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J Thorac Cardiovasc Surg 1998;115:1209-1214
© 1998 Mosby, Inc.

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

REVERSAL OF IATROGENIC MYOCARDIAL EDEMA AND RELATED ABNORMALITIES OFDIASTOLIC PROPERTIES IN THE PIG LEFT VENTRICLE

David A. Dean, MDa*, Mehrdad M. Amirhamzeh, MDa, Chao-Xiang Jia, MDa, Santos E. Cabreriza, MBAa, David G. Rabkin, BAa, Robert Sciacca, EngScD, Marc L. Dickstein, MDc, Henry M. Spotnitz, MDa**roles>

Supported in part by U.S. Public Health Service grant 1 RO1 HL-48109.Dr. Dickstein is supported by National Institutes of Health NRSA training grantHL09325-01.

Received for publication July 28, 1997. Revisions requested Oct. 6, 1997. Revisions received Dec. 24, 1997. Accepted for publication Dec. 29, 1997. Address for reprints: Henry M. Spotnitz, MD, Department of Surgery,Columbia University, College of Physicians and Surgeons, 622 West 168th St., PH1422, New York, NY 10032.


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Discussion
 References
 
Objective: This study examines theresolution of iatrogenic edema and related changes in systolic and diastolicproperties in the intact pig left ventricle. Methods:The coronary arteries were perfused for 50 to 60 seconds with diluted blood(hematocrit value 10% ± 1%, edema group,n = 5) or whole blood (hematocrit value 28%± 1%, control group, n = 6)infused into the aortic root during aortic crossclamping in conditioned,anesthetized pigs. After whole blood reperfusion, preload reduction by venacaval occlusion was used to define systolic and diastolic properties at15-minute intervals. Left ventricular pressure and conductance, aortic flow, andtwo-dimensional echocardiography were recorded.
Results:Left ventricular mass (wall volume) in the edema group increased significantlycompared with that in control pigs after crossclamp removal. Mass returned topreperfusion levels after 45 minutes. The ventricular stiffness constant (ß)increased significantly in the edema group versus the control group, returningto baseline by 30 minutes. The diastolic relaxation constant ({tau}) and baseconstant ({alpha}) did not differ between groups. There was no significantchange in contractility.
Conclusion:Increases in left ventricular mass and diastolic stiffness induced by coronaryperfusion with hemodiluted blood resolve after 45 minutes of whole bloodperfusion in pigs. This study defines physiologic effects of edema in the normalheart while eliminating most common confounding experimental errors. (J ThoracCardiovasc Surg 1998;115:1209-14)


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Discussion
 References
 
Analysis of the effects of cardiac surgery on left ventricular (LV)systolic and diastolic properties can be nullified by myocardial edema. Edema,usually caused by ischemic injuryGo 1or hemodilution,Go 2 or both, isidentified by increases in myocardial water content, LV weight, andechocardiographic LV mass (wall volume). A hallmark of edema is increased LVdiastolic stiffness.Go 2

Edema resulting from hemodilution is believed to be short-lived, fullyand easily reversible. Characterization of reversible edema is needed todifferentiate it from longer lasting ventricular injury. This task has beendifficult and has attracted many investigators.Go Go Go 4,3-10 Ideally, edema shouldbe induced and reversed without cardiac injury. Techniques that are highlylikely to cause edema, including cardiopulmonary bypass (CPB) and Langendorffperfusion, should be avoided.

Pursuing this, our laboratory induced edema in the intact circulation ofanesthetized rats by rapid proximal crystalloid perfusion of the distallyclamped aorta, discarding right atrial drainage. On the basis of myocardialwater content, edema was found to resolve after 15 minutes of whole bloodreperfusion.Go 11 Each timepoint required that a separate animal be put to death.

