Evidence map›Paper›PMID 17885551›Full record

Trial reportJournal of hypertension2007

Angiotensin-converting enzyme gene polymorphism predicts the time-course of blood pressure response to angiotensin converting enzyme inhibition in the AASK trial.

Vibha Bhatnagar, Daniel T O'Connor, Nicholas J Schork, Rany M Salem, Caroline M Nievergelt, Brinda K Rana, Douglas W Smith, George L Bakris, John P Middleton, Keith C Norris and 6 more

Open access · greenAbstract readMulticenter StudyRandomized Controlled Trial
In one paragraph

Trial report in Journal of hypertension, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Cardiovascular Pharmacogenomics: Does It Matter If You're Black or White?Annual review of pharmacology and toxicology · 2019
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Genetic determinants of hypertension: an update.Current hypertension reports · 2008
    Review
  17. 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

16 authors at 10 institutions in 1 country.

Vibha BhatnagarUniversity of California San Diego, La Jolla, USA. vbhatnag@ucsd.edu
Daniel T O'Connor
Nicholas J Schork
Rany M Salem
Caroline M Nievergelt
Brinda K Rana
Douglas W Smith
George L Bakris
John P Middleton
Keith C Norris
Jackson T Wright
Deanna Cheek
Leena Hiremath
Gabriel Contreras
Lawrence J Appel
Michael S Lipkowitz
University of California, San Diego · USCase Western Reserve University · USDuke University · USIcahn School of Medicine at Mount Sinai · USJohns Hopkins University · USMartin Luther King, Jr. Multi-Service Ambulatory Care Center · USThe Ohio State University · USUniversity of Chicago · USUniversity of Miami · USUniversity of South Carolina · US

Funding

ZIPRASIDONE (GEODON) AUGMENTATION IN SEROTONIN REUPTAKE INHIBITOR-RESISTANT OBM01RR000071 · NCRR · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI NEWCORN, JEFFREY H · 1985 to 2009
$41.5M
Trafficking of catecholamine storage vesicle proteinsP01HL058120 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZIEGLER, MICHAEL G. · 1999 to 2009
$18.5M
San Diego EXPORT Comprehensive NCMHD Research CenterP60MD000220 · NIMHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DALEY, SANDRA P · 2002 to 2011
$11.0M
AFRICAN AMERICAN STUDY OF KIDNEY DISEASE &HYPERTENSIONU01DK048689 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI LIPKOWITZ, MICHAEL · 1994 to 2007
$2.9M
ETIOLOGY OF NEPHROPATHY AND HYPERTENSION IN AASK PATIENTR01DK057867 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI LIPKOWITZ, MICHAEL S · 2000 to 2004
$1.9M
Sympathetic Outflow to Catecholamine Storage VesiclesR01DK060702 · NIDDK · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI O'CONNOR, DANIEL T · 2002 to 2006
$1.4M
FAMILY BLOOD PRESSURE PROGRAMU01HL064777 · NHLBI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SCHORK, NICHOLAS JOSEPH · 2000 to 2004
$1.1M
Pharmacogenomics and HypertensionK23RR020822 · NCRR · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BHATNAGAR, VIBHA · 2006 to 2010
$523k
NCRR NIH HHS K23 RR020822NCRR NIH HHS K23 RR020822-01A1NCRR NIH HHS M01 RR000071NCRR NIH HHS MO1-RR00071NHLBI NIH HHS 5U01 HL064777-07NHLBI NIH HHS HL58120NHLBI NIH HHS P01 HL058120NHLBI NIH HHS U01 HL064777NIDDK NIH HHS DK60702NIDDK NIH HHS R01 DK057867NIDDK NIH HHS R01 DK060702NIDDK NIH HHS R01 DK57867NIDDK NIH HHS U01 DK048689NIDDK NIH HHS U01 DK48689NIMHD NIH HHS MD000220NIMHD NIH HHS P60 MD000220
6 · The paper itself

Abstract

objectiveIt has yet to be determined whether genotyping at the angiotensin-converting enzyme (ACE) locus is predictive of blood pressure response to an ACE inhibitor.

methodsParticipants from the African American Study of Kidney Disease and Hypertension trial randomized to the ACE inhibitor ramipril (n = 347) were genotyped at three polymorphisms on ACE, just downstream from the ACE insertion/deletion polymorphism (Ins/Del): G12269A, C17888T, and G20037A. Time to reach target mean arterial pressure (</=107 mmHg) was analyzed by genotype and ACE haplotype using Kaplan-Meier survival curves and Cox proportional hazard models.

resultsIndividuals with a homozygous genotype at G12269A responded significantly faster than those with a heterozygous genotype; the adjusted (average number of medications and baseline mean arterial pressure) hazard ratio (homozygous compared to heterozygous genotype) was 1.86 (95% confidence limits 1.32-3.23; P < 0.001 for G12269A genotype). The adjusted hazard ratio for participants with homozygous ACE haplotypes compared to those heterozygous ACE haplotypes was 1.40 (1.13-1.75; P = 0.003 for haplotype). The ACE genotype effects were specific for ACE inhibition (i.e., not seen among those randomized to a calcium channel blocker), and were independent of population stratification.

conclusionsAfrican-Americans with a homozygous genotype at G12269A or homozygous ACE haplotypes responded to ramipril significantly faster than those with a heterozygous genotype or heterozygous haplotypes, suggesting that heterosis may be an important determinant of responsiveness to an ACE inhibitor. These associations may be a result of biological activity of this polymorphism, or of linkage disequilibrium with nearby variants such as the ACE Ins/Del, perhaps in the regulation of ACE splicing.

Indexed as

Polymorphism, Single NucleotideAdolescentAdultAgedAngiotensin-Converting Enzyme InhibitorsAntihypertensive AgentsBlood PressureFemaleGenotypeHaplotypesHumansHypertensionMaleMiddle AgedPeptidyl-Dipeptidase ARamiprilAngiotensin-Converting Enzyme InhibitorsAntihypertensive AgentsPeptidyl-Dipeptidase ARamipril

Identifiers

PMID17885551
PMCPMC2792638
OpenAlexW2043603709

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.