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J Thorac Cardiovasc Surg 2000;119:115-124
© 2000 Mosby, Inc.
SURGERY FOR ACQUIRED CARDIOVASCULAR DISEASE |
From the Division of Cardiothoracic Surgery, Department of Surgerya and The Department of Anesthesia,b School of Medicine of The University of California, San Francisco, and the San Francisco Veterans Affairs Medical Center, San Francisco, Calif.
This work was supported by California Heart Association grant-in-aid 97-241.
Address for reprints: Mark B. Ratcliffe, MD, VAMC Surgery 112D, San Francisco Veterans Affairs Medical Center, 4150 Clement St, San Francisco, CA 94121 (E-mail: ratcliffe.mark{at}sanfrancisco.va.gov).
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionConclusionAppendix AAppendix BReferences |
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAppendix BReferences |
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1-3 However, patients who have LV aneurysm repair for congestive heart failure have only minimal symptomatic and hemodynamic improvement, 1-4 and sheep that undergo LV aneurysm plication do not have an increase in resting cardiac output. 5
The inconclusive results associated with aneurysm plication have stimulated modifications of the standard aneurysm repair. 6,7 However, until the effect of LV aneurysm plication on ventricular function is understood, the effect of innovative modifications cannot be tested. We suggest that the success of an operation that surgically remodels ventricular size, shape, or regional stiffness depends on how the procedure affects both end-systolic and end-diastolic pressure-volume relationships and how those changes affect ventricular function. End-systolic and end-diastolic pressure-volume relationships, respectively termed elastance 8 and diastolic compliance, are determined by LV regional material properties (stiffness) and unloaded ventricular shapes. 9 Aneurysm plication changes the unloaded end-systolic and end-diastolic ventricular shapes and regional stiffness. As a consequence, postoperative end-systolic elastance, diastolic compliance, and ventricular function may be altered.
The primary goal of this study was to measure end-systolic elastance, diastolic compliance, and ventricular function (preload-recruitable stroke work [PRSW] and Starling relationships) before, immediately after, and 6 weeks after aneurysm plication. We hypothesize that LV aneurysm plication decreases ventricular volume, increases end-systolic elastance, decreases diastolic compliance, and improves ventricular function.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAppendix BReferences |
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Initial instrumentation
Castrated male Dorsett sheep were anesthetized (ketamine, 33 mg/kg intramuscularly; isoflurane maintenance, 2%-4% inspired) and their lungs were mechanically ventilated (tidal volume 15 mL/kg; model 309-0612-800, Ohio Medical Products, Madison, Wis). During a left thoracotomy, snares were placed around the left anterior descending and second left anterior descending diagonal coronary arteries at a point 40% of the distance from the apex to the base. As shown inFig 1, a pneumatic occluder (model OC20HD, In Vivo Metric Inc, Healdsburg, Calif) was placed around the inferior vena cava, and a transit-time flow probe (model 20S, Transonics Inc, Ithaca, NY) was placed around the ascending aorta. Flow probe leads, pneumatic catheters, and coronary snares were tunneled to the animal’s back. The thoracotomy was closed and the sheep was allowed to recover from anesthesia.
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Aneurysm plication
Ten weeks after myocardial infarction, a partial lower sternotomy was performed with the sheep under general anesthesia. Pericardial adhesions were divided. Aneurysm plication was performed without cardiopulmonary bypass. The transition between infarcted aneurysm and uninfarcted myocardium was palpated and the LV aneurysm was plicated between 2 strips of Dacron felt. Polypropylene sutures (2-0 Prolene, MH needle, Ethicon, Inc, Somerville, NJ) were passed through the felt, through and through the aneurysm at its border, and through the opposite strip of felt in a horizontal mattress fashion. The sternotomy was closed and the sheep was allowed to recover from anesthesia.
Data collection
Transdiaphragmatic echocardiography and conductance catheter measurements were obtained immediately before myocardial infarction, 10 weeks after infarction (preplication), and immediately after and 6 weeks after plication. Propranolol (0.1 mg/kg, given intravenously) and atropine (1.0 mg, given intravenously) were administered before data collection to decrease autonomic reflexes. All data were collected with the same level of anesthesia (1% inspired isoflurane [Forane]). Preplication data were obtained immediately before sternotomy, and postplication data were obtained immediately after chest closure but before the abdominal incision was closed so that the transdiaphragmatic echocardiogram could be obtained.
