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J Thorac Cardiovasc Surg 2006;132:610-620
© 2006 The American Association for Thoracic Surgery
Surgery for Acquired Cardiovascular Disease |
a Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands
b Department of Cardio-Thoracic Surgery, Leiden University Medical Center, Leiden, The Netherlands
Received for publication July 12, 2005; revisions received December 15, 2005; accepted for publication December 22, 2005. * Address for reprints: Paul Steendijk, PhD, Leiden University Medical Center, Department of Cardiology, PO box 9600, 2300 RC Leiden, The Netherlands (Email: p.steendijk{at}lumc.nl).
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Abstract |
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METHODS: In 3 patient groups (total, n = 33), pressure-volume loops were measured by conductance catheter before and after surgery. The main study group consisted of 10 patients with ischemic dilated cardiomyopathy (New York Heart Association class III/IV, left ventricular ejection fraction <30%) who had surgical ventricular restoration and coronary artery bypass grafting. In this group, 7 patients had additional restrictive mitral annuloplasty. To assess potential confounding effects of restrictive mitral annuloplasty and cardiopulmonary bypass, we included a group of 10 patients (New York Heart Association class III/IV, left ventricular ejection fraction <30%) who had isolated restrictive mitral annuloplasty and a group of 13 patients with preserved left ventricular function who had isolated coronary artery bypass grafting.
RESULTS: After surgical ventricular restoration, end-diastolic and end-systolic volumes were reduced from 211 ± 54 to 169 ± 34 mL (P = .03) and from 147 ± 41 to 110 ± 59 mL (P = .04), respectively. Left ventricular ejection fraction (from 27% ± 7% to 37% ± 13%, P = .04) and end-systolic elastance (from 1.12 ± 0.71 to 1.57 ± 0.63 mm Hg/mL, P = .03) improved. Peak wall stress (from 358 ± 108 to 244 ± 79 mm Hg, P < .01) and mechanical dyssynchrony (from 26% ± 4% to 19% ± 6%, P < .01) were reduced, whereas mechanical efficiency improved (from 0.34 ± 13 to 0.49 ± 0.14, P = .03). End-diastolic pressure increased (from 13 ± 6 to 20 ± 5 mm Hg, P < .01), whereas the diastolic chamber stiffness constant tended to be increased (from 0.021 ± 0.009 to 0.037 ± 0.021 mL–1, NS).
CONCLUSIONS: Surgical ventricular restoration achieves normalization of left ventricular volumes and improves systolic function and mechanical efficiency by reducing left ventricular wall stress and mechanical dyssynchrony.
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Introduction |
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Surgical ventricular restoration (SVR) by means of endoventricular circular patch plasty (Dor procedure) is beneficial in patients with left ventricular (LV) postinfarction aneurysm. Previous studies have shown that this procedure is safe and improves functional class, long-term survival, and LV ejection fraction.1,2 The exclusion of akinetic or dyskinetic segments achieves acute volume reduction, changes in LV shape, and decreases of LV dyssynchrony.3,4 These acute changes influence LV global and intrinsic systolic and diastolic function. The use of pressure-volume analysis to assess these effects is advantageous because pressure-volume relations accurately reflect intrinsic LV function and are relatively independent of loading conditions.5,6 Moreover, pressure-volume signals can be used to quantify mechanical dyssynchrony and LV wall stress.7
Theoretical studies predict that volume reduction surgery results in leftward and upward shifts of the end-systolic and end-diastolic pressure-volume relations in the pressure-volume diagram, indicating a positive effect on systolic function but an adverse effect on diastolic function.8,9 However, these effects are likely to be modulated by the material properties and the size of the resected or excluded region. Artrip and colleagues quantified the differential effects of volume reduction on end-systolic and end-diastolic function in a mathematical model.10 Their findings indicate that an overall negative effect on LV pump function results if weak but contracting myocardium is resected (like in the Batista procedure), beneficial effects if the excised region is dyskinetic, and equivocal effects with akinetic scar resection. However, whether these models are realistic is unknown because in vivo data on the effects of SVR and related procedures on LV pressure-volume relations in humans are very limited. One important aspect, which is not taken into account by these particular models, is (alterations in) mechanical dyssynchrony. Recent studies demonstrated that LV mechanical synchrony substantially improves after SVR, resulting in more efficient myocardial pump function.3,4 Furthermore, a recent special report from the RESTORE group emphasized the importance of considering interaction and (re)arrangement of myocardial layers and fiber orientation and stressed the need for additional studies to quantify the effects of SVR and to get a better insight in the underlying mechanisms.11
As SVR reversely remodels ventricular size and shape, this approach may alter systolic and diastolic function.11,12 Additionally, SVR may decrease LV wall stress and myocardial oxygen consumption by reducing end-diastolic volume, resulting in improved functioning of the remote myocardium.13 The aim of this study was to determine the acute effects of SVR on systolic and diastolic pressure-volume relationships, LV wall stress, and mechanical dyssynchrony and efficiency in patients with ischemic dilated cardiomyopathy.
