Effect of gadolinium-DTPA on the magnetic relaxation times of normal and infarcted myocardium.

Wesbey, George E.; Higgins, Charles B.; McNamara, Michael T.; Engelstad, Barry L.; Lipton, Martin J.; Sievers, Richard E.; Ehman, Richard L.; Lovin, Jeffrey; Brasch, Robert C.

doi:10.1148/radiology.153.1.6473778

Cited by 172 publications

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“…[14][15][16][17][18] In this study, the inhibitory effect of the β-blocker carvedilol on myocardial fibrosis in a hamster model of progressive dilated cardiomyopathy (TO2: Bio 53.58 hamster) was assessed by comparing the changes in LVDd and EF on echocardiography as well as MRI parameters (left ventricular myocardial volume, the enhanced area, and the relationship between the enhanced area and fibrosis on histopathological examination).…”

Section: Discussionmentioning

confidence: 99%

<b>Carvedilol Prevents Myocardial Fibrosis in Hamsters</b>

et al. 2006

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SUMMARYThe objective of the present study was to determine if carvedilol protects against myocardial degeneration and fibrotic change, and reduces mortality in TO2 hamsters.Carvedilol was administered intraperitoneally to 8 week-old TO2 hamsters for 21 weeks at a dose of 11 mg/kg/day. There were 15 TO2 hamsters in the carvedilol group (group C) and 10 in the untreated group (group N). The control group consisted of 11 Fb hamsters (group F). The mortality rate was determined from the number of surviving hamsters after 29 weeks. Myocardial fibrosis was evaluated by MRI and histopathological examination. EF and LVDd were determined by echocardiography at 8 and 29 weeks, while the MRI score was calculated at 29 weeks.Mortality, histopathological fibrosis, and MRI score were all lower in group C than in group N. Carvedilol had a protective effect against myocardial fibrosis and decreased the mortality rate in TO2 hamsters. ( 2-4) Following this, β-blocker therapy became used for the treatment of chronic heart failure.We previously performed MRI studies in a hamster model of cardiomyopathy (Bio 14.6 hamster) and found abnormal sites of enhancement as well as delayed enhancement. We proposed that the enhanced areas were regions of myocardial degeneration and fibrosis. 5) Carvedilol is a β-blocker that also has α-blocking and antioxidant effects, which have been shown to reduce the mortality rate of patients with moderate to severe chronic cardiac failure by 35% to 65%, in addition to also lowering the rehospitalization rate. 3,4) In the present study, we assessed the effects of carvedilol [6][7][8] in another hamster model of dilated cardiomyopathy, the BioFrom the

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Section: Discussionmentioning

confidence: 99%

<b>Carvedilol Prevents Myocardial Fibrosis in Hamsters</b>

et al. 2006

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“…Wesbey et al 21 showed increased T 1 shortening in transiently ischemic canine myocardium compared with normal tissue. In a canine model, after varying length of coronary occlusion and reperfusion, the size and three-dimensional shape of hyperenhancement correlated closely with irreversible damage defined by triphenyltetrazolium chloride staining.…”

Section: Hyperenhancement and Myocardial Viabilitymentioning

confidence: 94%

Assessment of Myocardial Viability With Contrast-Enhanced Magnetic Resonance Imaging

et al. 2002

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Background-Recent studies indicate that MRI, after administration of gadolinium-diethylenetriamine pentaacetic acid, can identify nonviable areas in dysfunctional myocardium. We compared MRI hyperenhancement with PET as a gold standard for detection and quantification of myocardial scar tissue. Methods and Results-Thirty-one patients with ischemic heart failure (ejection fraction, 28Ϯ9%) were imaged with PET and MRI. Scar was defined as regionally increased MRI signal intensity 20 minutes after injection of 0.2 mmol/kg gadolinium-diethylenetriamine pentaacetic acid and as concordantly reduced perfusion and glucose metabolism as defined by PET. Sensitivity and specificity of MRI in identifying patients and segments (nϭ1023)

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“…Recently, the time course and geometry of these alterations have been described (59) by late contrast-enhanced MRI, an imaging technique using injected gadolinium-diethylenetriamine pentaacetic acid (an extracellular contrast agent), which results in late high-resolution images in which myocardial damage appears hyperenhanced (Fig. 1c) (165,167). In this study, consistent ventricular dilation, together with changes in LV shape leading to an increased curvature radius, was shown in dogs subjected to coronary occlusion.…”

Section: Myocardial Wall Stressmentioning

confidence: 99%

Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning

Mazzadi

André‐Fouët²,

Costes³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Croisille, Didier Revel, and Marc F. Janier. Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning. Am J Physiol Heart Circ Physiol 291: H2570 -H2582, 2006. First published July 21, 2006 doi:10.1152/ajpheart.01249.2005.-Patients with severe chronic coronary artery disease (CAD) exhibit a highly altered myocardial pattern of perfusion, metabolism, and mechanical performance. In this context, the diagnosis of stunning remains elusive not only because of methodological and logistic considerations, but also because of the pathophysiological characteristics of the myocardium of these patients. In addition, a number of alternative pathophysiological mechanisms may act by mimicking the functional manifestations usually attributed to stunning. The present review describes three mechanisms that could theoretically lead to reversible mechanical dysfunction in these patients: myocardial wall stress, the tethering effect, and myocardial expression and release of auto-and paracrine agents. Attention is focused on the role of these mechanisms in scintigraphically "normal" regions (i.e., regions usually showing normal perfusion, glucose metabolism, and cellular integrity as assessed by nuclear imaging techniques), in which stunning is usually considered, but these mechanisms could also operate throughout the viable myocardium. We hypothesize that reversion of these three mechanisms could partially explain the unexpected functional benefit after reperfusion recently highlighted by high-spatial-resolution imaging techniques. stunned myocardium; hibernating myocardium; inotropic reserve; cardiac imaging; myocardial wall stress; ventricular remodeling SUMMARY OF CLINICAL PROBLEMIN RECENT YEARS, WIDESPREAD utilization of noninvasive cardiac imaging methods has greatly improved the synergy between clinical and basic investigation of cardiac ischemic pathophysiology. Thus imaging methods have shown that the reversible left ventricular (LV) dysfunction arising from brief coronary occlusion and reflow (myocardial stunning), first described in animal models (80), occurs in humans. Two major hypotheses explain this phenomenon: 1) the oxyradical hypothesis, which proposes that oxidant stress impairs LV function (18), and 2) the calcium hypothesis, which postulates that stunning results from disturbed myocyte calcium homeostasis (98). On the other hand, the hibernating myocardium (136, 137) was first discovered by imaging methods in humans, and it was originally defined as "resting LV dysfunction due to reduced coronary blood flow that can be partially or completely reversed by myocardial revascularization and/or by reducing myocardial oxygen demand" (136). The concept was refined when ultrastructural investigations showed a distinctive morphology for hibernating myocardium, generally without necrosis, but with loss of sarcomeres and myofibrils (suggesting a "dedifferentiation" process toward an embryonic phenotype), with loss of mitochondria and increased glycogen storage (9,19,27,162)...

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Effect of gadolinium-DTPA on the magnetic relaxation times of normal and infarcted myocardium.

Cited by 172 publications

References 0 publications

<b>Carvedilol Prevents Myocardial Fibrosis in Hamsters</b>

<b>Carvedilol Prevents Myocardial Fibrosis in Hamsters</b>

Assessment of Myocardial Viability With Contrast-Enhanced Magnetic Resonance Imaging

Mechanisms leading to reversible mechanical dysfunction in severe CAD: alternatives to myocardial stunning

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