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 ,
Jagat Narula, MD, DM, PhD, FACC ,
Martin G. St. John-Sutton, FRCP, FACC ,
L. Henry Edmunds, Jr, MD* and
Robert C. Gorman, MD*,*
* Harrison Department of Surgical Research, Philadelphia, Pennsylvania, USA
Department of Pathology, Philadelphia, Pennsylvania, USA
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
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Figure 1 Regional myocardial blood flow (ml/g/min) at baseline and at two, five, and eight weeks’ postinfarction, as determined by serial microsphere injections.
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Figure 2 Regional changes in fractional shortening during the cardiac cycle for three different myocardial segments (1 = infarct, 2 = borderzone, 3 = remote) before and at each time point after infarction. Note progressive expansion of all segments during remodeling and the progressive loss of contractility in segment 2 (borderzone) as remodeling progresses. AO = aorta; LAD = left anterior descending.
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Figure 3 Graphs depicting the relationship between the geometrical change (expansion) and functional change (contractile function) for each of 30 intertransducer segments in the left ventricular myocardium. Red symbols represent segments located within the anatomical infarction; green symbols represent segments located outside the infarction in normally perfused myocardium. No graph is shown for the preinfarction time point because changes (from baseline) in chord length and contractile function are plotted; before infarction all chords lie at the origin. The horizontal line y = 0 represents a segment of myocardium that has exactly the same fractional shortening as it had at the baseline study; segments that fall between that line and y = –100% are hypocontractile relative to baseline; segments falling below y = –100% demonstrate systolic dyskinesis. In the corresponding left ventricular diagrams, dashed lines indicate segments that fall below the line y = 0. Therefore, dashed green lines represent hypocontractile but perfused myocardium (borderzone myocardium) and dashed red lines represent infarcted myocardium. Note the progressive numerical increase and location of the hypocontractile, dashed segments. The data presented represent a composite constructed from averages of all eight animals. ES = end systole.
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Figure 4 At postinfarction and eight weeks, chord lengths were clustered by z-score using a k-clustering algorithm (with respect to percent change in contractility and percent change in chord length, perfusion status was not considered in the analysis). The plot above is similar to Figure 3, depicting each cluster using a different color. In this figure, each chord in the ventricular array is depicted using the color corresponding to the cluster to which it belongs. Dashed lines in the lower portion of the figure denote cord lengths with reduced contractility below baseline. Solid lines denote chord lengths with contractility at or above the baseline value. Note that the blue cluster includes all of the borderzone myocardium defined in Figure 3 as well as several infarcted segments. (The significance of this finding is presented in detail in the Discussion section.) The data presented represent a composite constructed from averages of all eight animals. ES = end systole.
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Figure 5 Percent expansion for myocardial chords within each cluster plotted over time. Clusters are identified by color as in Figure 4. Note that the rate of expansion is similar in all three myocardial regions after the immediate postinfarction period.
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Figure 6 A low magnification panoramic histologic view of the ovine model of anteroapical infarction (A, trichrome, 1x) is magnified to individually represent myocardial infarction region (B, trichrome, 20x), borderzone (C, trichrome, 20x), and remote myocardium (D, trichrome, 20x). The region of fibrosis stains blue and the viable myocytes stain red. The region of healed infarct (B) shows fibrosis; the borderzone (C) shows patchy interstitial and replacement fibrosis with myofibrillarlysis. The remote (D) area shows focal interstitial fibrosis.
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