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Methods |
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2 Note that some patients in the SVR group had additional RMA, whereas in both the SVR and the RMA groups, CABG was performed if indicated. Details are provided in the Results section. The study was approved by the institutional review committee and all patients gave informed consent. The patient characteristics of the 3 groups are summarized in Table 1.
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We anticipated that the heart failure patient would need inotropic support after surgery. As this would bias our LV function measurements, we started inotropic support directly after induction with a low loading dose of 0.25 mg/kg enoximone in 10 minutes and thereafter we gave continuous infusion at a rate of 0.50 µg/kg/min, which was maintained during the whole operation.
Surgical Techniques
Dor plasty
SVR was performed by means of endoventricular circular patch plasty as previously described by Dor and associates.15,16 Briefly, the LV was opened through the infarcted area. An endocardial encircling suture (Fontan stitch) was placed at the transitional zone between scarred and normal tissue. A balloon containing 55 mL/m2 saline was introduced into the LV, and the Fontan stitch was tightened to approximate the ventricular wall to the balloon. An oval dacron patch was tailored and used to close the residual orifice. The excluded scar tissue was closed over the patch to ensure hemostasis. Care was taken to eliminate all the septal scar and to delineate a new LV apex with the goal to restore the normal elliptical shape.
Mitral valve repair
A stringent restrictive (2 sizes smaller than measured) mitral annuloplasty was performed via an atrial transseptal approach using a Carpentier Edwards Physio ring (Edwards Lifesciences, Irvine, Calif). After weaning from cardiopulmonary bypass, transesophageal echocardiographic evaluation was performed in all patients to confirm disappearance of mitral regurgitation and assess the length of leaflet coaptation (aiming at 8 mm).
Study Protocol
Before and directly after cardiopulmonary bypass, conductance catheter measurements were performed as described previously.17 Briefly, temporary epicardial pacemaker wires were placed on the right atrium to enable measurements at fixed heart rates. A tourniquet was placed around the inferior caval vein to enable temporary preload reductions. An 8-French sheath was placed in the ascending aorta for introduction of the conductance catheter. The conductance catheter was introduced under transesophageal echocardiographic guidance and placed along the long axis of the LV. The position was optimized by inspection of the segmental volume signals. Conductance catheter calibration was performed using calibration factors alpha (
), derived from thermodilution, and parallel conductance correction volume (Vc), determined by hypertonic saline injections.5,18 Continuous LV pressure and volume signals derived from the conductance catheter were displayed and acquired at a 250-Hz sampling rate using a Leycom CFL-512 (CD Leycom, Zoetermeer, The Netherlands). Data were acquired during steady state and during temporary caval vein occlusion, all with the ventilator turned off at end-expiration. Acquisition was performed at a fixed atrial pacing rate of 80 beats/min. From these signals hemodynamic indexes were derived as described below.
Data Analysis
Global LV function
We determined indexes of global, systolic, and diastolic LV function. Cardiac output was obtained by thermodilution, heart rate, mean arterial pressure, stroke volume, LV ejection fraction, minimal and maximal rate of LV pressure change (dP/dtMIN and dP/dtMAX, respectively), end-diastolic volume, end-systolic volume, end-diastolic pressure, and end-systolic pressure and were obtained from steady-state beats using custom-made software. In addition, we assessed the early, active part of relaxation by the relaxation time constant (
), which was determined by fitting LV pressure decay (starting at the moment of minimal dP/dt) with an exponential curve, as described previously19: P(t) = A + B · exp(–t/). Time-varying wall stress, WS(t), was calculated from instantaneous LV pressure and volume signals (P(t) and V(t), respectively) as described by Arts and colleagues20: WS(t) = P(t) · [1 + 3 · V(t)/VWALL]. LV wall volume (VWALL) was estimated based on the diastolic posterior wall thickness derived from M-mode echocardiography.
