Expression of myosin heavy chain isoforms in skeletal muscle of patients with peripheral arterial occlusive disease

Abstract

Purpose: Peripheral arterial occlusive diseases (PAODs) not only compromise blood flow but lead to a series of subsequent metabolic and structural changes in the relevant muscles. Changes in myofibrillar proteins (eg, of myosin heavy chain [MHC] isoforms), one of the determinants of muscle structure as well as of muscular function, have not been reported in patients with PAOD and were therefore the aim of this study. Methods: Thirteen consecutive patients with PAOD were examined (clinical stage according to Fontaine II, three patients; III, three patients, and IV, seven patients) and compared with five age-matched control patients who had been in traffic accidents. A calf muscle sample (gastrocnemius muscle) in the ischemic region was taken for MHC isoform analysis by sodium dodecyl sulfate polyacrylamide gel electrophoresis and silver stain, and the relative content of MHC isoforms was measured. Results: Compared with the control patients, there was no significant change of MHC isoforms in patients with PAOD II. In patients with PAOD III, MHC IIb decreased significantly (P < .05) although MHC IIa remained unchanged; in patients with PAOD IV, both MHC IIa and IIb decreased significantly (P < .05). Accordingly, there was a progressive increase of the relative amount of MHC I with more critical ischemia in PAOD. Conclusion: In patients with PAOD, the content of MHC II decreased with a higher grade of ischemia. That seems to be consistent with an increased resistance to ischemia for myosin isoforms in the order of I more than in IIa more than IIb. Whether the decrease of MHC II in patients with PAOD is related to atrophy of muscle fibers or to muscle-fiber transition must be investigated further.