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
Loading...
Reduced CK flux in failing vs nonfailing LVH supports energy deficit hypothesis; hypothesis-generating and should not yet change practice.
Observational (n=34)
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.
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).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: