Impact of Baseline Glycemic Control on Residual Cardiovascular Risk in Patients With Diabetes Mellitus and High-Risk Vascular Disease Treated With Statin Therapy.
Aged
Biomarkers
/ blood
Blood Glucose
/ drug effects
Cardiovascular Diseases
/ mortality
Diabetes Mellitus, Type 2
/ blood
Double-Blind Method
Female
Glycated Hemoglobin
/ metabolism
Glycemic Control
Heart Disease Risk Factors
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
/ therapeutic use
Hypoglycemic Agents
/ therapeutic use
Male
Middle Aged
Predictive Value of Tests
Prospective Studies
Risk Assessment
Time Factors
Treatment Outcome
hemoglobin A1c
major adverse cardiovascular events
risk stratification
Journal
Journal of the American Heart Association
ISSN: 2047-9980
Titre abrégé: J Am Heart Assoc
Pays: England
ID NLM: 101580524
Informations de publication
Date de publication:
07 01 2020
07 01 2020
Historique:
entrez:
20
12
2019
pubmed:
20
12
2019
medline:
22
12
2020
Statut:
ppublish
Résumé
Background The contemporary impact of glycemic control on patients with diabetes mellitus at high cardiovascular risk remains unclear. We evaluated the utility of hemoglobin A1c (HbA1c) as a marker of risk on the composite end point of cardiovascular death, nonfatal myocardial infarction, stroke, hospitalization for unstable angina, and coronary revascularization in an optimally treated population with diabetes mellitus and established coronary artery disease enrolled in the ACCELERATE (Assessment of Clinical Effects of Cholesteryl Ester Transfer Protein Inhibition With Evacetrapib in Patients at a High Risk for Vascular Outcomes) trial. Methods and Results We included all patients with established diabetes mellitus and measured HbA1c (N=8145) and estimated Kaplan-Meier (KM) events rates, stratified by increasing baseline HbA1c levels censored at 30 months. We then performed a multivariable regression for the primary end point. Increasing baseline HbA1c was strongly associated with the occurrence of the primary end point (KM estimate, 12.6-18.2;
Identifiants
pubmed: 31852422
doi: 10.1161/JAHA.119.014328
pmc: PMC6988169
doi:
Substances chimiques
Biomarkers
0
Blood Glucose
0
Glycated Hemoglobin A
0
Hydroxymethylglutaryl-CoA Reductase Inhibitors
0
Hypoglycemic Agents
0
hemoglobin A1c protein, human
0
Banques de données
ClinicalTrials.gov
['NCT01687998']
Types de publication
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e014328Références
Diabetes Care. 2008 Aug;31(8):1473-8
pubmed: 18540046
N Engl J Med. 2017 May 18;376(20):1933-1942
pubmed: 28514624
Lancet. 1998 Sep 12;352(9131):837-53
pubmed: 9742976
N Engl J Med. 2008 Jun 12;358(24):2545-59
pubmed: 18539917
Am Heart J. 2015 Dec;170(6):1061-9
pubmed: 26678626
Diabetes Care. 2010 Jan;33 Suppl 1:S62-9
pubmed: 20042775
Eur Heart J. 2013 Oct;34(39):3035-87
pubmed: 23996285
N Engl J Med. 2009 Jan 8;360(2):129-39
pubmed: 19092145
Lancet. 2010 Jun 26;375(9733):2215-22
pubmed: 20609967
N Engl J Med. 2008 Jun 12;358(24):2560-72
pubmed: 18539916
N Engl J Med. 2011 Mar 03;364(9):829-841
pubmed: 21366474
Diabetes Care. 2009 Jul;32(7):1327-34
pubmed: 19502545
Eur Heart J. 2018 Jul 1;39(25):2368-2375
pubmed: 29236983
J Am Coll Cardiol. 2016 Dec 6;68(22):2479-2486
pubmed: 27908354
Rev Diabet Stud. 2014 Summer;11(2):138-52
pubmed: 25396402
Lancet. 2010 Feb 6;375(9713):481-9
pubmed: 20110121
Diabetes Care. 2006 Sep;29(9):2130-6
pubmed: 16936167
J Am Heart Assoc. 2020 Jan 7;9(1):e014328
pubmed: 31852422