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J Am Coll Cardiol, 2002; 40:1160-1167
© 2002 by the American College of Cardiology Foundation
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EXPERIMENTAL STUDY

Extension of borderzone myocardium in postinfarction dilated cardiomyopathy

Benjamin M. Jackson, MD*, Joseph H. Gorman, III, MD*, Sina L. Moainie, MD*, T. Sloane Guy, MD*, Navneet Narula, MD{dagger}, Jagat Narula, MD, DM, PhD, FACC§, Martin G. St. John-Sutton, FRCP, FACC{ddagger}, L. Henry Edmunds, Jr, MD* and Robert C. Gorman, MD*,*

* Harrison Department of Surgical Research, Philadelphia, Pennsylvania, USA
{dagger} Department of Pathology, Philadelphia, Pennsylvania, USA
{ddagger} Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
§ Center for Molecular Cardiology–MCP/Hahnemann University School of Medicine, Philadelphia, Pennsylvania, USA

Manuscript received May 7, 2001; revised manuscript received April 8, 2002, accepted June 12, 2002.

* Reprint requests and correspondence: Dr. Robert C. Gorman, Department of Surgery, 6 Silverstein, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA.
gormanr{at}uphs.upenn.edu

OBJECTIVES: This study tests the hypothesis that hypocontractile, borderzone myocardium adjacent to an expanding infarct becomes progressively larger and more hypocontractile as remodeling continues.

BACKGROUND: Early infarct expansion following anteroapical myocardial infarction (MI) is associated with progressive ventricular dilation and heart failure. The contribution of perfused, hypocontractile, borderzone myocardium to this process is unknown.

METHODS: Using a sheep model of anteroapical infarction, sonomicrometry array localization and serial microsphere injections were used to track changes in regional myocardial contractility, geometry, and perfusion. Eight sheep were studied before and after infarction and two, five, and eight weeks later. Thirty intertransducer chord lengths were analyzed to measure regional contractility and serial changes in regional geometry at end systole.

RESULTS: Beginning as a narrow band of fully perfused hypocontractile myocardium adjacent to the infarction, borderzone myocardium extends to involve additional contiguous myocardium that progressively loses contractile function as the heart remodels. Three distinct myocardial zones develop as a result of transmural MI: infarct, borderzone (perfused but hypocontractile), and remote (perfused and normally functioning).

CONCLUSIONS: This study demonstrates that hypocontractile, fully perfused borderzone myocardium extends to involve contiguous normal myocardium during postinfarction remodeling. This borderzone myocardium is a unique type of perfused, hypocontractile myocardium, which is distinct from hibernating or stunned myocardium. Preventing extension of borderzone myocardium by medical or surgical means offers the prospect of preventing late-onset heart failure following transmural expanding MIs.

Abbreviations and Acronyms
  ANOVA
  analysis of variance
  ECG
  electrocardiogram
  ED
  end diastole
  ES
  end systole
  %{Delta}ES
  percent change in end systolic chord length
  %{Delta}FS
  percent change in fractional shortening
  IV
  intravenous
  LV
  left ventricle
  LVP
  left ventricular pressure
  MDS
  multidimensional scaling
  MI
  myocardial infarction
  SAL
  sonomicrometry array localization
  SW
  stroke work




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