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(Circulation. 2008;117:2570-2572.)
© 2008 American Heart Association, Inc.

Editorial

Quest for Diastolic Prognostic Indicators of Clinical Outcome After Acute Myocardial Infarction

Martin St John Sutton, MD, FRCP

From the University of Pennsylvania Medical Centre, Philadelphia.

Correspondence to Martin St. John Sutton, John Bryfogle Professor of Cardiac Imaging, University of Pennsylvania Medical Centre, 3400 Spruce St, Philadelphia, PA 19104. E-mail suttonm@mail.med.upenn.edu

Key Words: Editorials • myocardial infarction • outcomes research

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Immediately after acute infarction, the region of the myocardium ceases to contract, and over the next 72 hours, the infarct zone stretches and thins, a process known as infarct expansion. This regional left ventricular wall thinning and failure to contract perturb the normally uniform distribution of the stress/strain relationship that preserves cardiac architecture and function. Simultaneous with these early biomechanical changes, myocyte necrosis releases a number of cytokines that, together with the local increase in the regional myocardial deformation, cause stretch activation of a portfolio of matrix metalloproteinases that initiate myocardial repair.

Article p 2591

The stability of myocardial repair after acute myocardial infarction is determined by the balance between the distending forces from ventricular dilatation resulting from infarct expansion and the restraining forces from deposition of a viscoelastic collagen scaffold by the extracellular matrix that increases the tensile strength of the scar. The dynamic equilibrium between collagen degradation and collagen deposition is modulated by a number of activated cytokines and neurohormones that normally result in buttressing the infarct and adjacent border zones, preventing progressive remodeling to heart failure.

Changes in the composition of the myocardium in terms of increased collagen content during and after repair of the infarct zone in forming a fibrous tissue scar alter the material properties of the myocardium after myocardial infarction and confer on the heart increased myocardial and chamber stiffness. These alterations in left ventricular composition, architecture, and chamber/myocardial stiffness affect left ventricular filling dynamics, the rate of detachment of cross-linking, and sequestration of . . . [Full Text of this Article]