Simulated left ventricular aneurysm and aneurysm repair in swine

J

THORAC CARDIOYASC SURG

1990;100:745-55

. Simulated left ventricular aneurysm and aneurysm . . repair In swine Patch reconstruction of left ventricular aneurysm may be superior to linear closure, but this hypothesis has not been tested experimentally. Accordingly, six anesthetized domestic pigs were instrumented to measure regional left ventricular wall thickening, stroke volume, systolic left ventricular pressure, and myocardial oxygen consumption. With total bypass and cardioplegia, a 6 by 8 em Dacron patch was inserted into the anteroapical left ventricle. Simulations were as foUows: left ventricular aneurysm, patch open; patch reconstruction, 50% patch plication; standard repair, ventriculotomy edges approximated. Global function, from stroke work (stroke volume X J left ventricular pressure)-left ventricular end-diastolic pressure curves, was depressed in aU three simulations compared with control. A tendency for stroke work to be greater for standard repair than for left ventricular aneurysm and patch reconstruction at higher preloads was not statistically significant. Mechanical efficiency, from stroke work/myocardial oxygen consumption (joules per milliliter oxygen per beat), was 2.43 ± 0.52 (mean ± standard error of the mean) (control), 2.22 ± 0.94 (standard repair), 1.27 ± 0.39 (patch reconstruction), and 1.09 ± 0.37 (left ventricular aneurysm) (no significant differences). Regional work was calculated as regional left ventricular wall thickening X J left ventricular pressure. The slope of the regional work-end-diastolic wall thickness relation decreased in the posterior wall14.0 ± 2.9 (control) versus 8.4 ± 2.0 (left ventricular aneurysm), 6.9 ± 1.4 (patch reconstruction), and 7.4 ± 1.4 (standard repair) (p < 0.05). In the anterior wall, contractility did not change significantly (7.4 ± 1.2, control; 7.8 ± 2.7, left ventricular aneurysm; 5.0 ± 0.4, patch reconstruction; and 5.3 ± 0.4, standard repair). Decreased end-diastolic wall thinning anteriorly suggested tethering. These results in the normal left ventricle suggest that patch ventriculoplasty is of no greater benefit than linear repair. Either repair may impede function of adjacent myocardium through restriction of regional diastolic lengthening.

Alfred C. Nicolosi, MD,* Zen-Chung Weng, MD, Paul W. Detwiler, MS, and Henry M. Spotnitz, MD, New York, N.Y.

h e importance of left ventricular (LV) geometry in both systolic and diastolic function has been discussed. 1• 2 Deviation from normal geometry is illustrated most dramatically in LV aneurysm, in which there is marked distortion of both chamber shape and size. Standard aneurysm repair, in which the thinned, from the Cardiovascular Surgery Research Laboratory, Department of Surgery, Columbia University College of Physicians and Surgeons, New York, N.Y. Received for publication July 17, 1989. Accepted for publication Jan. 4, 1990. Address for reprints: Henry M. Spotnitz, MD, Department of Surgery, Columbia University College of Physicians and Surgeons, 630 W. I 68th St., New York, NY 10032. *Recipient of National Research Service Award No. I f32HL07706. Supported in part by U.S. Public Health Service Grant No. JROJHL41163.

12/1/19697

scarred segment is resected and the edges of the ventriculotomy are reapproximated in linear fashion, frequently improves symptoms but has not been shown to consistently improve objective parameters of LV function. 3-5 It has been suggested that standard repair causes greater distortion of LV geometry than existed preoperatively, and some have advocated a repair that attempts to restore native chamber geometry. 6-8 Although studies of several acute models of LV aneurysm have appeared in the literature, 9- 11 they have concentrated on the issue of paradox rather than geometry. In these studies, accessory chambers made of a variety of materials are sutured to the LV free wall and are then connected to the main chamber by a small ventriculotomy. These models have shown the benefits of eliminating the aneurysmal segment; however, by their model design they do not address the issue of geometric properties of the remaining ventricular mass. The purpose of this study, 745

The Journal of Thoracic and Cardiovascular Surgery

7 4 6 Nicolosi et a/.

