Reduced Myocardial Creatine Kinase Flux in Human Myocardial Infarction An In Vivo Phosphorus Magnetic Resonance Spectroscopy Study
Background— Energy metabolism is essential for myocellular viability. The high-energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) are reduced in human myocardial infarction (MI), reflecting myocyte loss and/or decreased intracellular ATP generation by creatine kinase (CK), the...
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| Published in | Circulation (New York, N.Y.) Vol. 119; no. 14; pp. 1918 - 1924 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
14.04.2009
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 0009-7322 1524-4539 1524-4539 |
| DOI | 10.1161/CIRCULATIONAHA.108.823187 |
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| Abstract | Background—
Energy metabolism is essential for myocellular viability. The high-energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) are reduced in human myocardial infarction (MI), reflecting myocyte loss and/or decreased intracellular ATP generation by creatine kinase (CK), the prime energy reserve of the heart. The pseudo–first-order CK rate constant, k, measures intracellular CK reaction kinetics and is independent of myocyte number within sampled tissue. CK flux is defined as the product of [PCr] and k. CK flux and k have never been measured in human MI.
Methods and Results—
Myocardial CK metabolite concentrations, k, and CK flux were measured noninvasively in 15 patients 7 weeks to 16 years after anterior MI using phosphorus magnetic resonance spectroscopy. In patients, mean myocardial [ATP] and [PCr] were 39% to 44% lower than in 15 control subjects (PCr=5.4±1.2 versus 9.6±1.1 μmol/g wet weight in MI versus control subjects, respectively,
P
<0.001; ATP=3.4±1.1 versus 5.5±1.3 μmol/g wet weight,
P
<0.001). The myocardial CK rate constant, k, was normal in MI subjects (0.31±0.08 s
−1
) compared with control subjects (0.33±0.07 s
−1
), as was PCr/ATP (1.74±0.27 in MI versus 1.87±0.45). However, CK flux was halved in MI [to 1.7±0.5 versus 3.3±0.8 μmol(g · s)
−1
;
P
<0.001].
Conclusions—
These first observations of CK kinetics in prior human MI demonstrate that CK ATP supply is significantly reduced as a result of substrate depletion, likely attributable to myocyte loss. That k and PCr/ATP are unchanged in MI is consistent with the preservation of intracellular CK metabolism in surviving myocytes. Importantly, the results support therapies that primarily ameliorate the effects of tissue and substrate loss after MI and those that reduce energy demand rather than those that increase energy transfer or workload in surviving tissue. |
|---|---|
| AbstractList | Background—
Energy metabolism is essential for myocellular viability. The high-energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) are reduced in human myocardial infarction (MI), reflecting myocyte loss and/or decreased intracellular ATP generation by creatine kinase (CK), the prime energy reserve of the heart. The pseudo–first-order CK rate constant, k, measures intracellular CK reaction kinetics and is independent of myocyte number within sampled tissue. CK flux is defined as the product of [PCr] and k. CK flux and k have never been measured in human MI.
Methods and Results—
Myocardial CK metabolite concentrations, k, and CK flux were measured noninvasively in 15 patients 7 weeks to 16 years after anterior MI using phosphorus magnetic resonance spectroscopy. In patients, mean myocardial [ATP] and [PCr] were 39% to 44% lower than in 15 control subjects (PCr=5.4±1.2 versus 9.6±1.1 μmol/g wet weight in MI versus control subjects, respectively,
P
<0.001; ATP=3.4±1.1 versus 5.5±1.3 μmol/g wet weight,
P
<0.001). The myocardial CK rate constant, k, was normal in MI subjects (0.31±0.08 s
−1
) compared with control subjects (0.33±0.07 s
−1
), as was PCr/ATP (1.74±0.27 in MI versus 1.87±0.45). However, CK flux was halved in MI [to 1.7±0.5 versus 3.3±0.8 μmol(g · s)
−1
;
P
<0.001].
