Scar remodeling and transmural deformation after infarction in the pig.

Holmes, Jeffrey W.; Yamashita, Hirohisa; Waldman, Lewis K.; Covell, James W.

doi:10.1161/01.cir.90.1.411

Cited by 78 publications

(75 citation statements)

References 29 publications

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“…18,19 Indeed, transmission of cross-fiber shortening effects has been conclusively shown to occur between different layers of the myocardium in normal hearts. 20,21 In accordance with this mechanism, in nontransmurally infarcted regions, the inner infarcted layers might sustain deformation resulting from shortening in the outer noninfarcted layers. Similar interactions might also occur in the circumferential or longitudinal direction: Mechanical interaction or tethering has been shown to cause dysfunction in the noninfarcted rim of the infarct.…”

Section: Complex Relationship Between Local Function and Viability Inmentioning

confidence: 85%

Relation Between Gd-DTPA Contrast Enhancement and Regional Inotropic Response in the Periphery and Center of Myocardial Infarction

Gerber

Rochitte

Bluemke³

et al. 2001

Circulation

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Background-Gd-DTPA contrast-enhanced (CE) MRI identifies patterns of early hypoenhancement and delayed hyperenhancement in acute myocardial infarction, but their clinical significance for the prediction of myocardial viability remains controversial. Therefore, we closely examined the relationship between these CE patterns and regional inotropic response to low-dose dobutamine infusion at a regional level. Methods and Results-Thirteen dogs underwent CE and tagged MRI at rest and during 5 g · kg Ϫ1 · min Ϫ1 dobutamine 48 hours after MI. CE patterns and 3D regional strains were measured in 96 segments per animal. Segments were categorized as being normofunctional (nϭ828) if resting circumferential shortening was within the range of remote myocardium, or dysfunctional (nϭ420) if not. Inotropic response in resting dysfunctional segments was assessed according to CE patterns. Significant improvement of radial thickening (from ϩ12Ϯ1% [meanϮSEM] to ϩ22Ϯ2%, PϽ0.05) and circumferential shortening (from ϩ1Ϯ1% to Ϫ5Ϯ1%, PϽ0.05) strains occurred in dysfunctional myocardium with normal CE pattern but not in myocardium with early hypoenhancement. Delayed hyperenhanced myocardium displayed a more complex behavior. Circumferential stretching improved in the peripheral regions (from ϩ4Ϯ1% to Ϫ2Ϯ2%, PϽ0.05), where the infarct was nontransmural (38Ϯ3% transmurality), but not in centrally hyperenhanced regions (from ϩ4Ϯ1% to ϩ1Ϯ1% PϭNS), where the infarct was 66Ϯ3% transmural. Conclusions-Inotropic reserve was confined to dysfunctional myocardium with normal contrast enhancement but not to myocardium with early hypoenhancement. Inotropic response in delayed hyperenhanced myocardium is influenced by transmurality of necrosis. These observations support the use of CE MRI for the clinical detection of myocardial viability.

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Section: Complex Relationship Between Local Function and Viability Inmentioning

confidence: 85%

Relation Between Gd-DTPA Contrast Enhancement and Regional Inotropic Response in the Periphery and Center of Myocardial Infarction

Gerber

Rochitte

Bluemke³

et al. 2001

Circulation

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“…Permanent coronary ligation in swine tends to result in a well-demarcated, transmural scar, whereas the canine MI model in the present study is characterized by a relatively large volume of viable myocardium over the infarct zone. Holmes et al (18) studied systolic deformation of the infarct zone in a small region in the LV free wall by permanent occlusion of obtuse marginal branches of the left circumflex artery in swine. Despite impaired systolic shortening, they found significant systolic wall thickening (E rr ) still present at 3 wk, which is suggestive of passive deformation in the regions composed almost entirely of collagen (17).…”

Section: Discussionmentioning

confidence: 99%

Electromechanical analysis of infarct border zone in chronic myocardial infarction