LV

t

Right heart bypass

Total cardiopulmonary bypass

Roller pump

Fig. 1. Instrumentation and bypass circuit for pigs with experimental LV aneurysm and aneurysm repair. LV. Left ventricular; PA, pulmonary artery. Ultrasonic dimension crystals measure regional wall thickening in segments adjacent to and remote from the site of ventriculoplasty. All venous blood is diverted to the pump, and total CPB is accomplished by returning oxygenated blood to· the femoral artery. RHB, used to evaluate LV function, is accomplished by switching return to the left atrium. Coronary sinus flow is measured by timed drainage of a catheter in the right ventricle while the pulmonary artery is snared.

therefore, is to explore the acute effects of geometric changes on both global and regional LV function in a swine model of LV aneurysm and to compare standard linear repair with patch ventriculoplasty. Methods Surgical preparation. Domestic pigs (n = 6) (45 to 55 kg) were anesthetized with a single intramuscular injection of atropine (2 mg) and ketamine (20 mgfkg). After endotracheal

intubation, the animals' lungs were ventilated with a volumecycled ventilator, with supplemental oxygen and isoflurane (2.0% to 2.5%) used for maintenance of anesthesia. The animals were placed supine, and a median sternotomy was performed. After longitudinal pericardiotomy, the great vessels were isolated and the left hemiazygos vein was ligated. Two micromanometer-tipped catheters (Millar Instruments, Inc., Houston, Tex.) were introduced via peripheral arteries and advanced to the aortic root, where their signals were matched. One was then passed across the aortic valve to measure LV pressure. A fluidfilled port on this catheter was connected to a Statham P-23

Volume 100 Number 5 November 1990

Simulated LV aneurysm in swine

747

Fig. 2. Technique of experimental left ventricular aneurysm and aneurysm repair in swine. A, Normal pig heart, with dashed line indicating planned site and length of ventriculotomy in anterior wall of LV. 8, Separation of ventriculotomy edges. C, Insertion of a 6 by 8 em Dacron patch to simulate LV aneurysm. The suture line is reinforced by long Teflon pledgets on either side; D, Reduction of the patch with plicating sutures to simulate patched reconstruction after aneurysm resection. E, Simulation of standard aneurysm repair by drawing edges of ventriculotomy together in linear fashion. pressure transducer (Spectramed, Inc., Critical Care Division, Oxnard, Calif} Two pairs of ultrasonic dimension crystals (Sonotek Corp., San Diego, Calif.) were used to measure regional wall thickness in the left ventricle. One pair was placed in the anterior wall, adjacent to the planned site of longitudinal ventriculotomy and patch insertion, and the other was placed in the posterobasal region, remote from the planned ventriculoplasty. An electromagnetic flow probe (Carolina Medical Electronics, Inc., King, N.C.) of appropriate size was placed on the aortic root to measure phasic aortic flow. The animals were heparinized (300 IU /kg intravenously) and cannulated for both total cardiopulmonary bypass (CPB) and right heart bypass (RHB) (Fig. I). Superior and inferior caval drainage cannulas were inserted via the right atrium. Arterial inflow for CPB was accomplished via a femoral artery cannula, and for RHB, via a left atrial cannula connected to a separate roller pump. For coronary flow measurements the caval cannulas and pulmonary artery were snared so that only coronary sinus and thebesian venous drainage returned to the right side of the heart. Timed collection of the effluent from a right atrial-right ventricular catheter into a graduated cylinder was used to measure steady-state coronary venous return. Except during steady-state coronary venous return measurements, the pulmonary artery was vented to the pump. The heart-lung machine was primed with I L of whole blood from donor pigs and I L oflactated Ringer's solution mixed with 50 gm of human albumin. Blood was oxygenated with a bubble oxygenator (model S-070/S, Shiley, Inc., Irvine, Calif.), and blood gases were maintained in a physiologic range. After institution of bypass, lung ventilation and isoflurane were discontinued, and pentobarbital, in intermittent doses of approximately 300 mg, was used to maintain anesthesia. Protocol. After instrumentation and cannulation, CPB was begun at a rate 2:50 mljkgjmin. Phenylephrine was used as needed to maintain mean aortic pressure 2:60mm Hg. After stabilization, flow was gradually shifted from the arterial to the left atrial cannula to establish RHB at the same rate. Steady-