Conclusions—
These first observations of CK kinetics in prior human MI demonstrate that CK ATP supply is significantly reduced as a result of substrate depletion, likely attributable to myocyte loss. That k and PCr/ATP are unchanged in MI is consistent with the preservation of intracellular CK metabolism in surviving myocytes. Importantly, the results support therapies that primarily ameliorate the effects of tissue and substrate loss after MI and those that reduce energy demand rather than those that increase energy transfer or workload in surviving tissue. Energy metabolism is essential for myocellular viability. The high-energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) are reduced in human myocardial infarction (MI), reflecting myocyte loss and/or decreased intracellular ATP generation by creatine kinase (CK), the prime energy reserve of the heart. The pseudo-first-order CK rate constant, k, measures intracellular CK reaction kinetics and is independent of myocyte number within sampled tissue. CK flux is defined as the product of [PCr] and k. CK flux and k have never been measured in human MI. Myocardial CK metabolite concentrations, k, and CK flux were measured noninvasively in 15 patients 7 weeks to 16 years after anterior MI using phosphorus magnetic resonance spectroscopy. In patients, mean myocardial [ATP] and [PCr] were 39% to 44% lower than in 15 control subjects (PCr=5.4+/-1.2 versus 9.6+/-1.1 micromol/g wet weight in MI versus control subjects, respectively, P<0.001; ATP=3.4+/-1.1 versus 5.5+/-1.3 micromol/g wet weight, P<0.001). The myocardial CK rate constant, k, was normal in MI subjects (0.31+/-0.08 s(-1)) compared with control subjects (0.33+/-0.07 s(-1)), as was PCr/ATP (1.74+/-0.27 in MI versus 1.87+/-0.45). However, CK flux was halved in MI [to 1.7+/-0.5 versus 3.3+/-0.8 micromol(g . s)(-1); P<0.001]. These first observations of CK kinetics in prior human MI demonstrate that CK ATP supply is significantly reduced as a result of substrate depletion, likely attributable to myocyte loss. That k and PCr/ATP are unchanged in MI is consistent with the preservation of intracellular CK metabolism in surviving myocytes. Importantly, the results support therapies that primarily ameliorate the effects of tissue and substrate loss after MI and those that reduce energy demand rather than those that increase energy transfer or workload in surviving tissue. Energy metabolism is essential for myocellular viability. The high-energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) are reduced in human myocardial infarction (MI), reflecting myocyte loss and/or decreased intracellular ATP generation by creatine kinase (CK), the prime energy reserve of the heart. The pseudo-first-order CK rate constant, k, measures intracellular CK reaction kinetics and is independent of myocyte number within sampled tissue. CK flux is defined as the product of [PCr] and k. CK flux and k have never been measured in human MI.BACKGROUNDEnergy metabolism is essential for myocellular viability. The high-energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) are reduced in human myocardial infarction (MI), reflecting myocyte loss and/or decreased intracellular ATP generation by creatine kinase (CK), the prime energy reserve of the heart. The pseudo-first-order CK rate constant, k, measures intracellular CK reaction kinetics and is independent of myocyte number within sampled tissue. CK flux is defined as the product of [PCr] and k. CK flux and k have never been measured in human MI.Myocardial CK metabolite concentrations, k, and CK flux were measured noninvasively in 15 patients 7 weeks to 16 years after anterior MI using phosphorus magnetic resonance spectroscopy. In patients, mean myocardial [ATP] and [PCr] were 39% to 44% lower than in 15 control subjects (PCr=5.4+/-1.2 versus 9.6+/-1.1 micromol/g wet weight in MI versus control subjects, respectively, P<0.001; ATP=3.4+/-1.1 versus 5.5+/-1.3 micromol/g wet weight, P<0.001). The myocardial CK rate constant, k, was normal in MI subjects (0.31+/-0.08 s(-1)) compared with control subjects (0.33+/-0.07 s(-1)), as was PCr/ATP (1.74+/-0.27 in MI versus 1.87+/-0.45). However, CK flux was halved in MI [to 1.7+/-0.5 versus 3.3+/-0.8 micromol(g . s)(-1); P<0.001].METHODS AND RESULTSMyocardial CK metabolite concentrations, k, and CK flux were measured noninvasively in 15 patients 7 weeks to 16 years after anterior MI using phosphorus magnetic resonance spectroscopy. In patients, mean myocardial [ATP] and [PCr] were 39% to 44% lower than in 15 control subjects (PCr=5.4+/-1.2 versus 9.6+/-1.1 micromol/g wet weight in MI versus control subjects, respectively, P<0.001; ATP=3.4+/-1.1 versus 5.5+/-1.3 micromol/g wet weight, P<0.001). The myocardial CK rate constant, k, was normal in MI subjects (0.31+/-0.08 s(-1)) compared with control subjects (0.33+/-0.07 s(-1)), as was PCr/ATP (1.74+/-0.27 in MI versus 1.87+/-0.45). However, CK flux was halved in MI [to 1.7+/-0.5 versus 3.3+/-0.8 micromol(g . s)(-1); P<0.001].These first observations of CK kinetics