Evidence map›Paper›PMID 9429840›Full record

ReviewDrugs1997

Cardioprotective mechanisms of ACE inhibition. The angiotensin II-nitric oxide balance.

G H Gibbons

Abstract readReview
PubMed Publisher
In one paragraph

Review in Drugs, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

1 citing paper in PubMed, 15 citations in OpenAlex.

  1. 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

1 author at 1 institution in 1 country.

G H GibbonsMolecular and Cellular Vascular Biology Research Laboratory, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Brigham and Women's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current challenge facing clinicians is to develop pharmacotherapies that move beyond the treatment of symptoms towards a new agenda in cardiovascular therapeutics that includes interventions to actually prevent the development of end-stage coronary heart disease. The development of new strategies to alter the natural history of cardiovascular disease will be fostered by gaining insights into the fundamental pathobiological mechanisms that promote the morbidity and mortality associated with these disorders. An emerging body of evidence indicates that locally generated vasoactive substances such as angiotensin II and nitric oxide are important determinants of the natural history of vascular disease. It is anticipated that ongoing clinical trials will extend the concept that modulating the activity of vasoactive substances generated by the endothelium has important implications for altering the course of coronary heart disease.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin IIApoptosisCardiovascular DiseasesCoronary DiseaseEndothelium, VascularHumansMicrocirculationMyocardiumNitric OxideReactive Oxygen SpeciesVascular ResistanceVasodilationAngiotensin-Converting Enzyme InhibitorsAngiotensin IINitric OxideReactive Oxygen Species

Identifiers

PMID9429840
OpenAlexW2095406221

What OpenQuestion holds

Textmetadata
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.