9 results match your criteria: "Donald W. Reynolds Cardiovascular Research Center[Affiliation]"
Clin Chem
March 2013
Department of Internal Medicine, Donald W. Reynolds Cardiovascular Research Center, Dallas, TX, USA.
Background: ST2, part of the interleukin-1 receptor family, is released from cardiac myocytes under mechanical strain. Soluble ST2 (sST2) concentrations are associated with adverse cardiac events in high-risk cohorts. We evaluated the association of sST2 with all-cause and cardiovascular mortality in a large, low-risk population-based cohort.
View Article and Find Full Text PDFRev Cardiovasc Med
October 2010
Donald W. Reynolds Cardiovascular Research Center and Division of Cardiology, University of Texas Southwestern Medical Center, Dallas TX, USA.
Over the past decade, an evidence base has accumulated to support natriuretic peptide (NP) testing for diagnosis, risk assessment, and therapeutic monitoring and guidance of patients with heart failure. Investigators have also explored multiple other potential uses for these tests, including risk assessment of patients with suspected acute coronary syndromes (ACS). This article discusses the utility of NPs in the diagnosis and management of patients with ACS.
View Article and Find Full Text PDFJ Interferon Cytokine Res
May 2010
Donald W. Reynolds Cardiovascular Research Center and Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Specific chemokines contribute to vascular inflammation and may be useful biomarkers to detect atherosclerosis. The chemokines CXCL1 and CCL11 have previously been studied in animal or human models of atherosclerosis, while CXCL2 and CCL23 have not. Among 2,454 subjects enrolled in the Dallas Heart Study, a multi-ethnic population-based sample, we measured plasma CCL11, CCL23, CXCL1, and CXCL2, and associated levels with coronary artery calcium (CAC) by computed tomography, and aortic wall thickness, plaque burden, and compliance by magnetic resonance imaging.
View Article and Find Full Text PDFAm Heart J
April 2009
Donald W. Reynolds Cardiovascular Research Center, UT Southwestern Medical Center, Dallas, TX 75390-9047, USA.
Background: Identification of individuals in the community with left ventricular systolic dysfunction (LVSD) or left ventricular hypertrophy (LVH) may allow earlier initiation of disease-modifying treatment. We performed a comprehensive evaluation of the screening performance of B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) for LVSD or LVH.
Methods: In 2,429 subjects without a history of heart failure, myocardial infarction, valvular abnormalities, or a serum creatinine >2.
J Investig Med
July 2007
Center for Human Nutrition, the Donald W Reynolds Cardiovascular Research Center of the University of Texas Southwestern Medical Center at Dallas, TX 75390-9052, USA.
Low-density lipoprotein cholesterol (LDL-C) is the primary target of lipid-lowering therapy. However, all lipoproteins containing apolipoprotein B (apo B) appear to be atherogenic. Preferred targets of therapy therefore may include either the cholesterol in all apo B-containing lipoproteins (non-high-density lipoprotein cholesterol [non-HDL-C]) or total apo B itself.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
May 2007
Donald W. Reynolds Cardiovascular Research Center, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
Objective: Several lines of evidence implicate CD40 ligand (CD40L, CD154) as a mediator and marker of atherosclerosis. This study investigated the involvement of tumor necrosis factor receptor-associated factors (TRAFs) in CD40 signaling in endothelial cells (ECs) and their expression in atheromata and cells involved in atherogenesis.
Methods And Results: CD40L enhanced the basal expression of TRAF-1, -2, -3, and 6, but not TRAF-5 in ECs.
Physiol Genomics
September 2005
Donald W. Reynolds Cardiovascular Research Center, Division of Cardiovascular Medicine, Falk Cardiovascular Research Center, Stanford University, Stanford, California 94305, USA.
Large-scale gene expression studies provide significant insight into genes differentially regulated in disease processes such as cancer. However, these investigations offer limited understanding of multisystem, multicellular diseases such as atherosclerosis. A systems biology approach that accounts for gene interactions, incorporates nontranscriptionally regulated genes, and integrates prior knowledge offers many advantages.
View Article and Find Full Text PDFCardiovasc Res
January 2005
Donald W. Reynolds Cardiovascular Research Center, Division of Cardiovascular Medicine, Stanford University, Stanford, CA 94305, USA.
Objective: The endogenous peptide apelin is differentially regulated in cardiovascular disease but the nature of its role in cardiac function remains unclear.
Methods: We investigated the functional relevance of this peptide using ECG and respiration gated magnetic resonance imaging, conductance catheter pressure-volume hemodynamic measurements, and echocardiography in vivo. In addition, we carried out histology and immunohistochemistry to assess cardiac hypertrophy and to localize apelin and APJ in the adult and embryonic mouse heart.
Circulation
September 2003
Donald W. Reynolds Cardiovascular Research Center, Division of Cardiovascular Medicine, Falk CVRC, Stanford University, 300 Pasteur Dr, Stanford, Calif 94305, USA.
Background: Apelin is among the most potent stimulators of cardiac contractility known. However, no physiological or pathological role for apelin-angiotensin receptor-like 1 (APJ) signaling has ever been described.
Methods And Results: We performed transcriptional profiling using a spotted cDNA microarray with 12 814 unique clones on paired samples of left ventricle obtained before and after placement of a left ventricular assist device in 11 patients.