in prior human MI demonstrate that CK ATP supply is significantly reduced as a result of substrate depletion, likely attributable to myocyte loss. That k and PCr/ATP are unchanged in MI is consistent with the preservation of intracellular CK metabolism in surviving myocytes. Importantly, the results support therapies that primarily ameliorate the effects of tissue and substrate loss after MI and those that reduce energy demand rather than those that increase energy transfer or workload in surviving tissue.CONCLUSIONSThese first observations of CK kinetics in prior human MI demonstrate that CK ATP supply is significantly reduced as a result of substrate depletion, likely attributable to myocyte loss. That k and PCr/ATP are unchanged in MI is consistent with the preservation of intracellular CK metabolism in surviving myocytes. Importantly, the results support therapies that primarily ameliorate the effects of tissue and substrate loss after MI and those that reduce energy demand rather than those that increase energy transfer or workload in surviving tissue. |
| Author | Weiss, Robert G. Wu, Katherine C. Gerstenblith, Gary Schulman, Steven P. Steinberg, Angela Bottomley, Paul A. |
| AuthorAffiliation | 2 Cardiology Division, Department of Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD, 21287 USA 1 Division of MR Research, Department of Radiology, Johns Hopkins University, School of Medicine, Baltimore, MD, 21287 USA |
| AuthorAffiliation_xml | – name: 2 Cardiology Division, Department of Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD, 21287 USA – name: 1 Division of MR Research, Department of Radiology, Johns Hopkins University, School of Medicine, Baltimore, MD, 21287 USA |
| Author_xml | – sequence: 1 givenname: Paul A. surname: Bottomley fullname: Bottomley, Paul A. organization: From the Division of MR Research, Department of Radiology (P.A.B.), and Cardiology Division, Department of Medicine (K.C.W., G.G., S.P.S., A.S., R.G.W.), The Johns Hopkins University, School of Medicine, Baltimore, Md – sequence: 2 givenname: Katherine C. surname: Wu fullname: Wu, Katherine C. organization: From the Division of MR Research, Department of Radiology (P.A.B.), and Cardiology Division, Department of Medicine (K.C.W., G.G., S.P.S., A.S., R.G.W.), The Johns Hopkins University, School of Medicine, Baltimore, Md – sequence: 3 givenname: Gary surname: Gerstenblith fullname: Gerstenblith, Gary organization: From the Division of MR Research, Department of Radiology (P.A.B.), and Cardiology Division, Department of Medicine (K.C.W., G.G., S.P.S., A.S., R.G.W.), The Johns Hopkins University, School of Medicine, Baltimore, Md – sequence: 4 givenname: Steven P. surname: Schulman fullname: Schulman, Steven P. organization: From the Division of MR Research, Department of Radiology (P.A.B.), and Cardiology Division, Department of Medicine (K.C.W., G.G., S.P.S., A.S., R.G.W.), The Johns Hopkins University, School of Medicine, Baltimore, Md – sequence: 5 givenname: Angela surname: Steinberg fullname: Steinberg, Angela organization: From the Division of MR Research, Department of Radiology (P.A.B.), and Cardiology Division, Department of Medicine (K.C.W., G.G., S.P.S., A.S., R.G.W.), The Johns Hopkins University, School of Medicine, Baltimore, Md – sequence: 6 givenname: Robert G. surname: Weiss fullname: Weiss, Robert G. organization: From the Division of MR Research, Department of Radiology (P.A.B.), and Cardiology Division, Department of Medicine (K.C.W., G.G., S.P.S., A.S., R.G.W.), The Johns Hopkins University, School of Medicine, Baltimore, Md |
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| Keywords | Human Myocardial infarction Purine nucleoside Adenosine Enzyme Creatine kinase Transferases Cardiovascular disease Phosphorus magnetic resonance spectroscopy NMR spectrometry Triphosphates Metabolism Coronary heart disease Myocardial disease adenosine triphosphate |
| Language | English |
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| Snippet | Background—
Energy metabolism is essential for myocellular viability. The high-energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) are... Energy metabolism is essential for myocellular viability. The high-energy phosphates adenosine triphosphate (ATP) and phosphocreatine (PCr) are reduced in... |
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| SubjectTerms | Adenosine Triphosphate - metabolism Adult Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Coronary heart disease Creatine Kinase - metabolism Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Energy Metabolism Heart Humans Kinetics Magnetic Resonance Imaging - methods Male Medical sciences Myocardial Infarction - enzymology Myocardial Infarction - metabolism Myocardial Infarction - pathology Phosphocreatine - metabolism Phosphorus Reference Values |
| Subtitle | An In Vivo Phosphorus Magnetic Resonance Spectroscopy Study |
| Title | Reduced Myocardial Creatine Kinase Flux in Human Myocardial Infarction |
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