A similar study in pigs characterized induction and reversal of edema inthe same animal. Abnormalities of LV stiffness and LV mass resolved after 45minutes of whole blood reperfusion.Go 12Methodologic problems included myocardial ischemia and a transient need formechanical assistance. In the present study, we sought an improved model inwhich the functional effects of myocardial edema alone could be directly studiedin vivo for the first time.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Discussion
 References
 
Experimental protocol.
Animal care complied with the "Principles of Laboratory Animal Care"formulated by the Institute of Laboratory Animal Resources, "Guide for theCare and Use of Laboratory Animals" (NIH Publication No. 86-23, revised1985), and the position of the American Heart Association on Research AnimalUse.

Conditioned Hampshire pigs (40 to 50 kg), divided into edema (n = 5)and control groups (n = 6), were anesthetized, heparinized, andinstrumented as previously described.Go 12The left hemiazygos vein was ligated. A 7F conductance-micromanometer pressurecatheter (Sentron, Inc., Federal Way, Wash.) was placed in the LV through theapex. A pulmonary artery thermistor (Baxter Healthcare Corp., Irvine, Calif.)allowed determination of cardiac output.

Intravenous fluids (0.9% sodium chloride) were administered at arate of 5 ml/kg per hour. Hematocrit value and blood resistivity (whichdecreases with hemodilution) were not significantly different between groups atfour time points during the experiment. Digitized data and two-dimensionalechocardiography (2-DE) were recorded with the lungs deflated during preloadreduction by vena caval occlusion as previously described.Go 12

The coronary perfusate consisted of 167 ml of heparinized blood in 333 mlof Ringer's lactate solution (274 mOsm, hematocrit value 10%± 1%) in the edema group and 500 ml of whole blood (hematocritvalue 28% ± 1%) in the control group. Normal salinesolution was used for blood replacement milliliter for milliliter in eachanimal. An aortic cardioplegia needle and cannulas to vent the right and leftatria were introduced as previously described.Go 12 The heart was perfused asfollows: (1) The venae cavae and the main pulmonary artery were snared; (2) theaorta was crossclamped; (3) the atria were vented; (4) 500 ml of group-specificnormothermic aortic perfusate was injected at a rate of 50 to 60 mm Hg.Crossclamp time averaged less than 1 minute (edema group 57 ± 4seconds, control group 51 ± 4 seconds). During infusion, the heartwas manually compressed to avoid distention. All hearts maintained organizedrhythm during infusion.

The snares and aortic clamp were then released and the vents wereclamped. Epinephrine was infused (0.05 µg/kg per minute) for 2 to 3minutes until systolic blood pressure was greater than 60 mm Hg and heart ratewas less than 120 beats/min. Manual massage and circulatory support were notused.

As previously described,Go 12hemodynamics and 2-DE were recorded every 15 minutes for 90 minutes in thesteady state and during vena caval occlusion. The heart was then arrested withpotassium chloride solution. The LV was trimmed and weighed, and myocardialwater content was determined.

Conductance.
As previously described,Go 12arterial blood was collected to measure resistivity with the Leycom Sigma-5conductance module (Rijnsburg, The Netherlands). Parallel conductance wasmeasured before each data acquisition with injection of hypertonic salinesolution,Go 13 and 2-DE wasrecorded with a 5.0 MHz transducer, including multiple views previouslydescribed.Go 12 LV pressure andconductance were displayed with 2-DE,Go 14allowing correlation at end-diastole. Alpha ({alpha}), the dimensionlesscalibration factor that converts raw conductance volume to absolute volume, wasdetermined for each data set by comparing conductance-derived cardiac outputwith thermodilution and flow probe stroke volume.

Data analysis.
"Pre" refers to data before crossclamping. Postreperfusionpoints were "15 minutes," 3 to 15 minutes after reperfusion, "30minutes," 16 to 30 minutes after reperfusion, "45 minutes," 31to 45 minutes after reperfusion, "60 minutes," 46 to 60 minutesafter reperfusion, and "90 minutes," 61 to 90 minutes afterreperfusion.

