Document Detail


Biomarkers of chronic cardiac injury and hemodynamic stress identify a malignant phenotype of left ventricular hypertrophy in the general population.
MedLine Citation:
PMID:  23219305     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: The goal of this study was to determine if biomarkers of subclinical myocardial injury and hemodynamic stress identify asymptomatic individuals with left ventricular hypertrophy (LVH) at higher risk for heart failure (HF) and death.
BACKGROUND: The interaction between LVH, low but detectable cardiac troponin T (cTnT), and elevated N-terminal pro-B-type natriuretic peptide (NT-proBNP) on cardiovascular (CV) outcomes in the general population is unknown.
METHODS: Participants in the Dallas Heart Study without clinical HF, LV dysfunction, or chronic kidney disease underwent measurement of LV mass by magnetic resonance imaging (MRI), cTnT by highly sensitive assay, and NT-proBNP analysis (n = 2,413). Subjects were stratified according to LVH and by detectable cTnT (≥3 pg/ml) and increased NT-proBNP (>75th age- and sex-specific percentile) levels. For each analysis, participants were categorized into groups based on the presence (+) or absence (-) of LVH and biomarker levels above (+) or below (-) the predefined threshold.
RESULTS: Nine percent of participants were LVH+, 25% cTnT+, and 24% NT-proBNP+. Those LVH+ and cTnT+ and/or NT-proBNP+ (n = 144) were older and more likely to be male, with a greater risk factor burden and more severe LVH compared with those who were LVH+ biomarker- (p < 0.01 for each). The cumulative incidence of HF or CV death over 8 years among LVH+ cTnT+ was 21% versus 1% (LVH- cTnT-), 4% (LVH- cTnT+), and 6% (LVH+ cTnT-) (p < 0.0001). The interactions between LVH and cTnT (p(interaction) = 0.0005) and LVH and NT-proBNP (p(interaction) = 0.014) were highly significant. Individuals who were LVH+ and either cTnT+ or NT-proBNP+ remained at >4-fold higher risk for HF or CV death after multivariable adjustment for CV risk factors, renal function, and LV mass compared with those who were LVH- biomarker-.
CONCLUSIONS: Minimal elevations in biomarkers of subclinical cardiac injury and hemodynamic stress modify the association of LVH with adverse outcomes, identifying a malignant subphenotype of LVH with high risk for progression to HF and CV death.
Authors:
Ian J Neeland; Mark H Drazner; Jarett D Berry; Colby R Ayers; Christopher deFilippi; Stephen L Seliger; Vijay Nambi; Darren K McGuire; Torbjørn Omland; James A de Lemos
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-12-05
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  61     ISSN:  1558-3597     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2012-12-31     Completed Date:  2013-03-01     Revised Date:  2014-01-23    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  187-95     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Adult
Biological Markers / blood*
Cohort Studies
Death*
Female
Follow-Up Studies
Heart Failure / blood,  diagnosis*
Heart Injuries / metabolism
Heart Ventricles / pathology*
Hemodynamics / physiology
Humans
Hypertrophy, Left Ventricular / blood*
Incidence
Magnetic Resonance Imaging
Male
Middle Aged
Natriuretic Peptide, Brain / blood*
Peptide Fragments / blood*
Phenotype
Prevalence
Risk Factors
Troponin T / blood*
Grant Support
ID/Acronym/Agency:
T32 HL007360/HL/NHLBI NIH HHS; T32HL007360/HL/NHLBI NIH HHS; UL1RR02498/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Peptide Fragments; 0/Troponin T; 0/pro-brain natriuretic peptide (1-76); 114471-18-0/Natriuretic Peptide, Brain
Comments/Corrections

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