state control data were then collected. Flow was rapidly decreased to a minimum and increased to 20% to 25% above control for 15 to 20 seconds to vary preload during collection of LV function data. CPB was then resumed, body temperature was lowered to 28 o C, and a cardioplegia needle was inserted into the aortic root. The aorta was crossclamped, and the heart was arrested with cold, crystalloid cardioplegic solution ( 10 mljkg) and topical hypothermia. The cardioplegic soultion consisted of 5% dextrose in water (I L), to which was added potassium chloride (30 mEq), sodium bicarbonate (30 mEq), and mannitol ( 12.5 mg) to yield a tonicity of 431 mOsmjL and a pH of7.9. A longitudinal ventriculotomy was made in the anterolateral free wall of the LV (in a relatively avascular zone between the left anterior descending coronary artery and circumflex branches), extending from the upper third of the ventricle to the apex. A preclotted and baked, 6 by 8 em, elliptic Dacron (USCI Sauvage filamentous Dacron, Bard, Inc., Billerica, Mass; nominal thickness, 0.7mm) patch was then sutured into the ventriculotomy with polypropylene sutures. The suture line was reinforced by long Teflon pledgets on either side of the ventriculotomy so that there were no leaks. Interrupted horizontal mattress stitches were placed in the patch itself so that it could be plica tedto one half its original minor axis diameter, and large stitches were placed through the pledgets so that the edges of the ventriculotomy could be drawn together in linear fashion. The effect of patch size on LV geometry was estimated from a spherical model. Assuming a physiologic LV end-diastolic volume of70 mi, 12 LV endocardial surface area would be 82 cm2 • A 6 by 8 cmellipsoid patch (total area of38 cm 2) would increase this area 46%. When reduced to one half its minor axis diameter, the patch would increase LV surface area by approximately 23%. After the patch was sewn in, the animal was gradually rewarmed, the cross-clamp was removed, and the heart was deaired and defibrillated. After stabilization on CPB, RHB was resumed for data collection. Data were collected repeatedly with

The Journal of Thoracic and Cardiovascular Surgery

7 4 8 Nicolosi et a/.

120 100

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LVEDP (mm Hg) Fig. 3. Representative global function curves from pigs with experimental left ventricular aneurysm and aneurysm repair. LVA, LV aneurysm; L VEDP, left ventricular end-diastolic pressure. Stroke work is plotted versus L VEDP in each experimental condition. Control curve shows greater stroke work than any of the experimental curves at common levels of preload. There is no apparent difference in stroke work at any level of preload among the three sim· ulated conditions.

Table I. Mean ( ±SE) stroke work in swine model of experimental left ventricular aneurysm and (lneurysm repair (n = 6) LVEDP (mmHg) 10 12 14 16 18 20

Stroke work (ergs X Irl) 8.4 19.0 29.1 38.7 47.8 56.4

± ± ± ± ± ±

2.2 2.7 4.0 5.5 6.9 8.2

SR

PR

LVA 14.4 21.7 30.9 42.1 55.3 70.3

± ± ± ± ± ±

3.7 5.5 7.5 9.5 12 14.8

12.7 28.7 48.1 66.4 88.1 111.8

± ± ± ± ± ±

5.3 10.8 16.5 23.5 31.1 39.8

SE, Standard error; L VEDP, LV end-diastolic pressure; LV A, LV aneurysm; PR, patch reconstruction; SR, standard repair.

the patch in three configurations: patch fully open (LV aneurysm), patch partially plica ted, simulating patch reconstruction, and ventricular margins drawn together, simulating standard repair (Fig. 2). The order of data collection in these configurations was varied with each experiment. After final data collection, the heart was arrested with hyperkalemic injection into the aortic root, rapidly excised, and weighed. Data analysis. Data were acquired on a multichannel oscillograph (model DR-12, Electronics for Medicine, White Plains, NY) and digitized with a digital computer (Macintosh Plus, Apple computer), an x-y digitizing tablet (MacTablet, Summagraphics, Seymour, Conn.), and commercial software

(MacDraft, Innovative Data Design, Inc., Concord, Calif.). For each condition (control, LV aneurysm, patch reConstruction, standard repair), data were acquired in the steady state and during periods of preload variation. Global LV function was estimated from Frank-Starling curves, relating stroke work (SW) to LV end-diastolic pressure (LVEDP). Stroke work (in ergs) was calculated as follows: SW

