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September 5, 2006CirculationOpen Access

Patients with left ventricular hypertrophy and heart failure had a 65% reduction in net ATP flux through creatine kinase compared to normal subjects (1.1 vs 3.1 µmol/g/s, P<0.001).

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Population

34 subjects including patients with left ventricular hypertrophy, patients with LVH and chronic heart…

Design

Cross-sectional

Key result

Patients with left ventricular hypertrophy and heart failure had a 65% reduction in net ATP flux through creatine kinase compared to normal subjects (1.1 vs 3.1 µmol/g/s, P<0.001).

Authors

CSCraig S. SmithPBPaul A. BottomleySSSteven P. Schulman

Discussion

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Overview

Reduced CK flux in failing vs nonfailing LVH supports energy deficit hypothesis; hypothesis-generating and should not yet change practice.

Key Points

  • This research aims to investigate the energy supply dynamics in heart conditions like left ventricular hypertrophy (LVH) and chronic heart failure (CHF).
  • Measured myocardial creatine kinase metabolite concentrations and ATP synthesis
  • Compared data between LVH patients (n=10), LVH+CHF patients (n=10), and normal subjects (n=14)
  • Assessed relations between creatine phosphate levels and CK rate constants
  • Creatine phosphate levels were 35% lower in LVH patients than normal subjects (P < 0.006)
  • ATP flux decreased by 30% in LVH patients and 65% in LVH+CHF patients compared to normal subjects (P < 0.001)
  • Myocardial CK rate constant halved in LVH+CHF compared to normal (0.17 ± 0.06 s(-1) vs. 0.32 ± 0.06 s(-1), P < 0.001)

Study Design

Type

Observational (n=34)

Structured PICO

P
Population
34 subjects including patients with left ventricular hypertrophy (LVH, n=10), patients with LVH and chronic heart failure (LVH+CHF, n=10), and normal subjects (n=14).
O
Outcome
Myocardial creatine kinase (CK) metabolite concentrations and adenosine triphosphate (ATP) synthesis through CKsurrogate

Main Result

Absolute Event Rate: 1.1% vs 3.1%

p-value: p=<0.001

The kinetics of ATP turnover through creatine kinase, rather than metabolite pool sizes, distinguish failing from nonfailing hypertrophic human hearts, suggesting a deficit in energy delivery contributes to heart failure pathophysiology.

Cite This Study

Smith et al. (2006) conducted an observational in Left ventricular hypertrophy and chronic heart failure (n=34). Left ventricular hypertrophy with chronic heart failure vs. Normal subjects and nonfailing left ventricular hypertrophy was evaluated on Net ATP flux through creatine kinase (p=<0.001). Patients with left ventricular hypertrophy and heart failure had a 65% reduction in net ATP flux through creatine kinase compared to normal subjects (1.1 vs 3.1 µmol/g/s, P<0.001).

synapsesocial.com/papers/6a15da2d1362a77db8e3c516https://doi.org/10.1161/circulationaha.106.613646
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Metabolic Rates of ATP Transfer Through Creatine Kinase (CK Flux) Predict Clinical Heart Failure Events and Death2013 · 136 citations
  2. 2Mitochondrial Creatine Kinase Attenuates Pathologic Remodeling in Heart Failure2022 · 43 citations
  3. 3Energetic correlates of cardiac failure: Changes in the creatine kinase system in the failing myocardium1990 · 113 citations
  4. 4Cardiac work is related to creatine kinase energy supply in human heart failure: a cardiovascular magnetic resonance spectroscopy study2018 · 46 citations
  5. 5High-Energy Phosphate Metabolism and Creatine Kinase in Failing Hearts2001 · 126 citations