High-energy phosphate metabolism in normal, hypertrophied and failing human myocardium

This chapter examines the role of cardiac high-energy phosphate metabolism in normal, hypertrophied and failing human myocardium. Myocardial biopsies allow analysis of ATP, total adenine nucleotides, creatine kinase activity and total creatine content, while non-invasive 31P-magnetic resonance spect...

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Main Author: Neubauer, S
Format: Journal article
Language:English
Published: 1999
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author Neubauer, S
author_facet Neubauer, S
author_sort Neubauer, S
collection OXFORD
description This chapter examines the role of cardiac high-energy phosphate metabolism in normal, hypertrophied and failing human myocardium. Myocardial biopsies allow analysis of ATP, total adenine nucleotides, creatine kinase activity and total creatine content, while non-invasive 31P-magnetic resonance spectroscopy can be used to determine phosphocreatine/ATP ratios and, most recently, absolute levels of ATP and phosphocreatine. The failing human myocardium is characterized by reduced phosphocreatine and total creatine levels, normal or slightly reduced ATP levels and reduced creatine kinase activity. These changes are consistent with, but do not prove, a role of high-energy phosphate metabolism as a contributing factor in heart failure. An answer to the precise functional role of high-energy phosphate metabolism necessitates analysis of free ADP levels, free energy change of ATP hydrolysis and creatine kinase reaction velocity; these measurements may become feasible in coming years. However, analysis of energy metabolism in a compartmentalized manner, i.e., in the compartments relevant for contractile function such as the perimyofibrillar space, will remain elusive for the foreseeable future.
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spelling oxford-uuid:920d4a42-76ca-4189-ac20-18074fa8da082022-03-26T23:22:50ZHigh-energy phosphate metabolism in normal, hypertrophied and failing human myocardiumJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:920d4a42-76ca-4189-ac20-18074fa8da08EnglishSymplectic Elements at Oxford1999Neubauer, SThis chapter examines the role of cardiac high-energy phosphate metabolism in normal, hypertrophied and failing human myocardium. Myocardial biopsies allow analysis of ATP, total adenine nucleotides, creatine kinase activity and total creatine content, while non-invasive 31P-magnetic resonance spectroscopy can be used to determine phosphocreatine/ATP ratios and, most recently, absolute levels of ATP and phosphocreatine. The failing human myocardium is characterized by reduced phosphocreatine and total creatine levels, normal or slightly reduced ATP levels and reduced creatine kinase activity. These changes are consistent with, but do not prove, a role of high-energy phosphate metabolism as a contributing factor in heart failure. An answer to the precise functional role of high-energy phosphate metabolism necessitates analysis of free ADP levels, free energy change of ATP hydrolysis and creatine kinase reaction velocity; these measurements may become feasible in coming years. However, analysis of energy metabolism in a compartmentalized manner, i.e., in the compartments relevant for contractile function such as the perimyofibrillar space, will remain elusive for the foreseeable future.
spellingShingle Neubauer, S
High-energy phosphate metabolism in normal, hypertrophied and failing human myocardium
title High-energy phosphate metabolism in normal, hypertrophied and failing human myocardium
title_full High-energy phosphate metabolism in normal, hypertrophied and failing human myocardium
title_fullStr High-energy phosphate metabolism in normal, hypertrophied and failing human myocardium
title_full_unstemmed High-energy phosphate metabolism in normal, hypertrophied and failing human myocardium
title_short High-energy phosphate metabolism in normal, hypertrophied and failing human myocardium
title_sort high energy phosphate metabolism in normal hypertrophied and failing human myocardium
work_keys_str_mv AT neubauers highenergyphosphatemetabolisminnormalhypertrophiedandfailinghumanmyocardium