Mechanical work and efficiency
Stroke work (SW) was determined as the area of the pressure-volume loop, which represents the external work performed by the ventricle. Pressure-volume area (PVA), a measure of total mechanical work, was calculated as the sum of stroke work and potential energy. The latter represents mechanical energy loss converted to heat during the cardiac cycle and is quantified by the triangular area enclosed by the pressure-volume loop, the end-systolic pressure–volume relation, and the end-diastolic pressure–volume relation.21,22 Mechanical efficiency (ME) was calculated as the ratio of stroke work and pressure-volume area: ME = SW/PVA.23
Mechanical dyssynchrony
Nonuniform LV performance (dyssynchrony) was determined from the segmental LV conductance signals and quantified by calculating the percentage of time within the cardiac cycle that a specific segment is dyssynchronous (ie, opposite in phase with the global LV volume signal). Overall LV mechanical dyssynchrony was determined as the mean of the segmental dyssynchronies. In addition, we calculated the internal flow fraction, which quantifies the ineffective, segment-to-segment shifting of blood volume within the LV due to nonuniform contraction and filling. This approach was described and validated versus tissue Doppler imaging in a previous study.7
Systolic and diastolic pressure–volume relations
Ventricular function was assessed by systolic and diastolic pressure–volume relations derived from pressure-volume loops acquired during gradual preload reduction by vena cava occlusion. The end-systolic pressure–volume relation (ESPVR) was obtained as a linear fit to the end-systolic pressure–volume points and characterized by its slope, end-systolic elastance (EES), and the volume intercept at an end-systolic pressure of 80 mm Hg (ESV80). As illustrated in Figure 1, ESV80 is the end-systolic volume at a pressure of 80 mm Hg based on the curve fit of the ESPVR. The end-diastolic pressure–volume points were fitted with an exponential curve: EDP = A + B · exp (KED
· EDV). As shown in Figure 1, this relation was quantified by the diastolic stiffness constant (KED), the pressure intercept at an end-diastolic volume of 0 mL (EDP0), and the calculated volume intercept at an end-diastolic pressure of 14 mm Hg (EDV14).24,25 Overall ventricular performance was assessed by the preload recruitable stroke work relation (PRSW: relation between SW and end-diastolic volume), which reflects the Frank-Starling relationship in the intact heart.26 PRSW was characterized by its slope MPRSW and the position of the relation (volume intercept) at a SW of 4.5 mm Hg · L (EDV4.5). Note that the end-systolic pressure of 80 mm Hg, end-diastolic pressure of 14 mm Hg, and SW of 4.5 mm Hg · L, which were used to quantify the positions of the various relations, were retrospectively selected as the approximate mean values of these variables over all patients in the study.
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All data are presented as the mean ± standard deviation. |
Results |
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) was improved, and end-diastolic pressure was significantly increased. Mechanical dyssynchrony and the internal flow fraction were reduced in all groups; however, these changes were most pronounced and only reached statistical significance in the SVR group (Figure 3).
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Discussion |
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We quantified the immediate hemodynamic effects of SVR on load-independent systolic and diastolic LV pressure-volume relations in combination with effects on LV wall stress and mechanical dyssynchrony and efficiency in patients with ischemic dilated cardiomyopathy. Our results show that SVR significantly improved LV systolic function (LV ejection fraction, end-systolic pressure–volume relation) and reduced LV wall stress and mechanical dyssynchrony. In addition, LV mechanical efficiency was significantly improved. LV diastolic function, however, appeared to be compromised: the diastolic pressure–volume relation was significantly shifted toward smaller volumes and tended to be steeper, as evidenced by an increased diastolic stiffness constant, although the latter effect did not reach statistical significance.
