Captopril treatment for 5-6 weeks in patients with stable moderate heart failure increased subnormal skeletal muscle calcium and phosphofructokinase levels to the reference range (P<0.04).
RCT (n=12)
Double-blind
Does captopril improve skeletal muscle calcium and phosphofructokinase levels in patients with stable moderate heart failure?
Captopril treatment for 5-6 weeks upregulates depressed skeletal muscle calcium and phosphofructokinase levels in patients with stable moderate heart failure.
valor p: p=<0.04
The effects of the angiotensin converting enzyme inhibitor captopril, after treatment for 5-6 weeks with 25 mg t.i.d., were studied in 12 patients with stable moderate heart failure. Five patients received placebo treatment, and the two groups were comparable at baseline. Angiotensin II levels decreased in response to captopril therapy. Skeletal muscle potassium, magnesium and chloride levels did not differ from reference values. Calcium was subnormal (P less than 0.0001), but increased to the reference range during captopril treatment. Phosphofructokinase, a rate-limiting glycolytic enzyme, was in the lower reference range and increased (P less than 0.04) in response to captopril therapy. In conclusion, stable moderate heart failure is associated with low levels of skeletal muscle calcium and phosphofructokinase activity, these metabolic changes tending to return to normal levels with captopril treatment.
Sylvén et al. (Fri,) conducted a rct in stable moderate heart failure (n=12). Captopril vs. Placebo was evaluated on Skeletal muscle calcium and phosphofructokinase levels (p=<0.04). Captopril treatment for 5-6 weeks in patients with stable moderate heart failure increased subnormal skeletal muscle calcium and phosphofructokinase levels to the reference range (P<0.04).