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153. Rationale and Design of the Treatment of Hyponatremia Based on Lixivaptan in NYHA Class III/IV Cardiac Patient Evaluation (THE BALANCE) Study

Author

Abraham, William T., primary, Aranda, Juan M., additional, Boehmer, John P., additional, Elkayam, Uri, additional, Gilbert, Edward M., additional, Gottlieb, Stephen S., additional, Hasenfuβ, Gerd, additional, Kukin, Marrick, additional, Lowes, Brian D., additional, O’Connell, John B., additional, Tavazzi, Luigi, additional, Feldman, Arthur M., additional, Ticho, Barry, additional, and Orlandi, Cesare, additional

Published
2010
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157. An α 2C -Adrenergic Receptor Polymorphism Alters the Norepinephrine-Lowering Effects and Therapeutic Response of the β-Blocker Bucindolol in Chronic Heart Failure

Author

Bristow, Michael R., primary, Murphy, Guinevere A., additional, Krause-Steinrauf, Heidi, additional, Anderson, Jeffrey L., additional, Carlquist, John F., additional, Thaneemit-Chen, Surai, additional, Krishnan, Vaishali, additional, Abraham, William T., additional, Lowes, Brian D., additional, Port, J. David, additional, Davis, Gordon W., additional, Lazzeroni, Laura C., additional, Robertson, Alastair D., additional, Lavori, Phillip W., additional, and Liggett, Stephen B., additional

Published
2010
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170. Drug Therapy in the Heart Transplant Recipient

Author

Lindenfeld, JoAnn, primary, Page, Robert L., additional, Zolty, Ronald, additional, Shakar, Simon F., additional, Levi, Marilyn, additional, Lowes, Brian, additional, Wolfel, Eugene E., additional, and Miller, Geraldine G., additional

Published
2005
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171. Drug Therapy in the Heart Transplant Recipient

Author

Lindenfeld, JoAnn, primary, Miller, Geraldine G., additional, Shakar, Simon F., additional, Zolty, Ronald, additional, Lowes, Brian D., additional, Wolfel, Eugene E., additional, Mestroni, Luisa, additional, Page, Robert L., additional, and Kobashigawa, Jon, additional

Published
2004
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172. Hormone replacement therapy is associated with improved survival in women with advanced heart failure

Author

Lindenfeld, JoAnn, primary, Ghali, Jalal K, additional, Krause-Steinrauf, Heidi J, additional, Khan, Steven, additional, Adams, Kirkwood, additional, Goldman, Steven, additional, Peberdy, Mary Ann, additional, Yancy, Clyde, additional, Thaneemit-Chen, Surai, additional, Larsen, Rhonda L, additional, Young, James, additional, Lowes, Brian, additional, and Rosenberg, Yves D, additional

Published
2003
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174. The effect of diabetes on outcomes of patients with advanced heart failure in the BEST trial

Author

Domanski, Michael, primary, Krause-Steinrauf, Heidi, additional, Deedwania, Prakash, additional, Follmann, Dean, additional, Ghali, Jalal K, additional, Gilbert, Edward, additional, Haffner, Steven, additional, Katz, Richard, additional, Lindenfeld, JoAnn, additional, Lowes, Brian D, additional, Martin, Wade, additional, McGrew, Frank, additional, and Bristow, Michael R, additional

Published
2003
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175. Angiotensin-converting enzyme DD genotype in patients with primary pulmonary hypertension: increased frequency and association with preserved haemodynamics

Author

Abraham, William T, primary, Raynolds, Mary V, additional, Badesch, David B, additional, Wynne, Kristine M, additional, Groves, Bertron M, additional, Roden, Robert L, additional, Robertson, Alastair D, additional, Lowes, Brian D, additional, Zisman, Lawrence S, additional, Voelkel, Norbert F, additional, Bristow, Michael R, additional, and Perryman, M Benjamin, additional

Published
2003
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176. Myocardial Gene Expression in Dilated Cardiomyopathy Treated with Beta-Blocking Agents

Author

Lowes, Brian D., primary, Gilbert, Edward M., additional, Abraham, William T., additional, Minobe, Wayne A., additional, Larrabee, Patti, additional, Ferguson, Debra, additional, Wolfel, Eugene E., additional, Lindenfeld, JoAnn, additional, Tsvetkova, Tatiana, additional, Robertson, Alastair D., additional, Quaife, Robert A., additional, and Bristow, Michael R., additional

Published
2002
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180. Low-dose enoximone improves exercise capacity in chronic heart failure∗∗A list of the Enoximone Study Group Members and institutional affiliations is provided in the appendix.