= J LV X 1330 X SV

where J LV is the area under the LV pressure trace for a single beat (in mm Hg), as determined by planimetry, and SV is stroke volume for the same beat as determined by measuring the area under the aortic flow trace during ejection. For each beat, stroke work was plotted against L VED P and the points were fitted with a second-order polynomial equation by commercial software (Cricket Graph, Cricket Software, Malvern, Pa.). The equations were then solved at preload intervals of 2 mm Hg over the range of I 0 to 20 mm Hg. Regional LV function was estimated from regional stroke work-end-diastolic thickness relations in each state. Regional stroke work (RSW, in ergs X cm- 2) was calculated as follows: RSW =

J LV X 1330 X .:lth

where J LV is the area under the LV pressure curve as determined by planimetry and .:lth is the change in regional wall thickness from end-diastole to end-systole for the same beat. Regional stroke work was then plotted against the inverse of end-diastolic thickness (EDth- 1) for each beat and the points were fitted with a linear equation. (EDth- 1 was used to obtain

Volume 100 Number 5 November 1990

Simulated LV aneurysm in swine

749

120 100

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LVEDP (mm Hg) Fig. 4. Mean global function curves in pigs with experimental LV aneurysm and aneurysm repair (n = 6). LVA, LV aneurysm; L VEDP, left ventricular end-diastolic pressure. Data points for each condition were fit with a secondorde~ polynomial in each experiment, and stroke work was calculated at L VEDP intervals of 2 mm Hg over the range of 10 to 20 mm Hg. Although mean stroke work apppears higher with standard repair at most levels of preload, there are no statistical differences among the three groups at any level.

lines with positive slopes.) Similar methods, with use of global L Y dimensions and regional segment length rather than wall thickness, have shown that this is a highly linear relation in which changes in slope reflect changes in myocardial contractility.13 Global mechanical efficiency was estimated from the ratio of steady-state stroke work (in joules) and myocardial oxygen consumption (MV0 2) per beat. Stroke work was calculated as explained previously for three beats in the steady state and averaged. Myocardial oxygen consumption (ml 0 2/min) was calculated as follows:

Statistical significance was defined asap value <0.05. Data are presented as the mean ± standard error of the mean. All animals have received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and "Guide for the Care and Use of Laboratory Animals" prepared by the National Academy of Sciences and published by National Institutes of Health (NIH Publication No. 80-23, revised 1978).

MV02 = (A - CS) X Q

Global LV function curves from a representative experiment are shown in Fig. 3. Curve fits with secondorder polynomials yielded r values greater than 0.95 in most cases. Stroke work is higher in the control state at all levels of end-diastolic pressure in common with the subsequent experimental states. Mean results comparing global function in the three experimental states are presented in Fig. 4 and Table I. A tendency toward improved function is apparent with standard repair; however, none of the differences among the three simulated states was statistically significant. Mean values for the ratio of steady-state stroke work to myocardial oxygen consumption, reflecting myocardial mechanical efficiency, were 2.43 ± 0.52 in the control state, 2.22 ± 0.94 for standard repair, 1.27 ± 0.39 for

where (A - CS) is the differer..::e between arterial and coronary venous oxygen content in milliliters oxygen per minute and Q is coronary venous flow in milliliters per minute, collected from the right atrial-right ventricular catheter. Blood gases were measured on a model 713 analyzer (Instrumentation Laboratories, Inc., Lexington, Mass.). Myocardial oxygen consumption was divided by heart rate to obtain oxygen consumption on a per beat basis. Data in each patch configuration were averaged for the six experiments, and analysis of variance (ANOV A) for repeated measures was performed on global function values, the slope of regional function relations, and efficiency results. Heart rate, mean aortic pressure, left atrial flow, L VEDP, and peak systolic L Y pressure (LV peak) in the steady state were also compared by ANOVA. Regional systolic function in the adjacent and remote segments was compared in each state by paired t test.

Results

The Journal of Thoracic and Cardiovascular

7 5 0 Nicolosi et a/.