The relatively small changes in systolic function in the patients who had isolated restrictive mitral annuloplasty and in the patients who had elective CABG indicate that the systolic improvements in the SVR group were mainly related to LV restoration. The increase in LV ejection fraction after SVR was attributed to the surgical reduction in end-diastolic volume, as LV stroke volume was unchanged. However, LV ejection fraction may not be an accurate parameter of systolic improvement after SVR because loading conditions may have changed substantially after surgery. Thus, load-independent pressure–volume relations are needed to quantify alterations in systolic function. The slope of the end-systolic pressure–volume relation, end-systolic elastance EES, is a load-independent parameter of systolic function, and EES increased significantly after SVR. Moreover, the end-systolic pressure–volume relation was significantly shifted toward smaller volumes, also indicating improved systolic function.27,28 This improvement may be the result of increased systolic stiffness induced by exclusion of a large compliant area, as predicted by computational models,10 or due to improved function of the remote myocardium by reduced LV wall stress and reduced LV mechanical dyssynchrony after exclusion of the aneurysm.3,4
Regarding diastolic function, relaxation time constant was significantly reduced, indicating faster relaxation. This time-constant quantifies the speed of LV pressure decay during isovolumic relaxation (ie, between aortic valve closure and mitral valve opening, which represent the very early, and active, part of relaxation), which is considered to be importantly codetermined by systolic function.29 This change may result from coronary revascularization—which may enhance the oxygen-dependent reuptake process of calcium by the sarcoplasmic reticulum—or from an afterload reduction as active relaxation is afterload-dependent.30 Passive diastolic function was assessed by the diastolic pressure-volume relationship. Our results show that SVR induced a substantial leftward shift of the end-diastolic pressure-volume relation as quantified by the significant decrease in EDV14. In addition, the diastolic stiffness constant KED tended to increase, indicating by an enhanced steepness of the curve. Interestingly, diastolic chamber stiffness had a tendency to increase in all groups with a similar magnitude, although the effects did not reach statistical significance. This suggests that the increased diastolic stiffness may be contributed largely to the effect of the cardiopulmonary bypass and cardioplegic arrest leading to interstitial edema.31 In our center, normothermic cardiopulmonary bypass and intermittent antegrade warm blood cardioplegia is routinely used32 because this approach may provide metabolic benefits33,34 and less cell damage,35 possibly mediated by a better protection from ischemia-reperfusion injury. Our study was not designed to investigate whether alternative cardioplegic approaches have less effect on postoperative diastolic function, but previous experimental studies do not appear to show important differences regarding myocardial edema formation and postoperative diastolic compliance between warm and cold blood approaches.36
The results in our study are in line with predictions of Artrip and colleagues, which were based on a composite model of the left ventricle.10 The results of their study emphasize the importance of the material properties of the region being removed. It was predicted that resection of weak but contracting muscle such as may occur with the partial left ventriculectomy (Batista procedure) will lead to a greater leftward shift for the end-diastolic pressure–volume relation than for the end-systolic pressure–volume relation, resulting in an overall negative effects on cardiac performance. Schreuder and associates studied the acute effects of partial left ventriculectomy in humans with dilated cardiomyopathy on LV pressure–volume relations and found significant improvements of systolic function and mechanical synchrony after surgery.37 The effects on intrinsic diastolic function like that of the end-diastolic pressure–volume relation were not described in detail, but the significant increase of end-diastolic pressure 2 to 5 days after surgery suggests diastolic impairment after surgery. Most centers have abandoned the Batista procedure because of high surgical mortality and late return of heart failure, but studies by Suma's group indicate that by utilizing intraoperative echocardiography to select the optimal excision, partial left ventriculectomy may effectively treat severe heart failure in selected patients with nonischemic dilated cardiomyopathy.38
However, our study focuses on patients with ischemic dilated cardiomyopathy, for which case Artrip's model would predict improvement of overall cardiac pump function. Recent studies assessed the acute effects of SVR on pressure-volume relations and found improved systolic function and reduced mechanical dyssynchrony.4 However, the effects on diastolic load-independent indices, which may be important after volume reduction and insertion of an akinetic stiff patch, were not studied. To our best knowledge, the present study is the first to show the effects of SVR in patients with ischemic dilated cardiomyopathy on both systolic and diastolic pressure-volume relations in comparison with other surgical procedures. As expected, the results showed a leftward shift of both the end-systolic and the end-diastolic pressure-volume relations. Indexed by ESV80 and EDV14, respectively, the end-systolic pressure–volume relation shifted by –55 ± 18 mL, whereas the end-diastolic pressure-volume relation shifted by –84 ± 17 mL. Consequently, when compared at the same end-diastolic pressure (of 14 mm Hg), the hypothetical maximal total work, quantified by the area enclosed by the end-systolic pressure-volume relation, the end-diastolic pressure–volume relation, and the end-diastolic volume at 14 mm Hg, was decreased (from 13.4 to 10.1 mm Hg · L). According to the "maximal total work" concept introduced by Artrip and colleagues,10 this finding should be interpreted as a decrease in overall pump function. However, in practice, the LV worked at a higher end-diastolic pressure after SVR, resulting in a maintained stroke work and cardiac output. Moreover, under physiologic conditions the total work is only partly converted to effective external work (ie, the area of the pressure-volume loop, stroke work); the remainder is dissipated as heat (the potential energy component of the pressure-volume area). Interestingly, our results show that whereas stroke work remained fairly constant, the potential energy component was importantly reduced, indicating an improved mechanical efficiency of the ventricular contraction. This acute improvement presumably is caused by reduced mechanical dyssynchrony and reduced wall stress due to the restoration of LV shape. A widely used concept to assess overall ventricular performance is the preload recruitable stroke work. This relation reflects the Frank-Starling mechanism in the intact heart.26 Because the fundamental cellular processes responsible for the Frank-Starling mechanism presumably are myofilament overlap and length-dependent calcium sensitivity of the sarcomeres,39 stroke work is plotted as a function of end-diastolic volume as a reflection of diastolic fiber length (preload). Our findings show no significant changes in the preload recruitable stroke work relation after SVR. In many studies, end-diastolic (filling) pressure is used as a surrogate measure of preload, but if the diastolic pressure–volume relation is importantly altered (as in the present study), changes in the relation between stroke work and end-diastolic pressure cannot be directly interpreted in terms of altered Frank-Starling behavior. However, the finding in our study that maintained stroke work was obtained at a higher end-diastolic pressure is certainly a negative aspect because, even with an unchanged Frank-Starling curve, this indicates that the possibility to increase stroke work (or cardiac output) via this mechanism is limited.
