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Editorials

Insights into Myocardial Microstructure During Infarct Healing and Remodeling

Pathologists Need Not Apply

Christopher M. Kramer, MD

From the Departments of Medicine and Radiology, and the Cardiovascular Imaging Center, University of Virginia, Charlottesville.

Correspondence to Christopher M. Kramer, MD, University of Virginia Health System, Departments of Medicine and Radiology, Lee Street, Box 800170, Charlottesville, VA 22908. E-mail ckramer@virginia.edu

Key Words: magnetic resonance imaging • myocardial infarction • remodeling

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

Healing of acute myocardial infarction (MI) and subsequent increase in left ventricular (LV) cavity size or LV remodeling¹ is a complex process.² LV remodeling depends largely on infarct size³ and transmurality which in turn is determined by the status of the epicardial infarct artery⁴ and the microvasculature.⁵ Within a larger, near-transmural or transmural infarction, there is myocyte loss, in part because of apoptosis, and cellular slippage⁶ that leads to reduced tensile strength within the infarct zone and subsequent infarct expansion.⁷ Infarct expansion and wall thinning in the infarct zone then leads to regional cavity dilatation and increased wall stress throughout the LV. Elevated wall stress in turn activates the renin-angiotensin system and other autocrine-paracrine systems⁸ and cellular hypertrophy ensues.⁹ Cellular hypertrophy occurs primarily in noninfarcted regions adjacent to the infarcted segment and is eccentric due to the laying down of sarcomeres in series.^10,11 Eccentric cellular hypertrophy in noninfarcted regions together with fibrosis¹² contribute to mechanical dysfunction in adjacent noninfarcted regions that persists during remodeling.¹³ Remote noninfarcted regions are initially mildly dysfunctional in the first few days after large MI,¹⁴ but these recover over the next several weeks as global LV function improves.¹⁵ The sum total of these events is a deleterious increase in end-diastolic and -systolic cavity sizes. It is the latter that is the most important determinant of outcome after acute MI.¹⁶

Article see p 32

Until very recently, studies of the structural events that occur during LV remodeling have required painstaking histopathology and have been performed primarily in . . . [Full Text of this Article]

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