As previously described,Go 12data digitized at 200 Hz were analyzed with the use of IGOR software(Wavemetrics, Inc., Lake Oswego, Ore.). Raw conductance was corrected forparallel conductanceGo 13 and{alpha}. Corrected volume was then used in all calculations of systolic anddiastolic function.

End-diastole was defined as the point on the pressure trace coincidingwith the R wave on the electrocardiogram. Analysis of LV diastolicpressure-volume relationship consisted of exponential curve fitting ofend-diastolic pressure (EDP) and volume (EDV) by the least squares method(equation 1). ß is the LV stiffness constant and {alpha} is the baseconstant.

EDP = {alpha}aeßEDV   (1)

As suggested by Weiss, Frederiksen, and Weisfeldt,Go 15 the diastolic relaxationconstant, {tau}, was determined from the slope, A, of the natural log ofpressure versus time during isovolumic relaxation over 60 msec after peaknegative rate of pressure rise.

{tau} = –1/A   (2)

End-systole was defined by the upper left-hand corner of thepressure-volume loop.Go 16 Theend-systolic pressure-volume relation defined maximum systolic elastance.Go 16 Stroke work was determined foreach cardiac cycle by calculating the area within the pressure-volume loop.Preload recruitable stroke work (PRSW) was defined by the relationship betweenstroke work and end-diastolic volume.Go 17The slopes and volume intercepts were defined by linear regression. Volumeintercepts (x-axis intercepts) were calculated at the point where the fittedlinear regression line had a value of zero.

Echo techniques, previously described,Go 12 measured LV wall volume as thenumeric difference of the epicardial and endocardial shells, multiplied bymyocardial specific gravity (1.05 gm/ml) to determine LV mass.

Myocardial water content (MWC) was calculated from equation 3:

MWC (%) = ([Wet heart weight – Dry heart weight]/[Wet heartweight]) x 100   (3)

Statistical analysis.
For comparisons between groups, LV mass, diastolic properties ({alpha},ß, {tau}), systolic properties (systolic elastance and PRSW) were comparedby repeated-measures analysis of variance (ANOVA). Similarly, conductancecalibration before and after perfusion were compared by repeated-measures ANOVA.Post hoc comparisons were performed with the use of Tukey's procedure.Postmortem LV weight, LV myocardial water content, hematocrit value, perfusionpressure, and coronary perfusion time were compared by means of unpaired Student'st test.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Discussion
 References
 
Fig. 1 illustrates a representative pressure-conductance tracing duringvena caval occlusion. Raw conductance was converted to LVvolume by means of calibration routines based on injection of hypertonic salinesolution. Fig. 2 illustrates effects of edema on the LV diastolicpressure-volume relationship during a representative experiment; the data shiftupward and to the left in the edema group during reperfusion, reflectingincreased diastolic stiffness.



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  		Fig. 1. Representativepressure-volume data during preload reduction by inferior vena caval occlusion.Raw conductance was converted to absolute volume by means of calibrationroutines described in the text.

 


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  		Fig. 2. Representative LVpressure-volume data after infusion of hemodiluted blood, analyzed byexponential curve fitting. The curves are shifted upward and to the left 3 and18 minutes after reperfusion. LVM, LV mass by2-DE.

 
Fig. 3 presents the time course of average LV mass, as determined by 2-DEand ß. LV mass and ß increasedsignificantly in the edema group compared with the control group in the first15-minute interval after coronary perfusion, returning to control values by the45-minute time interval. There was no significant difference betweenpreperfusion LV mass and postmortem weight. Myocardial water content was notdifferent between the groups at the end of the experiment. Testing forsubjective planimetry errors was done with a blinded second observer, aspreviously described.Go Go Go Go 1,6,18,19 No intraobserverdifferences were noted. Postmortem LV weight correlated well with 2-DE LV mass.