Surgery

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Fig. 5. Representative regional function relations in pigs with experimental left ventricular aneurysm and aneurysm repair. LVA, LV aneurysm; EDth, end-diastolic thickness. The relation of regional stroke work to EDth- 1 is linear, with changes in slope directly reflecting changes in contractility. A, Changes in regional performance adjacent to the patch and suture line. Slope in all three experimental states is decreased somewhat from control. B, Changes in regional performance remote from the patch and suture line from the same experiment. Slope in all three experimental states is markedly decreased from control.

patch reconstruction, and 1.09 ± 0.37 for LV aneurysm (Table II). These differences were not statistically significant, although efficiency tended to be closest to control with standard repair. Representative regional function relations from a typ-

ical experiment are shown for adjacent and remote regions in Fig. 5. The regional stroke work-inverse of end-diastolic thickness relation is highly linear, with r values consistently greater than 0.95. The slope of the relation, a measure of contractility, decreases in both

Volume 100 Number 5 November 1990

Simulated LV aneurysm in swine

0

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Fig •. 6. Representative plot comparing end-diastolic thickness during volume loading in the anterior and posterior walls of pigs with experimental left ventricular aneurysm and aneurysm repair. LVA, LV aneurysm. The anterior wall is adjacent to the suture line, and the posterior wall is a remote site. The relations are highly linear. Slope in all three experimental states is greater than control, indicating a greater sensitivity of remote segment contractile elements to volume changes and suggesting a tethering of adjacent segment to the suture line.

Table II. Mean (±SE) mechanical efficiency in pigs

with experimental LV aneurysm and aneurysm repair (n = 6) Experimental condition Control LV aneurysm Patch reconstruction Standard repair

Efficiency (joules per milliliter oxygen per beat) 2.43 1.09 1.27 2.22

± 0.52 ± 0.37 ± 0.39 ± 0.94

SE, Standard error.

regions after a period of ischemic arrest and alteration of LV geometry; this change is more marked in the remote region. Mean results are shown in Table III. In the anterior wall, adjacent to the edge of the planned ventriculoplasty, mean slope of the relation was 7.43 ± 1.21 at control, 7.82 ± 2.70 for LV aneurysm, 5.33 ± 0.44 for standard repair, and 4.98 ± 0.38 for patch reconstruction. None of these differences was statistically significant. In the posterobasal segment, remote from the site of ventriculoplasty, mean slope was 14.02 ± 2.86 at control, 8.44 ± 2.05 for LV aneurysm, 7.36 ± 1.45 for standard repair, and 6.91 ± 1.37 for patch reconstruction

Table III Mean (±SE) slope of regional stroke work versus end-diastolic wall thickness relation in pigs with experimental LV aneurysm and aneurysm repair (n = 6)

Experimental condition Control LV aneurysm Patch reconstruction Standard repair

Adjacent* 7.43 7.82 4.98 5.33

± 1.21 ± 2.71

± 0.38 ± 0.44

Remotef 14.02 8.44 6.91 7.36

± 2.86 ± 2.05:j: ± 1.37:j: ± 1.45:j:

SE, Standard error of the mean. *Adjacent to site of anterolateral ventriculoplasty. tRemote from site of anterolateral ventriculoplasty. ;j:p < 0.05 versus control.

(p < 0.05 for LV aneurysm, standard repair, and patch reconstruction versus control). The three experimental conditions did not differ significantly from each other. The decrease in mean regional slope from control to LV aneurysm was statistically greater in the remote segment than in the adjacent segment ( -5.57 ± 2.26 versus 0.39 ± 2.08). Larger apparent decreases in mean slope for remote versus adjacent regions with patch reconstruction (-7.10 ± 1.91 versus -2.45 ± 1.04) and standard

The Joarnal of Thoracic and Cardiovascular Surgery

7 5 2 Nicolosi et a/.

50

40

30 LV = 175g Sphere EDV = 105 ml (no patch) Surface= 100 em sq (no patch) 20

;----r---r--~--------~--r---~--~--~--~

0

90 120 60 30 centimeters square Patch Size

150

Fig. 7. Computer prediction of effect of patch size on stroke volume (SV), ejection fraction (EF), and midwall systolic stress ( afterload) at a chamber pressure of I 00 mm Hg. The assumptions include a constant shortening fraction of the viable portion of the endocardial surface. The ventricle is defined as a uniformly contracting sphere despite the addition of an increasingly large akinetic section. Diastolic tethering, impaired shortening with increasing ~Iter­ load, and elimination of paradox are not Considered. The results predict a favorable effect of increasing patch size on stroke volume and adverse effects on ejection fraction and afterload. Since increasing afterload in reality decreases muscle shortening, patch reconstruction can increase stroke volume only if contractile reserve is sufficient to overcome the afterload resulting from increased ventricular size.