Ashikaga

Mickelsen

Ennis

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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. Electromechanical analysis of infarct border zone in chronic myocardial infarction. Am J Physiol Heart Circ Physiol 289: H1099 -H1105, 2005. First published May 20, 2005; doi:10.1152/ajpheart.00423.2005.-To test the hypothesis that alterations in electrical activation sequence contribute to depressed systolic function in the infarct border zone, we examined the anatomic correlation of abnormal electromechanics and infarct geometry in the canine post-myocardial infarction (MI) heart, using a high-resolution MR-based cardiac electromechanical mapping technique. Three to eight weeks after an MI was created in six dogs, a 247-electrode epicardial sock was placed over the ventricular epicardium under thoracotomy. MI location and geometry were evaluated with delayed hyperenhancement MRI. Three-dimensional systolic strains in epicardial and endocardial layers were measured in five short-axis slices with motion-tracking MRI (displacement encoding with stimulated echoes). Epicardial electrical activation was determined from sock recordings immediately before and after the MR scans. The electrodes and MR images were spatially registered to create a total of 160 nodes per heart that contained mechanical, transmural infarct extent, and electrical data. The average depth of the infarct was 55% (SD 11), and the infarct covered 28% (SD 6) of the left ventricular mass. Significantly delayed activation (Ͼmean ϩ 2SD) was observed within the infarct zone. The strain map showed abnormal mechanics, including abnormal stretch and loss of the transmural gradient of radial, circumferential, and longitudinal strains, in the region extending far beyond the infarct zone. We conclude that the border zone is characterized by abnormal mechanics directly coupled with normal electrical depolarization. This indicates that impaired function in the border zone is not contributed by electrical factors but results from mechanical interaction between ischemic and normal myocardium. electromechanical mapping; magnetic resonance imaging DEPRESSED SYSTOLIC FUNCTION in the ischemic border zone with normal perfusion has been recognized for several decades (23). The presence of hypocontractile border zone myocardium has consistently been substantiated by a variety of modalities, including echocardiography (19, 28), radiopaque bead arrays (30, 36), and, most recently, MRI (8,15,16,26). The abnormal mechanics of the border zone is clinically important because it may negatively affect ventricular remodeling and hypertrophy (4,20).The mechanism underlying the depressed function in the border zone has been explained primarily by mechanical factors. Most investigators have concluded that it results from mechanical interactions, or tethering, between normal and ischemic myocardium (10,11,28,30,34,36). However, the abnormal mechanics in the border zone may also involve a contribution of abnormal electrical activation. For example, the timing of electrical activation in the border zone may be delayed by abnormal electrical sequence in the infarct zone and depres...

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“…However, the mechanisms which caused this early loss of myocardial ECM within the MI region followed by ECM synthesis and deposition remained elusive. In serial studies utilizing biochemical and computer-assisted morphometric techniques, several laboratories reported a loss of normal collagen strut formation, increased release of hydroxyproline (an amino acid primarily found in collagen), and reduced collagen cross-linking within the ischemic region very early post-MI (76,166,182,184,185,226,270,350,426,432,434,468,474,496,497,535,543). These early ECM events occurred prior to the egress of inflammatory cells into the MI region.…”

Section: B Myocardial Remodeling In Myocardial Infarctionmentioning

confidence: 99%

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Spinale¹

2007

Physiological Reviews

1,005

1,023

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It is now becoming apparent that dynamic changes occur within the interstitium that directly contribute to adverse myocardial remodeling following myocardial infarction (MI), with hypertensive heart disease and with intrinsic myocardial disease such as cardiomyopathy. Furthermore, a family of matrix proteases, the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs), has been recognized to play an important role in matrix remodeling in these cardiac disease states. The purpose of this review is fivefold: 1) to examine and redefine the myocardial matrix as a critical and dynamic entity with respect to the remodeling process encountered with MI, hypertension, or cardiomyopathic disease; 2) present the remarkable progress that has been made with respect to MMP/TIMP biology and how it relates to myocardial matrix remodeling; 3) to evaluate critical translational/clinical studies that have provided a cause-effect relationship between alterations in MMP/TIMP regulation and myocardial matrix remodeling; 4) to provide a critical review and analysis of current diagnostic, prognostic, and pharmacological approaches that utilized our basic understanding of MMP/TIMPs in the context of cardiac disease; and 5) most importantly, to dispel the historical belief that the myocardial matrix is a passive structure and supplant this belief that the regulation of matrix protease pathways such as the MMPs and TIMPs will likely yield a new avenue of diagnostic and therapeutic strategies for myocardial remodeling and the progression to heart failure.

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Scar remodeling and transmural deformation after infarction in the pig.

Abstract: We conclude that infarct expansion and scar shrinkage may be controlled by different factors. In addition, we conclude that measurement of systolic wall thickening alone is not always adequate to assess postinfarction regional contractile function.

Cited by 78 publications

References 29 publications

Relation Between Gd-DTPA Contrast Enhancement and Regional Inotropic Response in the Periphery and Center of Myocardial Infarction

Relation Between Gd-DTPA Contrast Enhancement and Regional Inotropic Response in the Periphery and Center of Myocardial Infarction

Electromechanical analysis of infarct border zone in chronic myocardial infarction

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

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