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  		Fig. 3. Time course of mean LVmass (LVM) calculated by 2-DE and diastolicstiffness constant (ß for edema (n =5) and control groups (n = 6).Statistically significant increases occur in ß and LV mass in the edemagroup at 15 minutes and then return toward normal.

 
The base constant, {alpha}, and isovolumic relaxation constant, {tau},did not change significantly in the edema group as compared with the controlgroup. End-diastolic volume was not different between groups. However, withingroups, end-diastolic volume significantly decreased from baseline in the30-minute time interval in the control group, but remained lower in the edemagroup (p < 0.05, ANOVA). Heart rate didnot differ between groups, but within each group it was significantly higher inthe first 15-minute interval after removal of the aortic crossclamp, returningto baseline in the 30-minute interval in the control group only (Fig. 4).



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  		Fig. 4. Time course of heartrate (HR) and end-diastolic volume (EDV) for edema (n =5) and control groups (n = 6). Heart rateis increased significantly and end-diastolic volume is decreased significantlyat the 15-minute time point.

 
Table I presents indices for systolic function. Measures ofcontractility, end-systolic pressure-volume relationship and PRSW, were notstatistically different between groups (repeated-measures ANOVA). Cardiac outputdecreased after reperfusion in both groups, but the change was not statisticallysignificant.


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  		Table I. Systolic indices of LV
 
Average perfusion hematocrit value, time of perfusion, and perfusionpressure are presented in Table II. There was nodifference in perfusion pressure or time of perfusion between the two groups.


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  		Table II. Mean perfusion data
 

   Discussion
Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
References
 
The present experiment was designed from its inception to controlextraneous influences on cardiac function and edema. The data demonstrateincreased LV mass and impaired diastolic filling after coronary perfusion withhemodiluted blood. The LV end-diastolic pressure-volume relation shifts upwardand leftward, indicating decreased LV compliance and increased chamberstiffness. Forty-five minutes after whole blood reperfusion, LV mass andcompliance return to control values. These results for the normal pig heartdefine the transient effects of hemodilution on LV geometry and diastolicproperties and the minimum recovery time in the absence of specific treatment.

Many related observations have been reported. In isolated, hypothermicpig hearts, Hsu and coworkersGo 20demonstrated that hyposmolar coronary perfusion increased both heart weight (by30%) and myocardial water content (by 6.5%), consonant with simplemodels for fluid distribution.Go 2Foglia,Steed, and FolletteGo 7demonstrated that hypoosmotic cardioplegia increased LV myocardial water contentin a canine model undergoing CPB. Others reported a 16% increase in LVmass with hemodilutionGo Go 18,19 in dogs undergoing CPB;myocardial water content increased proportionately. A 22% increase in LVmass was also observed in dogs after 45 minutes of ischemic arrest on CPB.Go 6 These observations and additionalevidence support the view that increased LV mass in the present study reflectsmyocardial edema.

Several sources of error warrant discussion. Increased LV mass and LVwall thickness are interpreted in the present study to indicate myocardialedema. An alternate explanation for increased wall thickness is reactivehyperemia.Go 21 We believereactive hyperemia did not occur, because no increase in wall thickness occurredin a previous studyGo 12 after1 minute of ischemic ventricular fibrillation and reperfusion. Hyperemia is evenless likely in the present study, because fibrillation was avoided. We alsoargue that the hematocrit value of the perfusate was not a factor, because ahematocrit value of 9% is said to minimally impair myocardial oxygendelivery.Go Go 4,5 Any myocardial ischemia andhyperemia resulting from 1 minute of perfusion at this hematocrit value shouldhave been too short-lived to have affected the results. The degree ofhemodilution was based on a prior study.Go 22

Conductance in the open chest is affected by metallic objects,temperature, right ventricular volume, lung volume, and size of the pericardialcontact footprint.Go 23 Thesecan alter parallel conductance or the slope constant, or both. Frequentcalibration was used to compensate for this. Since we found the calibrationconstants extremely stable, myocardial edema apparently does not affectconductance calibration. A tendency for parallel conductance to increase duringreperfusion in our study could reflect changes in right ventricular volume, lungvolume, or temperature.Go 23