Consistent with our findings, Di Donato and colleagues recently demonstrated reduction of mechanical dyssynchrony after the Dor procedure.3 Usually, LV geometry in patients with chronic dilated cardiomyopathy is associated with a more transverse orientation of apicoseptal muscle fibers, and this orientation results in less efficient contraction and a decrease in LV pump function.12 SVR achieves restoration of the LV geometry toward a more elliptical shape,11,40 and the increase in systolic function after SVR, found in our study, may be partly the result of improvement of geometric rearrangement with restoration of LV apicoseptal fiber orientation.
Our approach involved the use of an intraventricular balloon filled with 55 mL/m2 saline to standardize the surgery, to avoid creating a too small cavity, and to achieve an elliptical shape of the left ventricle. Previous studies using a shaper device recommended a similar residual volume.41 However, at this point it is unknown which factors determine the optimal residual volume in individual patients. Also, the material properties of the patch may influence the results. A recent mathematical model study recommended repair without a patch whenever possible.42 Potentially, the modified linear closure described by Mickleborough and associates could be advantageous.43 However, this approach limits options for septal exclusion as compared with the Dor procedure. Therefore, as pointed out in a recent editorial by Buckberg,44 the linear closure would only be applicable to a selected patient population. Future studies are required to investigate these issues.
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Limitations |
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We anticipated that most of the patients with heart failure would need inotropic support after surgery. Therefore, to avoid bias, in the SVR and the RMA groups, inotropic support was started before surgery and, thus, pre- and postmeasurements were both done during inotropic support. In the CABG group none of the patients received inotropic support. This may have resulted in slightly less pronounced differences between the CABG group on the one hand and the SVR/RMA groups on the other hand.
A methodologic limitation may be present for the calculation of conductance catheter slope factor , which corrects underestimation of volume changes, which is due to electric field inhomogeneity and mismatch of the catheter segments with the LV long axis. In our study, this factor was calculated by matching the uncalibrated conductance stroke volume with stroke volume obtained by thermodilution. Because this comparison with right-sided stroke volume determined by thermodilution would be hampered in case of mitral insufficiency, we determined uncalibrated conductance catheter stroke volume as the volume at the moment of dP/dtMAX minus the volume at the moment of dP/dtMIN. With this approach pre- and postsystolic mitral insufficiency is not included in the uncalibrated conductance stroke volume. However, some overestimation of actual forward stroke volume is likely to remain, which theoretically would result in an underestimation of absolute volumes in patients with mitral insufficiency. Future studies using an independent method to determine absolute volume are required to address this issue.
In conclusion, SVR by endoventricular circular patch plasty leads to acute normalization of LV volumes with improved systolic function. At the expense of a higher diastolic pressure resulting from altered diastolic properties, cardiac pump function indexed by stroke work and cardiac output was not importantly altered. However, mechanical efficiency was significantly improved, presumably resulting from reduced wall stress and reduced mechanical dyssynchrony. Interestingly, the diastolic chamber stiffness constant was not more altered after SVR than after the surgical procedures in the other groups, suggesting that this effect was importantly related to procedure-induced myocardial edema and may be partially transient. Additional mitral valve repair is feasible and restores leaflet coaptation, although this procedure in itself does not importantly affect systolic and diastolic LV function in the acute phase. Future studies should be directed toward the long-term effects of SVR on systolic and diastolic pressure–volume relationships.
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| See related editorial on page 459.
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