Author

Lowes, Brian D, primary, Higginbotham, Michael, additional, Petrovich, Lawrence, additional, DeWood, Marcus A, additional, Greenberg, Mark A, additional, Rahko, Peter S, additional, Dec, G.William, additional, LeJemtel, Thierry H, additional, Roden, Robert L, additional, Schleman, Margo M, additional, Robertson, Alastair D, additional, Gorczynski, Richard J, additional, and Bristow, Michael R, additional

Published
2000
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187. Abstract 15319: Left Ventricular Assistant Device (lvad) Support Did Not Alter Mirna Expression in Heart Failure Patients

Author

Dhar, Kajari, Basma, Hesham, Um, John, Qiu, Fang, and Lowes, Brian D

Abstract

Introduction:Micro RNAs (miRNA) are crucial regulators of various biological processes including the pathogenesis of heart failure (HF). In this study, miRNA profiling was compared with pre and post LVAD and non-failing (NF) control heart patients. Our goal was to identify miRNAs involved in HF and responses to LVAD therapy.Methods:Myocardial RNAs were isolated from non-ischemic dilated cardiomyopathy patients (n=22) who went through LVAD placement (pre LVAD) and later transplant (post LVAD) along with 6 normal hearts as controls. NanoString technology was used to quantify miRNA expressions. NanoString miRNAs raw count data were preprocessed and normalized using solver 4.0 Analysis Software. Ingenuity Pathway Analysis (IPA) was done by differentially expressed miRNA to understand the biological pathways involved.Results:Our sample population exhibited 80% male and 95% Caucasian with an average age of 57 and ejection fraction was less than 25% at the time of LVAD placement. The average LVAD duration of patients was 525 days. One ninety-five miRNAs in pre and 120 miRNAs in post LVAD patients were differentially expressed compared to control using cutoff of for the FDR adjusted p-value 0.05 and at least 2-fold changes. There was no significant change in miRNA expression when post LVAD was compared with pre LVAD patients. IPA analysis revealed that there are 15 up-regulated miRNA that promote apoptosis with a net Z score of 2.155 in post LVAD versus control. There are 27 miRNAs with a net of apoptotic with a Z score 0f 0.766 in pre LVAD versus control. It was also noticed from IPA analysis that expression of 8 identical miRNAs in both pre and post LVAD patients were involved in heart fibrosis. LVAD therapy did not change the miRNA expressionConclusions:Our results identify many miRNAs that are associated with apoptosis and fibrosis in end stage heart failure. Molecular mechanisms of heart disease will be identified by miRNA profiling and function as potential biomarkers or therapeutic targets in future. LVAD therapy does not substantially reverse these epigenetic changes in this population.

Published
2022
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191. 901-94 The Angiotensin Converting Enzyme DD Genotype is Associated with Preserved Right Ventricular Function in Patients with Severe Primary Pulmonary Hypertension

Author

Abraham, William T., primary, Raynolds, Mary V., additional, Badesch, David B., additional, Lowes, Brian D., additional, Groves, Bertran M., additional, Wynne, Kristine M., additional, Voelkel, Norbert F., additional, Perryman, M. Benjamin, additional, and Bristow, Michael R., additional

Published
1995
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193. Importance of Angiotensin-Converting Enzyme in Pulmonary Hypertension

Author

Abraham, William T., primary, Raynolds, Mary V., additional, Gottschall, Brigitte, additional, Badesch, David B., additional, Wynne, Kristine M., additional, Groves, Bertron M., additional, Lowes, Brian D., additional, Bristow, Michael R., additional, Perryman, Benjamin, additional, and Voelkel, Norbert F., additional

Published
1995
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196. Worsening Renal Function in Patients With Acute Decompensated Heart Failure Treated With Ultrafiltration: Predictors and Outcomes.

Author

RAICHLIN, EUGENIA, HAGLUND, NICHOLAS A., DUMITRU, IOANA, LYDEN, ELIZABETH R., JOHNSTON, MICHAEL D., MACK, JOAN M., WINDLE, JOHN R., and LOWES, BRIAN D.

