3D Evaluation of Myocardial Edema: Experimental Study on 22 Pigs Using Magnetic Resonance and Tissue Analysis*

Albers, Jan; Schroeder, A.; Simone, Roberto De; Möckel, Regina; Vahl, CF; Hagl, S.

doi:10.1055/s-2001-16100

Cited by 19 publications

(11 citation statements)

References 17 publications

(20 reference statements)

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“…The systolic dysfunction is a manifestation of global decreases in contractility, while the diastolic dysfunction represents the extension of ischemic contracture into the post-resuscitation period and is characterized by left ventricular wall thickening with reduction in the end-diastolic volume, as well as by impaired relaxation [53,69]. The ''no-reflow'' phenomenon and the ischemia/ reperfusion injury exaggerate the existing myocardial edema, which results in greater diffusion distances for oxygen, increased myocardial stiffness, and enhanced myocardial dysfunction [52,[70][71][72]. A 2.6% gain in myocardial water results in 43% decline in left ventricular performance and compliance [73], while a 3.5% gain results in 30-50% decline in cardiac output [74].…”

Section: Pathophysiological Disturbances and Hemodynamics During Cardmentioning

confidence: 99%

Pathophysiology and pathogenesis of post-resuscitation myocardial stunning

2011

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The prognosis for cardiac arrest victims remains dismal, as only 17% survives to hospital discharge. Post-resuscitation myocardial stunning is the mechanical dysfunction that persists after the restoration of spontaneous circulation. Our knowledge regarding myocardial stunning has grown dramatically over the years, and several hypotheses have been proposed in order to explain its pathophysiology; however, the interrelationships among various mechanisms remain unclear. This review deals primarily with the basic aspects of the pathophysiology of post-resuscitation myocardial stunning. Given the large number of relevant studies and the fragmented information, an effort was made to summarize current knowledge in order to present a comprehensive pathophysiological mechanism. In this review, the pathophysiological disturbances occurring from the onset of cardiac arrest until the restoration of spontaneous circulation are addressed. Then, the pathophysiology of myocardial stunning during the post-resuscitation period is critically reviewed in 4 parts, the immediate, the early, the intermediate, and the recovery post-arrest phase. This article covers a huge gap in the existing literature regarding the pathophysiology of post-resuscitation period and provides a better understanding of the pathophysiology and pathogenesis of post-resuscitation myocardial stunning.

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Section: Pathophysiological Disturbances and Hemodynamics During Cardmentioning

confidence: 99%

Pathophysiology and pathogenesis of post-resuscitation myocardial stunning

2011

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“…Previous studies have used MRI to assess myocardial edema (16). In this study, in vivo water content was evaluated using MRI performed serially on anesthetized rats 24 hours following MI using a 4.7-T MR scanner (Bruker, Billerica, Massachusetts, USA).…”

Section: Methodsmentioning

confidence: 99%

“…MRI has previously been utilized to assess myocardial viability (18) and edema (16). In this study, to detect the spatial distribution of edematous myocardium we used MRI to evaluate short axis maps of the parameter T2 of the left ventricle (LV) obtained 24 hours following permanent LAD coronary artery occlusion in adult male rats receiving PP1 (n = 2), SKI-606 (n = 5), or vehicle (n = 5).…”

Section: Functional Effects Of Src Inhibition Following MImentioning

confidence: 99%

Src blockade stabilizes a Flk/cadherin complex, reducing edema and tissue injury following myocardial infarction

Weis¹,

Shintani²,

Weber³

et al. 2004

J. Clin. Invest.

297

113

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Ischemia resulting from myocardial infarction (MI) promotes VEGF expression, leading to vascular permeability (VP) and edema, a process that we show here contributes to tissue injury throughout the ventricle. This permeability/edema can be assessed noninvasively by MRI and can be observed at the ultrastructural level as gaps between adjacent endothelial cells. Many of these gaps contain activated platelets adhering to exposed basement membrane, reducing vessel patency. Following MI, genetic or pharmacological blockade of Src preserves endothelial cell barrier function, suppressing VP and infarct volume, providing long-term improvement in cardiac function, fibrosis, and survival. To our surprise, an intravascular injection of VEGF into healthy animals, but not those deficient in Src, induced similar endothelial gaps, VP, platelet plugs, and some myocyte damage. Mechanistically, we show that quiescent blood vessels contain a complex involving Flk, VE-cadherin, and β β-catenin that is transiently disrupted by VEGF injection. Blockade of Src prevents disassociation of this complex with the same kinetics with which it prevents VEGF-mediated VP/edema. These findings define a molecular mechanism to account for the Src requirement in VEGF-mediated permeability and provide a basis for Src inhibition as a therapeutic option for patients with acute MI. Cheresh is on the Scientific Advisory Board of TargeGen but is not an employee, board member, or a recipient of research funding from the company. TargeGen is developing small molecule therapies for use in treating ischemic diseases; however, these molecules are independent from those described in the current manuscript. Citation for this article:

