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Failure of critical protein connection at heart of cardiomyopathy

f years, it weakens the connection to the cell membrane. You literally beat your heart to death, he said.

The harder and faster the heart beats, the more likely it is to destroy the infrastructure of the myocardium (heart muscle), said Towbin. You put the heart to rest and it reconnects the end of the dystrophin molecule to the membrane.

In the studies with patients on the ventricular assist device, the Baylor team found that after four to six weeks on the pump, 90 percent of them saw a reduction in the number of cells with the defective dystrophin-membrane connection.

A second possible cause of the problem is that a chemical produced by the process of heart failure might target that portion of the dystrophin attached to the contractile apparatus and cell membrane, literally severing it at that critical link, suggested Bowles and Towbin.

Whatever the reason for the dystrophin problem, the finding has important implications for the development of new therapies for cardiomyopathy. The possibility that heart function can be restored in some patients raises the question as to whether some patients would be able to avoid transplantation, they said. Implanting a total artificial heart requires removal of the persons own heart, eliminating the possibility that it could be restored to near normal function by rest with the support of the pump.

However, Towbin and Bowles wonder if their finding indicates that the dilated cardiomyopathy will recur. If you take patients out of the heart failure state now, will they develop dilated cardiomyopathy again in the future? said Towbin.


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Contact: Lori Williams/Ron Gilmore
rgilmore@bcm.tmc.edu
713-798-4712
Baylor College of Medicine
14-Mar-2002


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