Myocardial edema in paroxysmal permeability disorders: The paradigm of Clarkson's disease

Cardioplegic arrest (CPA) is associated with interstitial myocardial edema, which has been shown to impair myocardial function. The accumulation of interstitial myocardial edema may be enhanced by impaired myocardial lymph flow. The purpose of this study was to investigate the effects of CPA on myocardial lymphatic function. In nine anesthetized dogs, we cannulated a prenodal cardiac lymphatic and measured myocardial lymph flow rate (QL), myocardial lymph driving pressure (PL), and myocardial lymph hyaluronan (Hya) concentration. We determined left ventricular function using pressure-volume curves derived by sonomicrometry and micromanometry. The dogs were placed on cardiopulmonary bypass (CPB) (28 degrees C) and subjected to 60 min of hypothermic, crystalloid CPA. With the onset of asystole both QL and PL decreased significantly from 70.7 +/- 31.8 (SD) to 3.3 +/- 4.0 microliters/min and from 19.9 +/- 8.0 to 10.4 +/- 1.8 mmHg, respectively (P < 0.01). Following return of sinus rhythm after separation from CPB, QL and PL increased significantly to 135.4 +/- 28.0 microliters/min and 27.3 +/- 7.5 mmHg, respectively (P < 0.01). Post-CPA myocardial edema was demonstrated by gravimetric wet-to-dry weight determination of 3.67 +/- 0.20 (normal 2.90 +/- 0.20, P < 0.001) and was associated with significantly decreased left ventricular function. Myocardial Hya turnover rate was 1.3 +/- 1.0% per day under baseline conditions and increased significantly to 2.7 +/- 0.9% per day post-CPA (P < 0.01). We conclude that organized myocardial contraction is the major determinant of myocardial lymph flow. Myocardial lymph flow impairment during CPA may contribute to post-CPA myocardial edema and left ventricular dysfunction.

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Basic determinants of epicardial transudation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.273.3.h1408 ◽

1997 ◽

Vol 273 (3) ◽

pp. H1408-H1414 ◽

Cited By ~ 8

Author(s):

R. H. Stewart ◽

D. A. Rohn ◽

S. J. Allen ◽

G. A. Laine

Keyword(s):

Reflection Coefficient ◽

Coronary Sinus ◽

Myocardial Edema ◽

Hydraulic Conductance ◽

Linear Increase ◽

Left Ventricular ◽

Edema Formation ◽

Anesthetized Dogs ◽

The Difference ◽

Osmotic Reflection Coefficient

Myocardial edema formation, which has been shown to compromise cardiac function, and increased epicardial transudation (pericardial effusion) have been shown to occur after elevation of myocardial venous and lymphatic outflow pressures. The purposes of this study were to estimate the hydraulic conductance and osmotic reflection coefficient for the epicardium and to determine the effect of coronary sinus hypertension and cardiac lymphatic obstruction on epicardial fluid flux (JV,e/Ae). A Plexiglas hemispheric capsule was attached to the left ventricular epicardial surface of anesthetized dogs. JV,e/Ae was determined over 30-min periods for three intracapsular pressures (-5, -15, and -25 mmHg) and two intracapsular solutions exerting colloid osmotic pressures of 7.0 and 2.0 mmHg. Hydraulic conductance was estimated to be 3.7 +/- 0.5 microliters.h-1.cm-2.mmHg-1. An osmotic reflection coefficient of 0.9 was calculated from the difference in JV,e/Ae of 16.5 +/- 8.4 microliters.h-1.cm-2 between the two solutions. Graded coronary sinus hypertension induced a linear increase in JV,e/Ae, which was significantly greater in dogs without cardiac lymphatic occlusion than in those with occlusion.

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Direct T2 Quantification of Myocardial Edema in Acute Ischemic Injury

JACC Cardiovascular Imaging ◽

10.1016/j.jcmg.2010.09.023 ◽

2011 ◽

Vol 4 (3) ◽

pp. 269-278 ◽

Cited By ~ 239

Author(s):

David Verhaert ◽

Paaladinesh Thavendiranathan ◽

Shivraman Giri ◽

Georgeta Mihai ◽

Sanjay Rajagopalan ◽

...

Keyword(s):

Ischemic Injury ◽

Myocardial Edema

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Abstract 10378: Characterization of Changes in Cardiac Structure and Function in Mice Treated With Anthracyclines Using Serial Cardiac Magnetic Resonance Imaging

Circulation ◽

10.1161/circ.132.suppl_3.10378 ◽

2015 ◽

Vol 132 (suppl_3) ◽

Author(s):

Pedro V Staziaki ◽

Hoshang Farhad ◽

Otávio Coelho-Filho ◽

Ravi V Shah ◽

Richard N Mitchell ◽

...

Keyword(s):

Cardiac Magnetic Resonance ◽

Magnetic Resonance ◽

Myocardial Fibrosis ◽

Myocardial Edema ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Post Contrast ◽

