The reduction in phosphocreatine depletion and in the increase in ADP during exercise, and the enhanced rate of phosphocreatine resynthesis in recovery (which is independent of muscle mass) indicate that a substantial correction of the impaired oxidative capacity of skeletal muscle in chronic heart failure can be achieved by exercise training.

Objective-To distinguish between the effects of reduced oxidative capacity and reduced metabolic efficiency on skeletal muscle bioenergetics during exercise in patients with congestive heart failure. Design and patients-Patients were studied by "P magnetic resonance spectroscopy during aerobic exercise and recovery, and results compared with controls. Results-In flexor digitorum superficialis muscle (26 patients) there was a 30% decrease in oxidative capacity compared with control (mean (SE) 36 (2) v 51 (4) mM/min) and also a 40% decrease in "effective muscle mass" (5 (1) v 9 (1) arbitrary units), probably at least partly the result of reduced metabolic efficiency. Both contribute to increased phosphocreatine depletion and intracellular acidosis during exercise. However, an increased concentration of ADP (an important mitochondrial regulator) during exercise permitted near-normal rates of oxidative ATP synthesis. Results were similar in gastrocnemius muscle (20 patients), with a 30% decrease in maximum oxidative capacity (29 (4) v 39 (3) mMlmin) and a 65% decrease in effective muscle mass (5 (1) v 13 (2) arbitrary units). Exercise training improved maximum oxidative capacity in both muscles, and in gastrocnemius effective muscle mass also. Conclusions-Skeletal muscle exercise abnormalities in patients with congestive heart failure result more from decreased metabolic efficiency than from the abnormalities in mitochondrial oxidation. Both decreased efficiency and defective mitochondrial oxidation result in an increased activation of glycogen phosphorylase, and may be improved by exercise training. (Heart 1996;76:35-41)

Chronic heart failure impairs the response of aortic rings to the endothelium dependent vasodilator acetylcholine in a rat model of heart failure. The response to sodium nitroprusside, an endothelium independent relaxing agent, is not impaired by heart failure. These findings may help to explain the raised systemic vascular resistance and the failure of vasodilatation in skeletal muscle vasculature which limits exercise capacity in subjects with heart failure.

No abstract

The introduction of fuzzy logic improves a system for the automatic quantification of renal artery lesions seen in digital subtraction angiograms. A two-step approach has been followed. An earlier system based on non-fuzzy syntactic analysis provided a clear symbolic description of the stenotic lesions. Although this system worked correctly, it did not take into account the variability and uncertainty inherent to image processing and to knowledge on the reference diameter. This system has been improved by the introduction of fuzzy logic in the representation of the reference diameter. It provides a description of the stenosis in terms of fuzzy quantities. To illustrate the benefits of the fuzzy approach, the results of the two systems have been compared by plotting the differences of an index of variability. It appears that the differences are statistically different when using a two-tailed paired t-test (t = 2.37; p = 0.025). The result shows that the fuzzy approach is better than a non-fuzzy approach in the sense that the index of variability is reduced significantly.