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Biomarkers of chronic cardiac injury and hemodynamic stress identify a malignant phenotype of left ventricular hypertrophy in the general population.

ABSTRACT: 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.

SUBMITTER: Neeland IJ

PROVIDER: S-EPMC3547631 | biostudies-literature | 2013 Jan

REPOSITORIES: biostudies-literature

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Biomarkers of chronic cardiac injury and hemodynamic stress identify a malignant phenotype of left ventricular hypertrophy in the general population.

Neeland Ian J IJ Drazner Mark H MH Berry Jarett D JD Ayers Colby R CR deFilippi Christopher C Seliger Stephen L SL Nambi Vijay V McGuire Darren K DK Omland Torbjørn T de Lemos James A JA

Journal of the American College of Cardiology 20121205 2

<h4>Objectives</h4>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.<h4>Background</h4>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.<h4>Methods</h4>Par ...[more]

PMID: 23219305

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Project description:Background Left ventricular hypertrophy (LVH) is associated with increased mortality risk and rehospitalization after transcatheter aortic valve replacement among those with severe aortic stenosis. Whether cardiac troponin (cTnT) and NT-proBNP (N-terminal pro-B-type natriuretic peptide) risk stratify patients with aortic stenosis and without LVH is unknown. Methods and Results In a multicenter prospective registry of 923 patients with severe aortic stenosis undergoing transcatheter aortic valve replacement, we included 674 with core-laboratory-measured LV mass index, cTnT, and NT-proBNP. LVH was defined by sex-specific guideline cut-offs and elevated biomarker levels were based on age and sex cut-offs. Adjusted Cox proportional hazards models evaluated associations between LVH and biomarkers and all-cause death out to 5 years. Elevated cTnT and NT-proBNP were present in 82% and 86% of patients with moderate/severe LVH, respectively, as compared with 66% and 69% of patients with no/mild LVH, respectively (P<0.001 for each). After adjustment, compared with no/mild LVH, moderate/severe LVH was associated with an increased hazard of mortality (adjusted hazard ratio [aHR], 1.34; 95% CI 1.01-1.77, P=0.043). cTnT and NT-proBNP each risk stratified patients with moderate/severe LVH (P<0.05). In a model with both biomarkers and LVH included, elevated cTnT (aHR, 2.08; 95% CI 1.45-3.00, P<0.001) and elevated NT-proBNP (aHR, 1.46; 95% CI 1.00-2.11, P=0.049) were each associated with increased mortality risk, whereas moderate/severe LVH was not (P=0.15). Conclusions Elevations in circulating cTnT and NT-proBNP are more common as LVH becomes more pronounced but are also observed in those with no/minimal LVH. As measures of maladaptive remodeling and cardiac injury, cTnT and NT-proBNP predict post-transcatheter aortic valve replacement mortality better than LV mass index. These findings may have important implications for risk stratification and treatment of patients with aortic stenosis.

Project description:BackgroundAortic stiffness shares a similar profile of risk factors with left ventricular hypertrophy (LVH) and can also lead to LVH by itself. Published data have demonstrated the correlation between aortic stiffness and LVH. Recent data have revealed estimated pulse wave velocity (ePWV) to be a simple and cost-effective marker of the severity of aortic stiffness. Our analysis aimed to explore the association between ePWV and LVH prevalence, and to investigate the incremental value of ePWV for the identification of LVH prevalence.MethodsThe present analysis based on a cross-sectional survey which included 11,597 participants from rural areas of southeastern China between Sep 2020 and Feb 2021. ePWV was formulated based on mean blood pressure and age according to a published algorithm.ResultsThe prevalence of LVH was 14.56%. With the adjustment of age, sex, education, income and physical activity level, current drinking and smoking status, BMI, waist circumference, serum creatinine, total cholesterol, high density cholesterol, mean blood pressure, fasting plasma glucose, anti-hypertensive therapy, anti-diabetic therapy, lipid-lowering therapy, and cardiovascular disease history, every standard deviation increment of ePWV associated with a 2.993 times risk of LVH prevalence. When dividing ePWV into quartiles, the top quartile had a 4.520 times risk of LVH prevalence when compared with the bottom quartile. Furthermore, smooth spline analysis displayed that the association was linear in the whole range of ePWV (p for non-linearity = 0.073). Additionally, subgroup analysis revealed the association was robust to sex, obesity and diabetes, and younger people and hypertensive population were more vulnerable to the increase of ePWV than their corresponding counterparts. Finally, ROC analysis showed a significant advancement when introducing ePWV into established risk factors (0.787 vs. 0.810, p for comparison < 0.001), and reclassification analysis also confirmed significant improvement from ePWV to identify LVH prevalence (category-free net reclassification analysis = 0.421, p < 0.001; integrated discrimination index = 0.023, p < 0.001).ConclusionOur analysis demonstrated a linear association between ePWV and LVH prevalence. Furthermore, our results suggest younger people and hypertensive population are more likely to have LVH prevalence with the increase of ePWV. More importantly, our findings implicate the incremental value of ePWV to optimize the identification of LVH prevalence in a general Chinese population.

Project description:BackgroundChronic pressure overload (such as arterial hypertension) may cause left ventricular (LV) remodeling, alterations in cardiac function, and the development of diastolic heart failure. Changes in the composition of the myocardial extracellular matrix may contribute to the development of pressure-overload-induced LV remodeling. We hypothesized that a specific pattern of plasma biomarker expression that reflected changes in these pathophysiological mechanisms would have diagnostic application to identify (1) patients who have development of LV hypertrophy (LVH) and (2) patients with LVH who have development of diastolic heart failure.Methods and resultsPlasma concentration of 17 biomarkers (matrix metalloproteinase [MMP]-1, -2, -3, -7, -8, and -9; tissue inhibitors -1, -2, -3, and -4; N-terminal propeptide of brain natriuretic peptide (NT-proBNP); cardiotrophin; osteopontin; soluble receptor for advanced glycation end products; collagen I teleopeptide; collagen I NT-proBNP; and collagen III N-terminal propetide [PIIINP]), an echocardiogram, and 6-minute hall walk were performed on 241 referent control subjects, 144 patients with LVH but no evidence of heart failure, and 61 patients with LVH and diastolic heart failure (DHF). A plasma multibiomarker panel consisting of increased MMP-7, MMP-9, TIMP-1, PIIINP, and NT-proBNP predicted the presence of LVH with an area under the curve of 0.80. A plasma multibiomarker panel consisting of increased MMP-2, TIMP-4, PIIINP, and decreased MMP-8 predicted the presence of DHF with an area under the curve of 0.79. These multibiomarker panels performed better than any single biomarker including NT-proBNP and better than using clinical covariates alone (area under the curve, 0.73 for LVH and 0.68 for DHF).ConclusionsPlasma biomarkers reflecting changes in extracellular matrix fibrillar collagen homeostasis, combined into a multibiomarker panel, have discriminative value in identifying the presence of structural remodeling (LVH) and clinical disease (DHF).

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Biomarkers of chronic cardiac injury and hemodynamic stress identify a malignant phenotype of left ventricular hypertrophy in the general population.

Publications

Biomarkers of chronic cardiac injury and hemodynamic stress identify a malignant phenotype of left ventricular hypertrophy in the general population.

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