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“…The doses of microspheres were one-eighth, one-fourth, or one-half of the acutely lethal dose for the selected microsphere diameter (26). Additionally, in 10 randomly chosen animals (1 animal for each size and dose of microspheres ϩ 1 control), the EBCT cine mode was used, as described previously (31) (17 scans/s throughout several cardiac cycles), before and 20 min after embolization, to assess the diastolic thickness of the anterior wall and the total volume of the LAD perfusion territory as an index of myocardial edema following the coronary microembolization (1,14,28,36). To distinguish the endocardial border from the contrast-filled LV cavity, the scans were obtained during continuous infusion of iopamidol.…”

Section: Methodsmentioning

confidence: 99%

Relationship between surface area of nonperfused myocardium and extravascular extraction of contrast agent following coronary microembolization

Malyar

Lerman

Gössl

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Malyar NM, Lerman LO, Gössl M, Beighley PE, Ritman EL. Relationship between surface area of nonperfused myocardium and extravascular extraction of contrast agent following coronary microembolization. Am J Physiol Regul Integr Comp Physiol 301: R430-R437, 2011. First published May 4, 2011 doi:10.1152/ajpregu.00428.2010.-Myocardial microvascular permeability and coronary sinus concentration of muscle metabolites have been shown to increase after myocardial ischemia due to epicardial coronary artery occlusion and reperfusion. However, their association with coronary microembolization is not well defined. This study tested the hypothesis that acute coronary microembolization increases microvascular permeability in the porcine heart. The left anterior descending perfusion territories of 34 anesthetized pigs (32 Ϯ 3 kg) were embolized with equal volumes of microspheres of one of three diameters (10, 30, or 100 m) and at three different doses for each size. Electron beam computed tomography (EBCT) was used to assess in vivo, microvascular extraction of a nonionic contrast agent (an index of microvascular permeability) before and after microembolization with microspheres at baseline and during adenosine infusion. A high-resolution three-dimensional microcomputed tomography (micro-CT) scanner was subsequently used to obtain ex vivo, the volume and corresponding surface area of the embolized myocardial islands within the perfusion territories of the microembolized coronary artery. EBCT-derived microvascular extraction of contrast agent increased within minutes after coronary microembolization (P Ͻ 0.001 vs. baseline and vs. control values). The increase in coronary microvascular permeability was highly correlated to the micro-CT-derived total surface area of the nonperfused myocardium (r ϭ 0.83, P Ͻ 0.001). In conclusion, myocardial extravascular accumulation of contrast agent is markedly increased after coronary microembolization and its magnitude is in proportion to the surface area of the interface between the nonperfused and perfused territories. microspheres; EBCT; micro-CT; microvascular permeability A BALANCE BETWEEN DELIVERY of vital nutrients and removal of waste products from the myocardium is pivotal for maintaining the physiological contractile function of the myocytes and for the coordinated electrical conductance along the cells' membranes. However, it has been shown that myocardial microvascular permeability can change under various pathologic and metabolic circumstances such as diabetes mellitus (24, 41), hypercholesterolemia (32), hypertension (31), and acute myocardial ischemia followed by reperfusion (29). Embolization of microscopic plaque debris into the distal coronary bed during coronary interventions is a common and frequent event (9, 10, 35) that might be associated with microinfarctions and with adverse clinical outcome (7, 10).We have previously demonstrated that experimental coronary microembolization leads to a decrease in regional myocardial contractility that is proportional to the surface...

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3D Evaluation of Myocardial Edema: Experimental Study on 22 Pigs Using Magnetic Resonance and Tissue Analysis*

Abstract: We validated 3D assessment of induced ME in pig hearts using MRI. The method may therefore become an exact tool in monitoring cardioplegia.

Cited by 19 publications

References 17 publications

Pathophysiology and pathogenesis of post-resuscitation myocardial stunning

Pathophysiology and pathogenesis of post-resuscitation myocardial stunning

Src blockade stabilizes a Flk/cadherin complex, reducing edema and tissue injury following myocardial infarction

Relationship between surface area of nonperfused myocardium and extravascular extraction of contrast agent following coronary microembolization

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