Echocardiography
A 2.5 MHz 2-dimensional echocardiography transducer (model 5000, General Electric Inc, Rancho Cordova, Calif) was inserted through a subxiphoid incision. As shown inFig 1
, an LV long-axis echocardiogram was used to confirm myocardial infarction, conductance catheter position, and to measure LV volume. LV long axis, short axis, and wall thickness at the equator and 30% of the distance from the apex to the base were measured (Imagevue, version 1.50, Nova Microsonics, Allendale NJ). LV volume was determined with the use of a single-plane disc volume Simpson rule.
Conductance catheter
A 7F pigtail 12-pole multielectrode conductance catheter (model 7212-12, Webster Laboratories, Baldwin Park, Calif) with a 2F catheter-tipped pressure transducer (model SPC-320, Millar Instruments, Inc, Houston, Tex) was used to measure LV pressure and volume. Lidocaine (100 mg, given intravenously) was administered to prevent ventricular arrhythmias. Position of the conductance catheter in the LV was confirmed by pressure waveform, the volume conductance signals, and the echocardiogram. The conductance catheter was connected to a volume conductance signal generator (model Sigma-5-DF, Leycom, Oegsteest, The Netherlands) using dual field mode. Blood conductance was measured in a 4-electrode cuvette. 11
LV pressure was amplified (model M2103B, Electronics for Medicine, PPG Industries, Lenexa, Kan), calibrated with a mercury manometer, and zeroed to the level of the right atrium. The aortic flow probe was connected to a transit-time flowmeter (model HT206, Transonics Inc, Ithaca, NY). The electrocardiogram, LV pressure, conductance catheter signals, and aortic blood flow were digitally sampled (200 Hz) with an 8-channel (bipolar), 12-bit analog-to-digital converter (model NB-M10-16, National Instrument Corp, Austin, Tex) housed in a personal computer (model Quadra 900, Apple Computer, Cupertino, Calif).
LV pressure, conductance catheter output, aortic blood flow, and electrocardiographic data were collected during four 20- to 30-second vena caval occlusions with respiration temporarily suspended. Vena caval occlusions were continued until LV peak pressure decreased to 40 mm Hg. In each case, echocardiograms were obtained before vena caval occlusion. Incisions were closed, and the sheep were allowed to recover from anesthesia.
Data analysis
Fifteen beats were selected from each vena caval occlusion (Custom Software). End-systole (ES) was identified as the point of maximal elastance. l2 End-diastole (ED) was defined as 40 ms before 40% of maximum positive rate of rise of LV pressure.
Conductance catheter data were used to calculate relative LV volume (VCONDi) as described by Baan and associates. 11 Stroke volumes (SV) were calculated according to the following equation:
SVcc = VCONDED – VCONDES.
Stroke volumes were also calculated from the aortic flow (AoFdt) according to the following equation:
SVFP=(ES
EDAoFdt)
Conductance catheter gain, 
, was set equal to SVCC,1/SVFP,1, where SVCC,1 and SVFP,1 are stroke volumes obtained from the first beat of each vena caval occlusion.
Parallel conductance was not measured and was not used to correct relative LV volume (VCONDi). Instead, absolute LV volume (LVVi) was calculated from conductance catheter and echocardiographic data according to the following equation (see Appendix A):
LVVi = VCONDi – VCONDED + VECHOED
where VCONDi is conductance catheter volume at time I, VCONDED is conductance catheter volume at end-diastole of the first beat of each vena caval occlusion, and VECHOED is the corresponding echocardiographic volume at end-diastole.
LV end-systolic pressure (LVPES) and volume (LVVES) were related by the following equation:
LVPES= EESLVVES+ LVPES,0
where LVPES,0 is the y (pressure) intercept and EES is the slope of the LV elastance. End-diastolic pressure (LVPED) and volume (LVVED) were related by the following equation:
LVPED= 
0e1LVVED
where 0 and 1 are the stiffness parameters of the LV diastolic compliance. The stroke work (SW) and LVPED were related by the following equation:
SW = mPRSWLVVED+ SW0
where SW0 is the stroke work intercept and mPRSW is the slope of the relationship.
The stroke volume (SV) and LVPED were related by the following equation:
SV = mStarlingLVPED + SV0
where SV0 is the stroke volume intercept and mStarling is the slope of the relationship.
Statistical analysis
All values were expressed as mean ± standard deviation. All baseline measurements(Table I) were compared with repeated-measures analysis of variance with the Bonferroni correction (Systat, version 6.11, SPSS Inc, Chicago, Ill).
Conductance catheter and flow probe measurement of stroke volume were compared by measurement agreement (see Appendix A). l3 Elastance, diastolic compliance, PRSW, and Starling relationships were compared with a repeated-measures multiple linear regression (Proc Regress, SAS system for Windows, version 6.12, SAS Institute, Cary, NC) (see Appendix B). 14,15
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAppendix BReferences |
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Repeated-measures analysis of baseline heart rate, LV pressure, stroke volume, ejection fraction, and stroke work at different time points are seen inTable I. Heart rate, LV pressure at end-systole, and peak LV pressure did not change significantly. LV pressure at end-diastole decreased immediately after plication.