Conductance was useful for measuring instantaneous LV volume in thisexperiment, particularly because edema causes artifacts in other measuringtechniquesGo Go 1,24 and because laboriouscalculations are required to extend quantitative 2-DE throughout the cardiaccycle. For these reasons, 2-DE was used to measure LV mass, whereas conductancewas used to measure LV volume. Conductance calibration based on 2-DE has beendescribed.Go 14

The last error source to be discussed is the use of exponential curvefitting for analysis of diastolic properties. This can be problematic at lowfilling pressures, where the curves are relatively flat and may even have areversed sigmoidal shape.Go 20Our approach is simplistic and could be inaccurate at pressures approachingzero. However, Fig. 2Go suggests thatexponential curve fitting was reasonable for the present data set. Theterminology for base and exponential constants has also been confusing; ßhas been used for the base or exponential constant by different authors.

Effects of edema on systolic properties are not well understood. Althoughedema could depress contractile function,Go Go 25,26 systolic performance has notbeen impaired by edema in several prior studies.Go Go 3,6Our data reveal no change in systolic elastance or PRSW after the first 5minutes of reperfusion. Cardiac output in both groups decreased transiently andinsignificantly after reperfusion, possibly reflecting changes in preload. Theassessment of contractility may have been affected by the use of inotropicagents immediately after crossclamping and by systemic reflexes, which were notblocked.

Many factors modifying edema were not explored in this study. Theseinclude ischemic injury, which affects membrane properties and ion pumps, andCPB, which releases cytokines and causes leaky membranes. Additional importantfactors are congestive heart failure, hypothermia, drug reactions,hypoproteinemia, sepsis, and transplant rejection. The purpose of the presentstudy was not to describe myocardial edema in all its forms, but rather todefine recovery from myocardial edema in its simplest form.

In summary, using a new model, myocardial edema was found to increaseventricular stiffness and wall volume. These changes resolved after 45 minutesof whole blood reperfusion. This model may facilitate testing cardioplegicagents and treatment for myocardial edema.


   Acknowledgments
 
We gratefully acknowledge the technical assistance of NatalyaChalik and Michael J. Sardo.


   Footnotes
 
*Current address: Dartmouth-Hitchcock Medical Center, Lebanon, N.H.

**George H. Humphreys II Professor of Surgery.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Discussion
 References
 

