Nishant R Shah1, Mark C Bieniarz2, Sukhdeep S Basra3, Robert D Paisley4, Pranav Loyalka5, Igor D Gregoric5, Douglas L Mann6, Biswajit Kar7. 1. Texas Heart Institute, Baylor College of Medicine, Houston, Texas. 2. New Mexico Heart Institute, Albuquerque, New Mexico. 3. Baylor College of Medicine, Houston, Texas. 4. 3-509th Infantry Airborne, US Army Joint Base Elmendorf-Richardson, Richardson, Alaska. 5. Texas Heart Institute, University of Texas Health Sciences Center, Houston, Texas. 6. Washington University School of Medicine, St. Louis, Missouri. 7. Texas Heart Institute, University of Texas Health Sciences Center, Houston, Texas. Electronic address: biswajit.kar@uth.tmc.edu.
Abstract
OBJECTIVES: The aim of this study was to characterize levels of serum biomarkers in patients with severe refractory cardiogenic shock (SRCS) and to document temporal changes in these levels during restoration of circulation. BACKGROUND: Patients with SRCS have been challenging to study because of their rapidly changing clinical condition while undergoing multiple simultaneous interventions. METHODS: Twenty-one patients with SRCS received circulatory support via a percutaneously implanted ventricular assist device (PVAD). Serum samples obtained prior to PVAD support initiation, at 24 h of PVAD support, and at 7 days of PVAD support were assayed for B-type natriuretic peptide (BNP), high-sensitivity C-reactive protein (hsCRP), soluble tumor necrosis factor receptor-1 (sTNFR1), soluble Fas (sFas), soluble Fas ligand (sFasL), endothelin-1, and procollagen III N-terminal peptide (PIIINP). Baseline biomarker levels were qualitatively compared to reference values; levels at 24 h of PVAD support and at 7 days of PVAD support were compared to baseline using 2-tailed Wilcoxon matched pair signed rank tests with Bonferroni correction for multiple comparisons. RESULTS: These patients with SRCS had elevated serum levels of BNP, hsCRP, sTNFR1, endothelin-1, and PIIINP. Ventricular unloading and restoration of circulation via PVAD support in patients with SRCS were associated with reductions in serum BNP, sFas, and endothelin-1 levels and increases in serum sFasL and PIIINP levels. CONCLUSIONS: This study characterizes several important baseline serum biomarker levels in patients with SRCS and introduces a novel PVAD-based protocol with the potential to "reverse"-model the pathophysiology of cardiogenic shock.
OBJECTIVES: The aim of this study was to characterize levels of serum biomarkers in patients with severe refractory cardiogenic shock (SRCS) and to document temporal changes in these levels during restoration of circulation. BACKGROUND:Patients with SRCS have been challenging to study because of their rapidly changing clinical condition while undergoing multiple simultaneous interventions. METHODS: Twenty-one patients with SRCS received circulatory support via a percutaneously implanted ventricular assist device (PVAD). Serum samples obtained prior to PVAD support initiation, at 24 h of PVAD support, and at 7 days of PVAD support were assayed for B-type natriuretic peptide (BNP), high-sensitivity C-reactive protein (hsCRP), soluble tumornecrosis factor receptor-1 (sTNFR1), soluble Fas (sFas), soluble Fas ligand (sFasL), endothelin-1, and procollagen III N-terminal peptide (PIIINP). Baseline biomarker levels were qualitatively compared to reference values; levels at 24 h of PVAD support and at 7 days of PVAD support were compared to baseline using 2-tailed Wilcoxon matched pair signed rank tests with Bonferroni correction for multiple comparisons. RESULTS: These patients with SRCS had elevated serum levels of BNP, hsCRP, sTNFR1, endothelin-1, and PIIINP. Ventricular unloading and restoration of circulation via PVAD support in patients with SRCS were associated with reductions in serum BNP, sFas, and endothelin-1 levels and increases in serum sFasL and PIIINP levels. CONCLUSIONS: This study characterizes several important baseline serum biomarker levels in patients with SRCS and introduces a novel PVAD-based protocol with the potential to "reverse"-model the pathophysiology of cardiogenic shock.
Authors: Anna J Meredith; Darlene L Y Dai; Virginia Chen; Zsuzsanna Hollander; Raymond Ng; Annemarie Kaan; Scott Tebbutt; Krishnan Ramanathan; Anson Cheung; Bruce M McManus Journal: ESC Heart Fail Date: 2015-11-24