repair (-6.66 ± 1.95 versus -2.10 ± 1.00) were not statistically significant. To analyze differences between remote and adjacent segments, the relation between adjacent and remote enddiastolic thickness during volume loading was examined; a typical example is shown in Fig. 6. The slope of the relation indicates the extent of preload change in one wall with respect to the other. If the slope of the line equals one, then they change at the same rate. As slope deviates from unity, then changing end-diastolic volume has a different effect on one wall than on the other. Mean slope of this relation for the six experiments was 0.79 ± 0.15 at control, 1.27 ± 0.15 for LV aneurysm, 1.32 ± 0.22 for patch reconstruction, and 1.80 ± 0.42 for standard repair. The difference between control and standard reconstruction was statistically significant (p < 0.05). Mean steady-state hemodynamics are presented in

Table IV. There were no significant differences between LV aneurysm, patch reconstruction, and standard repair. Mean RHB flow in LV aneurysm, patch reconstruction, and standard repair was significantly less than control (2613 ± 135 versus 2850 ± 178 mljmin, p < 0.05). Other statistically significant differences for LV aneurysm, patch reconstruction, and standard repair versus control were increased heart rate and decreased mean aortic pressure, stroke volume, and stroke work. There were no significant changes in LV, EDP, or peak LV pressure.

Discussion The present study employs a new animal model of LV aneurysm allowing repair techniques to be simulated. The results define changes in global and regional LV performance associated with acute changes in chamber geom-

Volume 100 Number 5 November 1990

Simulated LV aneurysm in swine

753

Table IV. Mean ( ±SE) steady-state hemodynamics in pigs with experimental LV aneurysm and aneurysm repair (n = 6)

Heart rate Left atrial flow LVEDP MAP LV peak Stroke volume

116 ± 8 2850± 178 12 ±I 69 ± 3 93 ± 2 29 ± 4

PR

LVA

Control

136 2613 14 55 85 19

± ± ± ± ± ±

8* 134* I 2* 4 2*

141 2613 13 56 83 20

± 13* ± 134* ±I ± 6* ± 2 ± 3*

SR 135 2613 15 58 88 23

± 9* ± 134* ±I ± 5* ± 5 ± 3*

SE, Standard error of the mean; LV A, LV aneurysm; PR, patch reconstruction; SR, standard repair; LVEDP, LV end-diastolic-pressure; MAP, mean aortic pressure; L Y peak, peak L Y systolic pressure. p < 0.05 versus control.

etry. We find no substantial benefit of patch ventriculoplasty compared with linear closure either in global LV function or in mechanical efficiency. The data also demonstrate restricted diastolic lengthening of myocardium adjacent to the anterior suture line. Acute animal models of LV aneurysm have been reported previously. 9- 11 Austen and colleagues9 reported the first of these, in which urinary bladder was fashioned into an accessory chamber, attached to the epicardial surface of the LV, and made continuous with the LV chamber by excising a disk of myocardium, 2 em in diameter. Such models produce little or no geometric change in radii of curvature of the ventricle, an important omission since radius is known to be an essential determinant of both preload and afterload through effects on wall stress. 14 In our model, a large ventriculotomy, extending from the upper third of the anterolateral wall to the apex, allowed wide separation of the ventriculotomy edges; interposition of a patch of variable size allowed effects of altered ventricular geometry to be assessed. Our data do not demonstrate any benefit of patch size on global LV function or efficiency when the perimeter of the patch (suture line) is maintained constant in length. This result may in part reflect use of an acute model based on a normal heart. LV aneurysm reflects postinfarction adaptive changes in regional wall thickness and radii of curvature evolving for days to weeks. 15 Clinical LV aneurysm also involves increased LV end-diastolic volume, a loss of muscle mass in the area of infarction, and a hypertrophic or myopathic response (or both) of remote myocardium. 16 It is thus possible that studies in infarcted hearts with LV aneurysm would differ from the present results. However, the present study defines methods that may be useful in such studies, including the immediate assessment of functional effects of changing geometry in the beating heart. On the other hand, the large body of clinical data suggesting that LV function is often not improved by LV aneurysm repair 3· 5 is consistent with our failure to dem-