Abstract

Background: Ultrafiltration (UF) is used to treat patients with diuretic-resistant acute decompensated heart failure. The aim of this study was to identify predictors and the effect of worsening renal failure (WRF) on mortality in patients treated with UF. Methods and Results: Based on changes in serum creatinine, 99 patients treated with UF were divided into WRF and control groups. Overall creatinine increased from 1.9 ± 9.7 to 2.2 ± 2.0 mg/dL (P < .001), and WRF developed in 41% of the subjects. The peak UF rate was higher in the WRF group in univariate analysis (174 ± 45 vs 144 ± 42 mL/h; P = .03). Based on multivariate analysis, aldosterone antagonist treatment (odds ratio [OR] 3.38, 95% confidence interval [CI] 1.17-13.46, P = .04), heart rate ≤65 beats/min (OR 6.03, 95% CI 1.48-48.42; P = .03), and E/E' ≥15 (OR 3.78, 95% CI 1.26-17.55; P = .04) at hospital admission were associated with WRF. Patients with baseline glomerular filtration rate (GFR) ≤60 mg/dL who developed WRF during UF had a 75% 1-year mortality rate. Conclusions: WRF occurred frequently during UF. Increased LV filling pressures, lower heart rate, and treatment with aldosterone antagonist at hospital admission can identify patients at increased risk for WRF. Patients with baseline GFR ≤60 mg/dL and WRF during UF have an extremely high 1-year mortality rate. [ABSTRACT FROM AUTHOR]

Published
2013
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197. Association of DJ-1/PTEN/AKT- and ASK1/p38-mediated cell signalling with ischaemic cardiomyopathy.

Author

Klawitter, Jelena, Klawitter, Jost, Agardi, Erika, Corby, Kyler, Leibfritz, Dieter, Lowes, Brian D., Christians, Uwe, and Seres, Tamas

Subjects
CARDIOMYOPATHIES, SERINE/THREONINE kinases, CELLULAR signal transduction, CELL metabolism, GENE expression, HEART cells, APOPTOSIS, NF-kappa B
Abstract

Aims Dilated cardiomyopathies from chronic ischaemia (ISCM) or idiopathic (IDCM) pathological mechanisms are accompanied by similar clinical symptoms but may differ in protein expression, cell metabolism, and signalling processes at the cellular level. Using a combination of proteomic and metabolomic profiling, we sought to decipher the relationships between the metabolism and cellular signalling pathways in human heart tissues collected from patients with ISCM, IDCM, and those without heart disease and dilation. Methods and results The comparative analysis suggested a decrease in glycolysis, Krebs cycle, and malate–aspartate shuttle activities in both types of cardiomyopathies and an increase in ketone body oxidation only in ISCM. Chronic ischaemic injury was associated with increased DJ-1 and decreased phosphatase and tensin homolog (PTEN) protein expression. The reduced PTEN expression was accompanied by increased phosphorylation of cell-protective AKT. Phosphorylation at T845 of apoptosis signal-regulating kinase 1 and p38 mitogen-activated protein kinase proteins, with no change in the phosphorylation of extracellular signal-regulated kinases, was also observed. The downregulation of peptidyl–prolyl cis/trans isomerase and NF-κB essential modulator potentially inhibits NF-κB-initiated processes. Conclusion The present study characterized differences in the molecular mechanisms, metabolism, and pathological cell signalling associated with ISCM and IDCM, which may provide novel targets for intervention at the cellular level. [ABSTRACT FROM PUBLISHER]

Published
2013
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198. Adora2b-elicited Per2 stabilization promotes a HIF-dependent metabolic switch crucial for myocardial adaptation to ischemia.

Author

Eckle, Tobias, Hartmann, Katherine, Bonney, Stephanie, Reithel, Susan, Mittelbronn, Michel, Walker, Lori A, Lowes, Brian D, Han, Jun, Borchers, Christoph H, Buttrick, Peter M, Kominsky, Douglas J, Colgan, Sean P, and Eltzschig, Holger K

Subjects
MYOCARDIAL infarction, ADENOSINES, ISCHEMIA, GLYCOLYSIS, LABORATORY mice
Abstract

