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Altered Creatine Kinase Adenosine Triphosphate Kinetics in Failing Hypertrophied Human Myocardium
Open accessAbstract
Background— The progression of pressure-overload left ventricular hypertrophy (LVH) to chronic heart failure (CHF) may involve a relative deficit in energy supply and/or delivery. Methods and Results— We measured myocardial creatine kinase (CK) metabolite concentrations and adenosine triphosphate (ATP) synthesis through CK, the primary energy reserve of the heart, to test the hypothesis that ATP flux through CK is impaired in patients with LVH and CHF. Myocardial ATP levels were normal, but creatine phosphate levels were 35% lower in LVH patients (n=10) than in normal subjects (n=14, P <0.006). Left ventricular mass and CK metabolite levels in LVH were not different from those in patients with LVH and heart failure (LVH+CHF, n=10); however, the myocardial CK pseudo first-order rate constant was normal in LVH (0.36±0.04 s −1 in LVH versus 0.32±0.06 s −1 in normal subjects) but halved in LVH+CHF (0.17±0.06 s −1 , P <0.001). The net ATP flux through CK was significantly reduced by 30% in LVH (2.2±0.7 μmol · g −1 · s −1 , P =0.011) and by a dramatic 65% in LVH+CHF (1.1±0.4 μmol · g −1 · s −1 , P <0.001) compared with normal subjects (3.1±0.8 μmol · g −1 · s −1 ). Conclusions— These first observations in human LVH demonstrate that it is not the relative or absolute CK metabolite pool sizes but rather the kinetics of ATP turnover through CK that distinguish failing from nonfailing hypertrophic hearts. Moreover, the deficit in ATP kinetics is similar in systolic and nonsystolic heart failure and is not related to the severity of hypertrophy but to the presence of CHF. Because CK temporally buffers ATP, these observations support the hypothesis that a deficit in myofibrillar energy delivery contributes to CHF pathophysiology in human LVH.
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“The same quantitative 31P magnetic resonance spectroscopy protocols for measuring human myocardial metabolite concentrations and CK kinetics used here, previously revealed significant reductions in myocardial CK flux inpatients with non-ischemic dilated cardiomyopathy7, and left ventricular hypertrophy secondary to hypertension6.”
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“The present work extends the observation of reduced kf and CK flux in patients who have both heart failure and hypertrophy produced by pressure overload6, to those with hypertrophy of genetic origin–specifically those with an Arg403Gln point mutation in MH.”
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“Indeed, the magnitude of the reduction is comparable, albeit less than, the 50–65% reductions observed previously in other heart failure patients6,7.”
From iRhythm ZIO: The Diagnostic Yield of a 14-day Continuous Ambulatory ECG Monitor (Turakhia et al., diagnostic yield of extended ambulatory ECG monitoring) (2013) · cites this paper as [6]
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“With inorganic phosphate [Pi] conservatively estimated at 1μmol/g wet wt6,7 in both control and HC patients, the free-energy release with ATP hydrolysis is similar in both groups (ΔG~ATP. −58.5±0.4 vs −58.3±1.3 kJ/mol).”
From iRhythm ZIO: The Diagnostic Yield of a 14-day Continuous Ambulatory ECG Monitor (Turakhia et al., diagnostic yield of extended ambulatory ECG monitoring) (2013) · cites this paper as [6]
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Self-citation
Metadata
- Authors
- Smith, C. S., Bottomley, P. A., Schulman, S. P., Gerstenblith, G., & Weiss, R. G.
- Affiliations
- Johns Hopkins University (US)
- Venue
- Circulation
- Published
- 2006-09-12
- Volume
- 114
- Issue
- 11
- Pages
- 1151-1158
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- PMC
- PMC1808438
- OpenAlex
- W2111571221
- Cited by
- 204
- References
- 53
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 8 · 2023: 8 · 2022: 8 · 2021: 6 · 2020: 12 · 2019: 13 · 2018: 8 · 2017: 11 · 2016: 11 · 2015: 12 · 2014: 11 · 2013: 13 · 2012: 9
- FWCI
- 7.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Donald W. Reynolds Foundation
- National Heart, Lung, and Blood Institute (HL61912, HL-63030, R01HL063030, R01HL061912, R01HL056882, HL56882)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- creatine kinase, adenosine triphosphate, left ventricular hypertrophy, chronic heart failure, myocardial energy metabolism, phosphocreatine, ATP turnover, pressure overload, heart failure pathophysiology
- MeSH terms
- Adenosine Triphosphate, Adult, Aged, Cardiac Output, Low, Creatine Kinase, Energy Metabolism, Female, Heart, Heart Ventricles, Humans, Male, Middle Aged, Myocardium, Severity of Illness Index, Hypertrophy, Left Ventricular, Disease Progression
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