ReviewCardiovascular drugs and therapy1996
Angiotensin-converting enzyme inhibitors and coronary artery disease.
Review in Cardiovascular drugs and therapy, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed, 6 citations in OpenAlex.
- Angiotensin I-converting enzyme: genotype and disease associations.The Journal of molecular diagnostics : JMD · 2000Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The renin-angiotensin system and angiotensin converting enzyme (ACE) are increasingly being implicated in the pathogenesis of coronary artery disease and its sequelae. Genetic studies of ACE gene polymorphism hint at an association between the ACE genotype and atherosclerosis. Animal studies have demonstrated the potential beneficial effects of ACE inhibition at a variety of sites, including improvement of endothelial function, inhibition of platelet aggregation, reduction of atherosclerosis, and inhibition of myointimal proliferation. Although these have not all been validated in human studies, the reduction of ischemic events in studies of ACE inhibition in left ventricular dysfunction cannot be explained solely by improved hemodynamics, and it is possible that actions on the endothelium, the atherosclerotic process, and platelets are at least in part responsible. The results of studies in humans looking more directly at the influence of ACE inhibitors on atherosclerosis and ischemic heart disease are awaited.
Indexed as
Identifiers
What 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.