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(Circulation. 1995;92:2022-2023.)
© 1995 American Heart Association, Inc.

Articles

Meeting Highlights

David A. Clayton, PhD; R. Sanders Williams, MD; Isabella Y. Liang, PhD

From the National Heart, Lung, and Blood Institute, Bethesda, Md.

	Introduction

 
A workshop entitled "Mitochondrial DNA Mutations and Cardiomyopathy, Heart Failure, and Ischemic Heart Disease," chaired by Dr David A. Clayton and sponsored by the Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute, was convened on May 15 and 16, 1995, in Bethesda, Md.

There is now convincing evidence that proper functioning of human mitochondrial DNA (mtDNA) is critical to normal cellular metabolism and that mutations in mtDNA can result in severe disease phenotypes. It is also clear that cardiac dysfunction is one of the most important problems in human health and is a condition that presents not only in mature adults but in infants as well. Therefore it is appropriate and timely to address the role of mtDNA mutation in heart disease and then to focus on appropriate strategies to elucidate the physiological cause-and-effect relationship between alterations in this genome and pathological phenotypes. The purposes of this workshop were: to review the current state of knowledge about mtDNA mutations; to provide a forum for dialogue between investigators interested specifically in the heart with those whose work is mainly in other organs/tissues/cells; to allow the clinical investigators to become aware of current knowledge concerning mtDNA and the powerful techniques available to study mitochondrial function; and to make recommendations concerning the direction of future research on the mtDNA mutations to improve prevention, diagnosis, and treatment of heart failure and ischemic heart disease. The workshop, attended by about 50 people, was very well received.

	The Clinical Perspective

 
Evidence that mutations in mtDNA . . . [Full Text of this Article]

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