onstrate effects of LV chamber geometry on global performance.lt has also been shown clinically that effects of LV aneurysm resection are dependent on preoperative global function, specifically that preoperative ejection fraction less than 45% in the contractile segment remote from the infarction predicts increased morbidityP· 18 One possible implication of this is that effects of variation in chamber geometry may be affected by contractility. Discussion of a possible mechanism follows. The present results, based on prior evidence that wall thickness is equivalent to muscle length for contractility analysis, 19· 20 provide unique insight into regional effects of reconstruction. Thus contractility in the remote (posterior) wall segment, .measured from the slope of the regional work-inverse of end-diastolic thickness, was significantly depressed after reconstruction compared with control, consistent with global data. In contrast, no significant change in contractility was observed in the adjacent (anterior) crystal pair. The simulated LV aneurysm repairs also demonstrate no reduction of early systolic paradox in segments adjacent to the aneurysm, an effect documented in a previous clinical study from our laboratory. 21 We speculate that the observed difference in behavior of the anterior and posterior segments primarily reflects myocardial tethering, which conceals depressed contractility anteriorly by limiting diastolic thinning. We must also account for what appear to be regional differences in contractility in the control state. This reflects a recognized problem with regional contractility analysis based on wall thickness, that is, the extent to which crystal placement reflects this thickness. The regional volume of myocardium influencing thickness in the segment under observation is also a factor, and this could be influenced by heterogeneity of fiber orientation.14· 22 For these reasons, regional wall thickness analysis is primarily useful for demonstrating changes in function within a given region. Conversely, current methods for regional contractility analysis have not been shown to be useful for comparison of absolute levels of function

The Journa·l of

7 5 4 Nicolosi et a/.

in different regions or in different hearts. Validity of proposed "normalization" techniques has not been confirmed.l9, 20 As stated, our results appear to refleet strongly a previously unappreciated or underemphasized local effect of the suture line on adjacent myocardium. The evidence for this is a statistically significant change in the slope relating anterior and posterior end-diastolic wall thickness during volume loading. The change is such that, after geometric reconstruction, thinning of the posterior wall becomes disproportionately greater than simultaneous thinning of the anterior wall. We conclude that thinning of the anterior wall (and increasing fiber and sarcomere length) is restricted by patch reconstruction. In contrast to diastolic tethering, our data show minimal change in end-systolic wall thickness after reconstruction. This indicates that adverse effects of the patch and suture line on adjacent tissues in our model are primarily diastolic rather than systolic effects. Attachment of a longitudinal patch or a Teflon strip, or both, would be expected to have greater effect toward the apex, where the proportion of obliquely oriented fibers becomes greater. 22 Whether tethering is important clinically in LV aneurysm repair will depend on the degree to which the scar resected before reconstruction is restrictive. Conversely, when compliant myocardium is replaced or augmented by a patch, as in infarctectomy or repair of congenital heart disease, the tethering effect described here is likely to apply. Knowledge of regional variation in wall thickness with volume loading is incomplete. We do not find a slope different from 1.0 in the control state in Fig. 6 indicative of methodologic problems, but the precise causes are unknown. Contributing factors include differences in fiber orientation22 and heterogeneity of the myocardial redistribution mechanism, which allows wall thickness to change during changes in end-diastolic volume. 23 Diastolic tethering might also minimize global effects of changing geometry, including the tendency for indices of global LV function and efficiency to improve .with standard repair as compared with patch reconstruction and LV aneurysm. Klein, Herman, and Gorlin 24 noted impaired global LV performance in patients whose aneurysm comprised more than 20% of LV surface area, but not in those whose aneurysm was less than 15% of LV surface area. Similarly, Weisman and colleagues 15 showed global cardiac dilatation in rats surviving transmural infarction of more than 22% of LV mass, while infarcts less than this are associated with no global remodeling. LV aneurysm resection is highly complex, reflecting a large spectrum of clinical presentation. Acute and chron-

