| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10953984 | Journal of Molecular and Cellular Cardiology | 2010 | 9 Pages |
Abstract
⺠The passive stiffness of skinned HCM cardiac myocytes was similar to that of normal (donor) myocytes. ⺠Maximum Ca-activated force production was reduced by 40% in HCM vs donor myocytes. ⺠This loss of force could contribute to systolic dysfunction in HCM hearts. ⺠Myofibrillar Ca sensitivity was higher in HCM than in donor myocytes. ⺠The enhanced Ca sensitivity could compensate for the smaller maximum force but would tend to cause diastolic dysfunction. ⺠These characteristics were common to all HCM patients studied, suggesting the changes were secondary consequence of the underlying genetic variants.
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Authors
Anita C. Hoskins, Adam Jacques, Sonya C. Bardswell, William J. McKenna, Victor Tsang, Cristobal G. dos Remedios, Elisabeth Ehler, Kim Adams, Shapour Jalilzadeh, Metin Avkiran, Hugh Watkins, Charles Redwood, Steven B. Marston, Jonathan C. Kentish,