circulation. Cardiovascular genetics · 2011Pooled it
- Genetics of Arterial-Wall-Specific Mechanisms in Atherosclerosis: Focus on Mitochondrial Mutations.Current atherosclerosis reports · 2020Review
- Role of somatic mutations in vascular disease formation.Expert review of molecular diagnostics · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The manifestations of coronary artery disease are varied. They all arise as a consequence of the deposition of atherosclerotic plaque within the vessel wall. The most feared sequela of coronary artery disease is sudden and unexpected death in the ostensibly healthy patient. Plaque rupture of hemodynamically insignificant atherosclerotic plaques and ensuing thrombosis is likely responsible for a large proportion of such deaths. Identifying populations at increased risk for sudden death would represent a major advance. Such screening is contingent upon identification of DNA sequence variants that predispose individuals to plaque rupture. Phenotyping is not sufficiently nuanced to detect such variants on a large scale, so we are limited to end points that are crude surrogates for plaque rupture. As imaging modalities are refined and our ability to recruit large numbers of appropriate patients is facilitated by the formation of alliances, our ability to probe this conundrum via a genome-wide approach will improve.
Indexed as
Identifiers
19563728What OpenQuestion holds
Registered trials
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.