Selective microembolization of the circumflex coronary artery in an ovine model: dilated, ischemic cardiomyopathy and left ventricular dysfunction

Monreal, Gretel; Gerhardt, Mark A.; Kambara, Atsushi; Abrishamchian, A. Reza; Bauer, John; Goldstein, Andrew H.

doi:10.1016/j.cardfail.2003.08.013

Cited by 26 publications

(20 citation statements)

References 33 publications

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“…Mechanical dysfunction (dyskinesia) of the posterior LV may torque normal septal contraction and/or indirectly augment global wall stress to impart additional stress on remaining viable myocytes. This is a plausible explanation, since we observed regional wall motion abnormalities in our model (Monreal et al, 2004). Although there are conflicting data on the contributions of myocyte hypertrophy to contractile dysfunction in HF (Di Somma et al, 2000;Harding and Del Monte, 2002;Narayan et al, 1989), it seems more likely that desmin accumulation may be a mechanism for hypertrophy rather than vice versa since hypertrophy occurred after desmin upregulation in our model.…”

Section: Extracellular Fibrosis and Myocyte Hypertrophymentioning

confidence: 65%

“…In order to better define molecular remodeling, LV EF, LVESA, and LVEDA were obtained via transthoracic echocardiography at baseline (pre-microembolization), month-4, and -12 HF as described previously (Monreal et al, 2004) (Fig. 1A).…”

Section: Resultsmentioning

confidence: 99%

“…Our laboratory has developed a pathology-driven ovine model of HF resulting from small-vessel infarction via coronary microembolization, which recapitulates HF observed in humans (Monreal et al, 2004). Using a proteomics approach, we identified desmin as a specific protein that is strikingly upregulated in HF myocardium from our model.…”

Section: Introductionmentioning

confidence: 81%

“…We developed an ovine model of small-vessel model HF (Monreal et al, 2004;Goldstein et al, 2005). Sheep underwent selective microembolization of the circumflex coronary artery (LCx) to induce HF.…”

Section: Methodsmentioning

confidence: 99%

“…We previously reported gross anatomical hypertrophy of the LV anterior and anterior septal cardiac walls in HF sheep (Monreal et al, 2004). To investigate hypertrophy at the cellular level, we used IHC digital image analysis to quantify the myocyte cellular/nuclear area ratio as an index of hypertrophy (Hein et al, 2002).…”

Section: Myocyte Hypertrophymentioning

confidence: 99%

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Cytoskeletal remodeling of desmin is a more accurate measure of cardiac dysfunction than fibrosis or myocyte hypertrophy

et al. 2008

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Section: Extracellular Fibrosis and Myocyte Hypertrophymentioning

confidence: 65%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 81%

Section: Methodsmentioning

confidence: 99%

Section: Myocyte Hypertrophymentioning

confidence: 99%

See 3 more Smart Citations

Cytoskeletal remodeling of desmin is a more accurate measure of cardiac dysfunction than fibrosis or myocyte hypertrophy

et al. 2008

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Magnetic resonance imaging quantification of left ventricular dysfunction following coronary microembolization

Carlsson¹,

Martin²,

Ursell³

et al. 2008

Magnetic Resonance in Med

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Microembolization is common after coronary interventions, and therefore this MRI study aimed to quantify the effect of coronary microembolization on left ventricular (LV) function. The left anterior descending artery (LAD) was selectively catheterized in an XMR suite (Philips Medical Systems, Best, The Netherlands) in eight pigs to deliver MR contrast media to measure the LAD territory using first-pass perfusion and for intracoronary delivery of the embolic agent. Cine, tagged, and delayed contrastenhanced MRI (DCE-MRI) was performed to assess LV volumes, ejection fraction, radial and circumferential strain, and viability at baseline, 1 h, and 1 week after microembolization. Histopathology and histochemical staining were used to characterize and measure the extent of microinfarction. The LAD territory was 35% ؎ 2% LV mass. Patchy microinfarction on DCE-MRI at 1 week was 22.0% ؎ 3.6% LAD territory (7.5% LV mass). Microembolization caused persistent decline in ejection fraction (baseline ‫؍‬ 49% ؎ 1%, 1 h ‫؍‬ 29% ؎ 1%, P ‫؍‬ 0.02 and 1 week ‫؍‬ 36% ؎ 1%, P ‫؍‬ 0.03) and increased end-diastolic (79.6 ؎ 3.9 ml, 85.5 ؎ 4.5 ml, P ‫؍‬ 0.03 and 92.4 ؎ 6.2 ml, P ‫؍‬ 0.06, respectively) and end-systolic (40.8 ؎ 2.1 ml, 60.2 ؎ 3.4 ml, P ‫؍‬ 0.02 and 59.3 ؎ 4.8 ml, P ‫؍‬ 0.03, respectively) volumes. The microembolized territory was manifested as dysfunctional regions for 1 week on cine and tagged MRI. Histopathology revealed occlusive microemboli surrounded by necrotic tissue undergoing repair. Microinfarction was visualized after coronary microembolization and caused LV dysfunction disproportionate to the size of myocardial damage. It also changed LV geometry and decreased radial and circumferential strain over the course of 1 week. Magn Reson Med 61:595-602, 2009.

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Iatrogenic, Transgenic, and Naturally Occurring Models of Cardiomyopathy and Heart Failure

Gross

2009

Animal Models in Cardiovascular Research

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Selective microembolization of the circumflex coronary artery in an ovine model: dilated, ischemic cardiomyopathy and left ventricular dysfunction

Cited by 26 publications

References 33 publications

Cytoskeletal remodeling of desmin is a more accurate measure of cardiac dysfunction than fibrosis or myocyte hypertrophy

Cytoskeletal remodeling of desmin is a more accurate measure of cardiac dysfunction than fibrosis or myocyte hypertrophy

Magnetic resonance imaging quantification of left ventricular dysfunction following coronary microembolization

Iatrogenic, Transgenic, and Naturally Occurring Models of Cardiomyopathy and Heart Failure

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