Thoracic and Cardiovascular Surgery

ic effects of surgery on ventricular size, contractility, coronary blood flow, and mitral integrity all must be considered. A large, paradoxic aneurysm resulting from single-vessel disease in a ventricle with large cavity size and excellent function of uninvolved myocardium is usually dealt wilth successfully. The globally hypokinetic ventricle with multivessel disease and a large, akinetic transmural scar is far more difficult. Computer analysis based on geometric considerations alone indicates that an akinetic patch of increasing size will, in theory, increase stroke volume while increasing afterload and decreasing ejection fraction (Fig. 7). If this is correct, the mark of inadequate chamber size would be a vigorous LV with clinically inadequate stroke volume, whereas the mark of excessive size would be a dilated, hypokinetic ventricle associated with biventricular power failure. The present results suggest that diastolic tethering resulting from LV aneurysm repair may also be of clinical importance. These concepts are difficult, and previous analytic methods have been unable to synthesize a simple, consistent solution. The present study represents a first step in an empiric approach, defining a model that allows geometry to be varied in the beating heart. Further progress requires a reproducible animal model of LV aneurysm, perhaps based on recent methods. 25 • 26 Both acute and chronic studies are needed to explore not only hemodynamics and regional function, but also myocardial sarcomere length and LV fiber distribution. 14• 22 The results cannot be predicted. Perhaps mathematic rules derived from finite element analysis 27 or other computer techniques can define optimum functional geometry for individual patients. Perhaps an empiric approach, varying geometry while measuring function on CPB, will prove useful. A method to allow full diastolic lengthening of myocardium adjacent to the repair similarly has not been defined, and the role of diastolic loading conditions in ventricular reconstruction also merits further study. In summary, we have defined an acute model of LV aneurysm based on the normal heart. The model employs acute variation of ventricular geometry to simulate effects of current methods of aneurysm repair. Functional analysis is derived from both global and regional data. On the basis of this model, we conclude that patch repair offers no advantage over linear closure if ventricular size is sufficient. Furthermore, either repair may impede function of adjacent myocardium through a tethering effect, which impairs regional diastolic lengthening. Further studies are needed to determine tbe relevance o\ tbese resu\ts to tbe clinical problem of LV aneurysm. We wish to acknowledge Anthony Cuffy, Santos Cabreriza, and Lars Weiss, whose technical support was invaluable.

Volume 100

Simulated LV aneurysm in swine

Number 5 November 1990

REFERENCES I. Burton A C. The importance of the shape and size of the heart. Am Heart J 1957;54:801-10. 2. Hutchins GM, Bulkley BH, Moore GW, Piasio MA, Lohr FT. Shape of the human cardiac ventricles. Am J Cardia! 1978;41 :646-54. 3. Froehlich RT, Falsetti HL, Doty DB, Marcus ML. Prospective study of surgery for left ventricular aneurysm. Am J Cardia! 1980;45:923-31. 4. Taylor NC, Barber R, Crossland P, Wraight EP, English T AH, Petch MC. Does left ventricular aneurysmectomy improve ventricular function in patients undergoing coronary bypass surgery? Br Heart J 1985;54:145-52. 5. Dymond DS, Stephens JD, Stone DL, Elliott AT, Redes GM, Spurrell RAJ. Combined exercise radionuclide and hemodynamic evaluation of left ventricular aneurysmectomy. Am Heart J 1982;104:977-87. 6. Hutchins GM, Brawley RK. The influence of cardiac geometry on the results of ventricular aneurysm repair. Am J Pathol1980;99:221-7. 7. Jatene AD. Left ventricular aneurysmectomy-resection or reconstruction. J THORAC CARDIOVASC SURG 1985; 89:321-331. 8. Dor V, Saab M, Coste P, Kornaszewska M, Montiglio F. Left ventricular aneurysm: a new surgical approach. Thorae Cardiovasc Surg 1.989;37:11-9. 9. Austen WG, Tsunekawa T, Bender HW, Ebert PA, Morrow AH. The acute hemodynamic effects of left ventricular aneurysm-an experimental study in dogs. J Surg Res 1962;2: 161-7. 10. Tyson K, Mandelbaum I, Shumacker HB. Experimental production and study of left ventricular aneurysms. J THO.. RAC CARDIOVASC SURG 1962;44:731-7. II. Derrick JR, Del Williams R, Humphrey AL. Hemodynamic consideration of aneurysms of the heart. Ann Thorae Surg 1966;2:607 -II. 12. Weng Z-C, Schierman SW, Goldstein A W, Nicolosi AC, Spontnitz HM. Effects of perfusate tonicity on myocardial edema and compliance. Circulation 1988;78(Pt 2):11446. 13. Glower DO, Spratt JA, Snow NO, eta!. Linearity of the Frank-Starling relationship in the intact heart: the concept of preload recruitable stroke work. Circulation 1985; 71:994-1003. 14. Streeter DO, Vaishnav RN, Patel OJ, Spotnitz HM, Ross J Jr, Sonnenblick EH. Stress distribution in the canine left

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