The effect of aneurysm formation and aneurysm plication on long-axis echocardiogram is seen inFig 2 andTable II. During aneurysm formation, the equatorial short axis and distal short axis increase. Immediately after plication the LV long axis and equatorial short axis decrease and wall thickness increases. However, 6 weeks after aneurysm repair, the LV long axis increases and wall thickness decreases to near prerepair values. LV volume is seen inFig 3. End-diastolic and end-systolic LV volumes significantly increase with aneurysm formation. Note that immediately after plication end-diastolic and end-systolic volumes return to preinfarction values. However, both end-diastolic and end-systolic volumes return to preplication values 6 weeks after plication.
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). In conjunction with the postplication decrease in LV end-diastolic pressure and increase in wall thickness, these changes probably represent a small decrease in preload at the end of the surgical aneurysm repair. Both stroke volume and stroke work increase by 6 weeks after plication but do not reach preinfarction values. Ejection fraction decreases from 57.6% to 30.4% with infarction and aneurysm formation, increases to 48.6% with plication, but decreases to 36.3% 6 weeks after aneurysm repair.
Pressure-volume relationships
The effect of aneurysm formation and plication on end-systolic elastance is seen inFig 4 andTable III. Note that elastance moves to the right on the pressure-volume diagram with aneurysm formation, moves back to the left with plication, and then returns to the right 6 weeks after aneurysm repair. The slope of elastance decreases with infarction and aneurysm formation, is unchanged with aneurysm plication, but then decreases 6 weeks after plication.
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. Note that compliance changes, in general, mirror changes in elastance. Compliance moves to the right on the pressure-volume diagram with aneurysm formation, moves back to the left with plication, and then returns to the right 6 weeks after aneurysm repair. Both the multiplication term, 0, and the exponential term, 1, decrease significantly with aneurysm formation, increase with aneurysm plication, but then decrease 6 weeks after plication.
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. PRSW moves to the right on the stroke work/end-diastolic volume plot with infarction and aneurysm formation. It moves to the left immediately after plication but shifts back to the right 6 weeks after plication. The slope of the PRSW relationship decreases with infarction and aneurysm formation, increases with aneurysm plication, but then again decreases 6 weeks after plication.
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. The Starling relationship undergoes a slight upward parallel shift on the stroke volume/end-diastolic pressure plot with infarction and aneurysm formation. The Starling relationship then undergoes a parallel downward shift immediately after plication and remains at that position 6 weeks after plication. There are no significant changes in Starling relationship slope. The stroke volume intercept of the Starling relationship increases with infarction and aneurysm formation, decreases with aneurysm plication, but then increases 6 weeks after plication.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAppendix BReferences |
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Short-term changes in end-systolic elastance and diastolic compliance with aneurysm plication
This study found that the slopes of both LV end-systolic elastance and diastolic compliance increase after aneurysm plication. In human beings, aneurysm patch repair decreases both end-systolic and end-diastolic LV volume, 6 and linear aneurysm plication probably reduces LV volume further. Patch repair removes the aneurysm wall and replaces it with patch material 7; linear repair replaces aneurysm with a surgical repair of felt and scar.
LV function
Improvements in ejection fraction, end-systolic elastance, or PRSW are associated with an improvement in systolic function. 8,16 However, it is incorrect to conclude that overall ventricular function has improved if ejection fraction, end-systolic elastance, or PRSW increase after aneurysm repair or partial ventriculectomy. For instance, in this study, ejection fraction increased from 30.4% to 48.6% with aneurysm plication, but stroke volume decreased from 26 to 18.2 mL. Similarly, Di Donato and associates 17 found that ejection fraction increased from 39% to 49% whereas stroke volume decreased after patch aneurysmorrhaphy. However, in a later group of patients with severely depressed preoperative ventricular function, an increase in ejection fraction from 17% to 37% was associated with an increase in stroke volume although cardiac index did not change significantly. 6 Partial left ventriculectomy may also cause an increase in ejection fraction that does not represent an increase in LV function. 18,19 Although these findings are difficult to interpret because end-diastolic pressure is often lower in the postoperative period, 6 they suggest that ejection fraction is not a reliable indicator of ventricular function in operations that surgically remodel the left ventricle.
