Left Ventricular Performance and Remodeling in Rabbits After Myocardial Infarction

Mahaffey, Kenneth W.; Raya, Thomas E.; Pennock, Gregory D.; Morkin, Eugene; Goldman, Steven

doi:10.1161/01.cir.91.3.794

Cited by 94 publications

(66 citation statements)

References 23 publications

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“…Given the anatomy of coronary arterial trees, the distal LCx ligation was a standard method to induce myocardial infraction at the apical portion of rabbit LV (Mahaffey et al. 1995). To mimic the sequelae of human cardiomyopathy, Schmitto et al.…”

Section: Discussionmentioning

confidence: 99%

“…Post‐MI rabbits through a distal LCx ligation showed the impaired LV function as well as the activation of neurohormonal and inflammatory systems (Mahaffey et al. 1995; Rungwerth et al. 2004), which presented high similarity to the large animal models of MI (Pfeffer and Braunwald 1990; Moainie et al.…”

Section: Discussionmentioning

confidence: 99%

“…1995). Four suture ligations were performed transmurally on four vessel segments of the LV including the left anterior descending (LAD) artery and three primary branches of the LCx arterial tree, which created multiple, patchy areas of myocardial infarction on the anterior and apical locations of the free wall, as shown in Figure 1.…”

Section: Methodsmentioning

confidence: 99%

“…1992; Muders and Elsner 2000), myocardial infarction induced by a distal ligation of left circumflex artery (LCx) in rabbits has become the gold standard in the study of ischemic HF (Mahaffey et al. 1995; White et al. 2000; Edwards et al.…”

Section: Introductionmentioning

confidence: 99%

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The Structure-function remodeling in rabbit hearts of myocardial infarction

Niu

et al. 2017

Physiol Rep

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Animal models are of importance to investigate basic mechanisms for ischemic heart failure (HF). The objective of the study was to create a rabbit model through multiple coronary artery ligations to investigate the postoperative structure‐function remodeling of the left ventricle (LV) and coronary arterial trees. Here, we hypothesize that the interplay of the degenerated coronary vasculature and increased ventricle wall stress relevant to cardiac fibrosis in vicinity of myocardial infarction (MI) precipitates the incidence and progression of ischemic HF. Echocardiographic measurements showed an approximately monotonic drop of fractional shortening and ejection fraction from 40% and 73% down to 28% and 58% as well as persistent enlargement of LV cavity and slight mitral regurgitation at postoperative 12 weeks. Micro‐CT and histological measurements showed that coronary vascular rarefaction and cardiac fibrosis relevant to inflammation occurred concurrently in vicinity of MI at postoperative 12 weeks albeit there was compensatory vascular growth at postoperative 6 weeks. These findings validate the proposed rabbit model and prove the hypothesis. The post‐MI rabbit model can serve as a reference to test various drugs for treatment of ischemic HF.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Structure-function remodeling in rabbit hearts of myocardial infarction

Niu

et al. 2017

Physiol Rep

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“…This agent has been shown to attenuate symptoms of heart failure after myocardial infarction through its positive inotropic effects (13,15,21). The favorable changes with DITPA treatment of rats or rabbits following coronary artery ligation and infarction include increased maximal positive and negative pressure development over time (dP/dt), increased basal time constant of isovolumic relaxation, and increased circumferential shortening and restoration of repolarizing transient outward K ϩ current (8,13,16,31). Unlike thyroxine, DITPA is not significantly chronotropic (13) and accordingly is a safer therapeutic agent.…”

mentioning

confidence: 99%

DITPA stimulates bFGF, VEGF, angiopoietin, and Tie-2 and facilitates coronary arteriolar growth

Wang

Zheng

Christensen

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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.-Previous studies from our laboratory and those of others have shown thyroxine to be a stimulator of coronary microvascular growth. The present study tested the hypothesis that 3,5-diiodothyropropionic acid (DITPA), a thyroid hormone analog with inotropic but not chronotopic characteristics, is angiogenic in the nonischemic heart. Daily injections (3.75 mg/kg sc) of DITPA to Sprague-Dawley rats affected protein increases in vascular endothelial growth factor (VEGF)164, VEGF188, basic fibroblast growth factor (bFGF) (FGF-2), angiopoietin-1, and Tie-2 during the first few days of treatment. After 3 wk of treatment, arteriolar length density and the relative number of terminal arterioles (Ͻ10 m diameter) increased in the left ventricle as determined by image analysis of perfuse-fixed hearts. These findings occurred in hearts that did not undergo changes in mass nor in increases in capillary length density. We conclude that DITPA, which is known to improve ventricular function after infarction, is angiogenic in normal nonischemic hearts. growth factors; angiogenesis; 3,5-diiodothyroproprionic acid; basic fibroblast growth factor; vascular endothelial growth factor CORONARY ANGIOGENESIS during prenatal and postnatal growth is a well-established phenomenon. However, in the nonischemic adult heart, angiogenesis may or may not occur when the heart enlarges. Although some significant vascular growth may occur in certain animal models of hypertension (reviewed in Ref. 28), in patients with long-term left ventricular (LV) hypertrophy due to aortic stenosis, coronary reserve is usually markedly depressed even in the absence of coronary artery disease (5). In contrast, when hypertrophy occurs in response to volume overload, capillary and arteriolar growth are usually proportional to the magnitude of hypertrophy, and maximal coronary perfusion is maintained (2, 28). These findings support the concept that the stimulus evoking the hypertrophy is a determinant of angiogenesis. Perhaps the best example supporting this concept is thyroid hormone-induced hypertrophy, which is associated with a rapid and marked capillary growth (1,3,7,14,(24)(25)(26)30). Moreover, we have documented a normal maximal myocardial perfusion in rat hearts in which hypertrophy was induced with thyroxine, a finding that indicates compensatory growth of resistance vessels as well (25).In a previous study, we showed that 3,5-diiodothyropropionic acid (DITPA), a thyroxine analog, stimulates modest, early growth of the capillary bed in the myocardium surviving infarction (29). This agent has been shown to attenuate symptoms of heart failure after myocardial infarction through its positive inotropic effects (13,15,21). The favorable changes with DITPA treatment of rats or rabbits following coronary artery ligation and infarction include increased maximal positive and negative pressure development over time (dP/dt), increased basal time constant of isovolumic relaxation, and increased circumferential shortening and restoration of repolarizing transient outward...

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Rapid Down-regulation of Thyroid Hormones in Acute Myocardial Infarction

Friberg¹,

Werner²,

Eggertsen³

et al. 2002

Arch Intern Med

134

105

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The thyroid hormone system is rapidly down-regulated in AMI. This may be beneficial during acute ischemia. Patients with angina had higher levels of interleukin 6 and C-reactive protein and more depressed thyroid hormone system in early samples. Thyroid level depression in patients with angina may possibly have been present before the infarction process started. This novel finding needs further evaluation in large studies to sort out cause-and-effect relationships.

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Left Ventricular Performance and Remodeling in Rabbits After Myocardial Infarction

Cited by 94 publications

References 23 publications

The Structure-function remodeling in rabbit hearts of myocardial infarction

The Structure-function remodeling in rabbit hearts of myocardial infarction

DITPA stimulates bFGF, VEGF, angiopoietin, and Tie-2 and facilitates coronary arteriolar growth

Rapid Down-regulation of Thyroid Hormones in Acute Myocardial Infarction

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