  1. Haasler GB, Rodigas PC, Collins RH, Wei J,Meyer FJ, Spotnitz AJ, et al. Two-dimensional echocardiography in dogs:variation of left ventricular mass, geometry, volume, and ejection fraction oncardiopulmonary bypass. J Thorac Cardiovasc Surg 1985;90:430-40.[Abstract]
  2. Spotnitz HM, Hsu DT. Myocardial edema:importance in the study of left ventricular function. Adv Card Surg 1994;5:1-25.[Medline]
  3. Cross CE, Rieben PA, Salisbury PF. Influenceof coronary perfusion and myocardial edema on pressure-volume diagram of leftventricle. Am J Physiol 1961;201:102-8.[Abstract/Free Full Text]
  4. Laks H, Standeven J, Blair O, Hahn J,Jellinek M, Willman VL. The effects of cardiopulmonary bypass with crystalloidand colloid hemodilution on myocardial extravascular water. J ThoracCardiovasc Surg 1977;73:129-38.[Abstract]
  5. Geffin GA, Vasu MA, O'Keefe D,Pennington DG, Erdmann AJ, Lowenstein E, et al. Ventricular performance andmyocardial water content during hemodilution in dogs. Am J Physiol 1978;235:767-75. \ %
  6. Lazar HL, Hassler GB, Collins RH, DubroffJM, Meisner J, Spotnitz HM. Compliance, mass, and shape of the canine leftventricle after global ischemia analyzed with two-dimensional echocardiography.J Surg Res 1985;39:199-208.[Medline]
  7. Foglia RP, Steed DL, Follette DM. Iatrogenicmyocardial edema with potassium cardioplegia. J Thorac Cardiovasc Surg 1979;78:217-22.[Abstract]
  8. Foglia RP, Lazar HL, Steed DL, Follette DM,Manganaro AJ, Deland E, et al. Iatrogenic myocardial edema with crystalloidprimes: effects on left ventricular compliance, performance, and perfusion. SurgForum 1978;29:312-5.
  9. Vogel WM, Cerel AW, Apstein CS.Post-ischemic cardiac chamber stiffness and coronary vasomotion: the role ofedema and effects of dextran. J Mol Cell Cardiol 1986;18:1207-18.[Medline]
  10. Schaff HV, Gott VL, Goldman RA, FrederiksenJW, Flaherty JT. Mechanism of elevated left ventricular end-diastolic pressureafter ischemic arrest and reperfusion. Am J Physiol 1981;240:H300-7.
  11. Takoudes TG, Amirhamzeh MMR, Hsu DT, WiseBR, Odeh SO, Spotnitz HM. Time course of resolution of perfusion-inducedmyocardial edema in the rat heart. J Surg Res 1994;57:641-6.[Medline]
  12. Amirhamzeh MMR, Dean DA, Jia C-X, et al.Iatrogenic myocardial edema: increased diastolic compliance and time course toresolution in vivo. Ann Thorac Surg 1996;62:737-43.[Abstract/Free Full Text]
  13. Burkhoff D, Van der Valde ET, Kass D, BaanJ, Maughan WL, Sagawa K. Accuracy of volume measurement by conductance catheterin isolated, ejecting canine hearts. Circulation 1985;72:440-7.[Abstract/Free Full Text]
  14. Cabreriza SE, Amirhamzeh MMR, Jia C-X,Spotnitz HM. Conductance-echocardiography correlations during changes in leftventricular volume. ASAIO J 1995;41:M669-73.[Medline]
  15. Weiss JL, Frederiksen JW, Weisfeldt ML.Hemodynamic determinants of the time-course of fall in the canine leftventricular pressure. J Clin Invest 1976;58:751-60.
  16. Sagawa K. The ventricular pressure-volumediagram revisited. Circ Res 1978;43:677-86.[Free Full Text]
  17. Glower DD, Spratt JA, Snow ND, Kabas JS,Davis JW, Olsen CO, et al. Linearity of the Frank-Starling relationship in theintact heart: the concept of preload recruitable stroke work. Circulation 1985;71:994-1009.[Abstract/Free Full Text]
  18. Collins RH, Haasler GB, Krug JH, Colt C,Spotnitz AJ, Martin EC, Spotnitz HM. Canine left ventricular volume and massduring thoracotomy by two-dimensional echocardiography. J Surg Res 1982;33:294-304.[Medline]
  19. Hassler HB, Rodigas PC, Spotnitz HM. Theabsence of temperature effects on end-diastolic pressure-volume relations in thecanine left ventricle determined by two-dimensional echocardiography. J ThoracCardiovasc Surg 1982;83:878-90.[Abstract]
  20. Hsu DT, Weng Z-C, Nicolosi AC, Detwiler PW,Sciacca R, Spotnitz HM. Quantitative effects of myocardial edema on the leftventricular pressure volume relation in the isolated stored pig heart. J ThoracCardiovasc Surg 1993;106:651-7.[Abstract]
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  24. Spotnitz WD, Clark MB, Rosenblum HM, LazarHL, Haasler GB, Collins RH, et al. Effect of cardiopulmonary bypass and globalischemic on human and canine left ventricular mass: evidence for interspeciesdifferences. Surgery 1984;96:230-8.[Medline]
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