Border zone geometry increases wall stress after myocardial infarction: contrast echocardiographic assessment

Jackson, Benjamin M.; Gorman, Joseph H.; Salgo, Ivan S.; Moainie, Sina L.; Plappert, Theodore; John-Sutton, Martin St.; Edmunds, L. Henry; Gorman, Robert C.

doi:10.1152/ajpheart.00360.2002

Cited by 76 publications

(68 citation statements)

References 17 publications

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“…10,25,26 Reducing these stresses may in turn minimize stress-induced apoptosis and border zone extension and expansion, reducing further remodeling and preventing the progression into CHF. Although the average level of stress reduction is on the order of 20%, it is important to note that the resulting border zone fiber stress levels are equivalent to those calculated in the remote region.…”

Section: Discussionmentioning

confidence: 99%

Theoretical Impact of the Injection of Material Into the Myocardium

et al. 2006

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Background-To treat cardiac injuries created by myocardial infarcts, current approaches seek to add cells and/or synthetic extracellular matrices to the damaged ventricle to restore function. Because definitive myocardial regeneration remains undemonstrated, we propose that cardiac changes observed from implanted materials may result from altered mechanisms of the ventricle. Methods and Results-We exploited a validated finite element model of an ovine left ventricle with an anteroapical infarct to examine the short-term effect of injecting material to the left ventricular wall. The model's mesh and regional material properties were modified to simulate expected changes. Three sets of simulations were run: (1) single injection to the anterior border zone; (2) therapeutic multiple border zone injections; and (3) injection of material to the infarct region.Results indicate that additions to the border zone decrease end-systolic fiber stress proportionally to the fractional volume added, with stiffer materials improving this attenuation. As a potential therapy, small changes in wall volume (Ϸ4.5%) reduce elevated border zone fiber stresses from mean end-systole levels of 28.2 kPa (control) to 23.3 kPa (treatment), similar to levels of 22.5 kPA computed in remote regions. In the infarct, injection improves ejection fraction and the stroke volume/end-diastolic volume relationship but has no effect on the stroke volume/end-diastolic pressure relationship. Conclusions-Simulations indicate that the addition of noncontractile material to a damaged left ventricular wall has important effects on cardiac mechanics, with potentially beneficial reduction of elevated myofiber stresses, as well as confounding changes to clinical left ventricular metrics.

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Section: Discussionmentioning

confidence: 99%

Theoretical Impact of the Injection of Material Into the Myocardium

et al. 2006

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“…However, local activation of stretch activated signaling could explain the greater hypertrophy and fibrosis in the peri-infarct region. Tethering of the noncontractile infarct to adjacent viable myocardium amplifies wall stresses in the peri-infarct region, and biomechanical strain can trigger stretch activated signaling pathways in cardiomyocytes [29]. This might also account for the significantly greater increase of ANP protein in the peri-infarct region compared to the remote region.…”

Section: Discussionmentioning

confidence: 99%

Extracellular superoxide dismutase protects the heart against oxidative stress and hypertrophy after myocardial infarction

Deel

et al. 2008

Free Radical Biology and Medicine

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Extracellular SOD (EC-SOD) contributes only a small fraction to total SOD activity in the heart, but is strategically located to scavenge free radicals in the extracellular compartment. EC-SOD expression is decreased in myocardial infarction (MI)-induced failing heart, but whether EC-SOD can abrogate oxidative stress or modify MI-induced ventricular remodeling has not been previously studied. Subsequently, the effect of EC-SOD gene deficiency (EC-SOD KO) on left ventricular (LV) oxidative stress, hypertrophy, and fibrosis were studied in EC-SOD KO and wild type mice under control conditions, 4 weeks and 8 weeks after permanent coronary artery ligation. EC-SOD KO had no detectable effect on LV function in normal hearts, but caused small but significant increases of LV fibrosis. Eight weeks after MI, EC-SOD KO mice developed significantly more LV hypertrophy (LV mass increased 1.64-fold in KO mice as compared to 1.35-fold in wild type mice, p<0.01), and more fibrosis and myocyte hypertrophy which was more prominent in the peri-infarct region than in the remote myocardium. EC-SOD KO mice had greater increases of nitrotyrosine in the peri-infarct myocardium, and this was associated with a greater reduction of LV ejection fraction, a greater decrease of Sarcoplasmic or Endoplasmic Reticulum Calcium 2 ATPase (SERCA2a) and a greater increase of atrial natriuretic peptide (ANP) in the peri-infarct zone compared to wild type mice. EC-SOD KO was associated with more increases of phosphorylated p38 (p-p38 Thr180/Tyr182 ), p42/44 extracellular signal-regulated kinase (p-Erk Thr202/Tyr204 ) and c-Jun N-terminal kinase (p-JNK Thr183/Tyr185 ) under both control conditions or after MI, indicating that EC-SOD KO increases activation of mitogen-activated protein kinase (MAPK) signaling pathways. These findings demonstrated that EC-SOD plays an important role in protecting the heart against oxidative stress and infarction induced ventricular hypertrophy.

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“…Variation may reflect the degree of border zone coverage and stress reduction, 28 as well as biological variability in intrinsic myocardial susceptibility to remodeling and heart failure-for example, based on adrenergic responsiveness or response to mechanical stress.…”

Section: Mechanistic Implicationsmentioning

confidence: 99%

Persistent Reduction of Ischemic Mitral Regurgitation by Papillary Muscle Repositioning

et al. 2007

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Background-Recurrent ischemic mitral regurgitation (IMR) is frequent despite initial reduction by annuloplasty becausecontinued LV remodeling increases tethering to the infarcted papillary muscle (PM). We have previously shown that PM repositioning by an external patch device can acutely reduce IMR. In this study, we tested the hypothesis that IMR reduction persists despite possible continued LV remodeling. Methods and Results-In 7 sheep, we used a chronic ischemic posterior infarct model that produces LV dilatation and MR over 10 weeks. An epicardial patch device was adjusted under echo guidance to reduce MR, with follow-up over a further 8 weeks and evaluation by 3D echo and sonomicrometry. In all 7 sheep, moderate IMR resolved with acute patch application and PM repositioning (6.5Ϯ1.8 mm to 0.6Ϯ1.3 mm proximal jet width, PϽ0.001) without decrease in LVEF (43Ϯ3% to 44Ϯ8%). Eight weeks after PM repositioning, MR was not significantly greater (0.6Ϯ1.3 mm versus 1.0Ϯ1.0 mm, PϭNS) despite an increase in LV volumes in 3 animals (2 had increases of 50Ϯ15%). On average, LV volumes did not change significantly (ESV: 46Ϯ8 mL versus 49Ϯ15 mL; PϭNS and EDV: 85Ϯ16 mL versus 89Ϯ30 mL; PϭNS). LVEF was unchanged from acute to chronic patch (44Ϯ8% versus 43Ϯ8%). Contractility as end-systolic elastance did not decrease from the chronic MI to the acute and chronic patch stages, nor were there any significant changes in dP/dt, LV stiffness constant, or time constant of LV relaxation (Tau). Conclusion-PM

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Border zone geometry increases wall stress after myocardial infarction: contrast echocardiographic assessment

Cited by 76 publications

References 17 publications

Theoretical Impact of the Injection of Material Into the Myocardium

Theoretical Impact of the Injection of Material Into the Myocardium

Extracellular superoxide dismutase protects the heart against oxidative stress and hypertrophy after myocardial infarction

Persistent Reduction of Ischemic Mitral Regurgitation by Papillary Muscle Repositioning

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