End-systolic elastance and PRSW have been proposed as load-independent measures of ventricular contractility. 8,16 In this study, the slope of the end-systolic elastance and PRSW relationships increase with aneurysm plication. Although the stroke volume intercept decreased, the slope of the Starling relationship did not change. These equivocal results (improved end-systolic elastance and PRSW but depressed Starling relationship) are caused by the relative shifts in end-systolic elastance and diastolic compliance that occurs with aneurysm plication. Although end-systolic elastance is increased after plication, the relative decrease in diastolic compliance may be greater. As a direct consequence, stroke volume and the Starling relationship decrease, and for stroke volume and cardiac output to be maintained after aneurysm plication, end-diastolic pressure and stroke work must increase. The improvement in PRSW is therefore caused by the increase in stroke work and by the reduction in absolute LV volume. Mathematical models of partial left ventriculectomy demonstrate this paradoxic increase in end-systolic elastance and PRSW with a decrease in the Starling relationship. 18,19 End-diastolic pressure and resulting pulmonary congestion may ultimately be the clinically limiting factor, making the Starling relationship the more important measure of ventricular function after aneurysm repair.
Postoperative remodeling
Surprisingly, the left ventricle was found to dilate and both end-diastolic and end-systolic volumes returned to preplication values 6 weeks after plication. Both end-systolic elastance and diastolic compliance decreased at 6 weeks after plication, in large part because of the increase in end-diastolic and end-systolic volumes. Although not reported with linear aneurysm plication, patients who have undergone both LV patch aneurysmorrhaphy 7 and partial left ventriculectomy 20 have experienced LV dilation at 1 year. Dor and associates 7 found that end-systolic and end-diastolic ventricular volume increased 22% and 29%, respectively, after patch repair. Stolf and coworkers 20 reported that end-systolic and end-diastolic ventricular volume increased after partial left ventriculectomy.
The cause of the postoperative remodeling is unclear but may include progression of the underlying biologic disease process, lack of pericardial support, and failure of the repair to reduce wall stress in the border zone and remote uninfarcted myocardium. A reduction in wall stress after aneurysm repair may be the most important factor and may be necessary if LV function is to be improved and postoperative remodeling prevented. Savage and coworkers 5 measured regional deformation after aneurysm plication and found the effect on circumferential wall stress to be heterogeneous. Wall stress was increased in the remote anterior wall at end-diastole but decreased in the posterior wall throughout the cardiac cycle. Although longitudinal stress was not measured, Savage’s group 5 did note an increase in longitudinal dimensions and suggested that longitudinal stress was increased(Fig 8). Therefore, aneurysm plication may replace high border zone stress caused by the aneurysm 21 with high closing or residual stress in the border zone and remote myocardium. The sheep model of aneurysm formation and repair would seem to be ideal for the investigation of these important clinical issues.
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Conclusion |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAppendix BReferences |
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The relative effects of patch aneurysm repair are unknown but should be tested both in the sheep aneurysm model and with finite element models of LV aneurysm and repair. Finally, understanding the mechanism of postoperative ventricular remodeling is important both for aneurysm repair and for partial ventriculectomy (Batista operation). The sheep is an ideal model with which to investigate possible mechanisms of postoperative remodeling.
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Appendix A |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAppendix BReferences |
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22 provides a continuous analog measurement of ventricular volume. Gain, , has been previously compared with an electromagnetic flowmeter, 22 sonomicrometry crystals, 23 and serial ventriculography 24 and found to be generally accurate. However, the conductance catheter has not been previously used to measure intracavitary LV volume in an aneurysmal heart.
In
Fig 8, stroke volume measurements by conductance catheter and flow probe are compared. All stroke volume data are included (287 data points from 20 vena caval occlusions). Standard deviation of stroke volume measurement difference is 7.9 mL. The conductance catheter is therefore a reasonable measure of relative changes in LV volume.
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Appendix B |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAppendix BReferences |
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14,15 The regression model used was as follows:
ß2iAi
+ ß3iAi
LVVES + ß4iTi + ß5iTi
LVVES 14,15 For instance, the Ai term represents the effect of an individual animal on the pressure intercept, LVVES,0, and the AiLVVES term represents the effect on slope, EES. Dummy variable methods of this type are a standard way of allowing for between-subject variability in linear regression analysis. 14,15
As with elastance, a repeated-measures multiple linear regression model was used where dummy variables represented the experimental time points and individual animals. The regression model used was as follows:
Ln(LVPED
+ 1) = ß0
+ ß1LVVED + ß2iAi + ß3i Ai
LVVED
+ ß4iTi
+ ß5iTi
LVVED
where Ai and Ti are defined as above. A log transformation was used. 15
PRSW and Starling relationship analysis was similar to EES analysis.
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Acknowledgments |
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References |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionAppendix AAppendix BReferences |
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