Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2881934 | The Annals of Thoracic Surgery | 2007 | 8 Pages |
Abstract
An equivalent increase in LV end-diastolic (ED) volume in both groups, coupled with unchanged ED and end-systolic remodeling strains as well as systolic circumferential, longitudinal, and radial strains, argue against a global LV or regional myocardial geometric basis for the cardiomyopathy associated with IMR. Further, similar systolic fiber shortening in both groups militates against an intracellular (cardiomyocyte) mechanism. The differences in subepicardial E12 and E13 shears, however, suggest a causal role of altered interfiber (cytoskeleton and extracellular-matrix) interactions.
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Authors
Tom C. MD, Allen MD, Frank MD, Filiberto MD, Robert A. MD, Akinobu MD, Daniel B. PhD, David MD, PhD, George T. MS, Neil B. PhD, D. Craig MD,