Adenosine signaling has been implicated in cardiac adaptation to limited oxygen availability. In a wide search for adenosine receptor A2b (Adora2b)-elicited cardioadaptive responses, we identified the circadian rhythm protein period 2 (Per2) as an Adora2b target. Adora2b signaling led to Per2 stabilization during myocardial ischemia, and in this setting, Per2?/? mice had larger infarct sizes compared to wild-type mice and loss of the cardioprotection conferred by ischemic preconditioning. Metabolic studies uncovered a limited ability of ischemic hearts in Per2?/? mice to use carbohydrates for oxygen-efficient glycolysis. This impairment was caused by a failure to stabilize hypoxia-inducible factor-1? (Hif-1?). Moreover, stabilization of Per2 in the heart by exposing mice to intense light resulted in the transcriptional induction of glycolytic enzymes and Per2-dependent cardioprotection from ischemia. Together, these studies identify adenosine-elicited stabilization of Per2 in the control of HIF-dependent cardiac metabolism and ischemia tolerance and implicate Per2 stabilization as a potential new strategy for treating myocardial ischemia. [ABSTRACT FROM AUTHOR]

Published
2012
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199. An α2C-Adrenergic Receptor Polymorphism Alters the Norepinephrine-Lowering Effects and Therapeutic Response of the β-Blocker Bucindolol in Chronic Heart Failure.

Author

Bristow, Michael R., Murphy, Guinevere A., Krause-Steinrauf, Heidi, Anderson, Jeffrey L., Cariquist, John F., Thaneemit-Chen, Surai, Krishnan, Vaishali, Abraham, William T., Lowes, Brian D., Port, J. David, Davis, Gordon W., Lazzeroni, Laura C., Robertson, Alastair D., Lavori, Phillip W., and Stephen B. Liggett

Subjects
HEART failure, ALPHA adrenoceptors, BETA adrenoceptors, ADRENERGIC beta blockers, SYMPATHOLYTIC agents, GENETIC polymorphisms, GENETICS
Abstract

The article focuses on a study which investigated whether alpha-2C-adrenergic receptor (AR) polymorphisms affect sympatholytic effects of bucindolol in patients with chronic heart failure. Outcomes of chronic heart failure were determined by adrenergic activation. The study concluded that alpha-2Creceptor genotype influenced the Beta-Blocker Evaluation of Survival Trial AR polymorphism substudy, the norepinephrine lowering and clinical therapeutic responses to bucindolol.

Published
2010
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200. Myocardial FFA metabolism during rest and atrial pacing in humans.

Author

Bergman, Bryan C., Tsvetkova, Tatiana, Lowes, Brian, and Wolfel, Eugene E.

Subjects
MYOCARDIAL infarction, FATTY acids, OXIDATION, BLOOD flow, CATHETERS, FAT, LIPIDS
Abstract

There is limited in vivo data in humans evaluating myocardial fat utilization during increased heart work. This study was done to determine myocardial free fatty acid (FFA) metabolism during rest and atrial pacing, which increases cardiac work without changing arterial sub-strate concentration. We studied seven healthy men and women (age = 49.7 ± 3.9 yr, BMI = 23.4 ± 1.1 kg/m2, Vo2max = 35.5 ± 3.0 ml-kg-1 min-1, ejection fraction = 68 ± 3%). After 3 days of dietary control, coronary sinus, femoral arterial and venous, and peripheral venous catheters were placed. Subjects received [13C]bi- carbonate followed by a continuous infusion of [1-13C]palmitate through the end of the study. Arterial and coronary sinus blood sampling and measurements of resting coronary sinus blood flow were made during rest and atrial pacing to 120 beats/mm. MVo2 increased (P < 0.05) from rest to atrial pacing. Coronary sinus FFA concentration was significantly lower than arterial through rest and atrial pacing (P 0.007). Isotopically measured myocardial palmitate uptake increased significantly from rest to atrial pacing (P = 0.03). Approximately one-third of palmitate delivery was extracted by the niyocardium during rest and atrial pacing. Myocardial V13CO2 production and palmitate oxidation increased significantly from rest (P < 0.01) to atrial pacing. Net glycerol balance was significantly greater than zero during rest (P = 0.04) but not different from zero during atrial pacing (P = 0.13). These data suggest that myocardial lipid uptake and oxidation increase with greater heart work during atrial pacing, with a similar relative proportion of fat oxidation to total myocardial energy expenditure. [ABSTRACT FROM AUTHOR]

Published
2009
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