Cardiac Edema ◽

Early Increase ◽

Acute Increase

Introduction: Anthracyclines are a standard chemotherapeutic agent. However, the anthracyclines are associated with a late reduction in left ventricular ejection fraction (LVEF) and heart failure. Pathologically, anthracycline-induced cardiotoxicity (AIC) is characterized by the development of cardiac edema and fibrosis and cardiac magnetic resonance (CMR) is the gold-standard imaging technique for edema and fibrosis. Hypothesis: We hypothesized that a) cardiac edema and fibrosis would be detected by CMR after anthracyclines and b) edema and fibrosis would provide prognostic information. Methods: We performed a longitudinal CMR and histological study of 45 wild-type mice randomized to doxorubicin (DOX, n=30, 5 mg/kg/week for 5 weeks) or placebo (n=15). Measurements were performed at baseline, 5, 10, and 20 weeks after DOX or placebo. Measures of interest were LVEF, myocardial edema and fibrosis. Edema was assessed by T2 mapping, fibrosis by calculating the extracellular volume (ECV) from pre- and post-contrast T1 measurements. Results: In DOX-treated mice vs. placebo, myocardial edema at 5 weeks was increased (T2 values of 32±4 vs. 21±3 ms, P<0.05, Fig. A), while LVEF was unchanged. At 10 weeks, there was a reduction in LVEF (54±6 vs. 63±5% μL, P<0.05) and an increase in myocardial fibrosis (ECV of 0.34±0.03 vs. 0.27±0.03, P<0.05, Fig. B). There was a correlation between T2 measures and cardiac water weight (r=0.79, P=0.007, Fig. C) and between the ECV and histological myocardial fibrosis (r=0.90, P<0.001; Fig. D). Both the early increase in edema and the sub-acute increase in fibrosis predicted the late DOX-induced mortality (P<0.001, Fig. E and F). Conclusions: Our data suggest that, in mice, CMR can detect the early increase in edema and sub-acute increase in fibrosis after anthracyclines, that an increase in edema precedes a reduction in LVEF, that the increase in edema and fibrosis are linked and both are predictive of late animal mortality.

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Myocardial Edema without Fibrosis by Magnetic Resonance T2 Mapping in Acute Chagas' Myocarditis

Arquivos Brasileiros de Cardiologia ◽

10.5935/abc.20170113 ◽

2017 ◽

Author(s):

Andréa Silvestre de Sousa ◽

Maria Eduarda Derenne ◽

Alejandro Marcel Hasslocher-Moreno ◽

Sérgio Salles Xavier ◽

Ilan Gottlieb

Keyword(s):

Magnetic Resonance ◽

T2 Mapping ◽

Myocardial Edema

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Isoproterenol-induced Creatine Kinase Leakage in Langendorff-perfused Rat Heart Associated with Significant Myocardial Edema.

Japanese Heart Journal ◽

10.1536/ihj.39.513 ◽

1998 ◽

Vol 39 (4) ◽

pp. 513-525 ◽

Cited By ~ 3

Author(s):

Keita ODASHIRO ◽

Shin-ichi HIRAMATSU ◽

Toru MARUYAMA ◽

Yoshikazu KAJI ◽

Shozo KANAYA ◽

...

Keyword(s):

Creatine Kinase ◽

Rat Heart ◽

Myocardial Edema ◽

Perfused Rat Heart

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Effect of sarcolemmal anion transport system blockers on the development of ischemia-induced myocardial edema and recovery of contractile function during reperfusion

Bulletin of Experimental Biology and Medicine ◽

10.1007/bf02433381 ◽

1999 ◽

Vol 127 (4) ◽

pp. 363-365

Author(s):

V. V. Alabovskii ◽

E. J. Cragow ◽

A. A. Vinokurov

Keyword(s):

Transport System ◽

Contractile Function ◽

Myocardial Edema ◽

Anion Transport ◽

Anion Transport System

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Contrasting Effects of Colloid and Crystalloid Resuscitation Fluids on Cardiac Vascular Permeability

Anesthesiology ◽

10.1097/00000542-200606000-00018 ◽

2006 ◽

Vol 104 (6) ◽

pp. 1223-1231 ◽

Cited By ~ 128

Author(s):

Matthias Jacob ◽

Dirk Bruegger ◽

Markus Rehm ◽

Ulrich Welsch ◽

Peter Conzen ◽

...

Keyword(s):

Hydroxyethyl Starch ◽

Perfusion Pressure ◽

Ex Vivo ◽

Myocardial Edema ◽

Endothelial Glycocalyx ◽

Perfused Heart ◽

Fluid Filtration ◽

Fluid Extravasation ◽

The Impact ◽

Krebs Henseleit Buffer

Background Fluid extravasation may lead to myocardial edema and consequent reduction in ventricular function. Albumin is presumed to interact with the endothelial glycocalyx. The authors' objective was to compare the impact of different resuscitation fluids (human albumin, hydroxyethyl starch, saline) on vascular integrity. Methods In an isolated perfused heart model (guinea pig), Krebs-Henseleit buffer was augmented with colloids (one third volume 5% albumin or 6% hydroxyethyl starch 130/0.4) or crystalloid (0.9% saline). Perfusion pressure and vascular fluid filtration (epicardial transudate formation) were assessed at different flow rates. After global, stopped-flow ischemia (37 degrees C, 20 min), hearts were reperfused with the same resuscitation fluid additives. In a second series, the authors applied the respective perfusates after enzymatic digestion of the endothelial glycocalyx (heparinase, 10 U over 15 min). Results Both 5% albumin and 6% hydroxyethyl starch decreased fluid extravasation versus saline (68.4 +/- 5.9, 134.8 +/- 20.5, and 436.8 +/- 14.7 microl/min, respectively, at 60 cm H(2)O perfusion pressure; P < 0.05), the corresponding colloid osmotic pressures being 2.95, 5.45, and 0.00 mmHg. Digestion of the endothelial glycocalyx decreased coronary integrity in both colloid groups. After ischemia, a transient increase in vascular leak occurred with Krebs-Henseleit buffer containing hydroxyethyl starch and saline, but not with albumin. The authors observed no difference between intravascular and bulk interstitial colloid concentration in the steady state. Notwithstanding, electron microscopy revealed an intact endothelial glycocalyx and no interstitial edema in the albumin group. Conclusion Ex vivo, albumin more effectively prevented fluid extravasation in the heart than crystalloid or artificial colloid. This effect was partly independent of colloid osmotic pressure and may be attributable to an interaction of albumin with the endothelial glycocalyx.

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