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Eur J Cardiothorac Surg 2000;17:52-57
© 2000 Elsevier Science NL
a Deutsches Herzzentrum Berlin, Augustenburger Platz 1, 13353 Berlin, Germany
b Division of Cardio-thoracic Surgery, UCLA Medical School, Los Angeles, CA, USA
Corresponding author. Tel.: +49-30-4593-1000; fax: +49-30-4593-1003
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Abstract |
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 Top Abstract 1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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Key Words: Reversed remodeling • Batista procedure • Heart failure
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1. Introduction |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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Conceptual cardio-reduction models do not start with a damaged heart to stimulate clinical events. A present requirement is an in vivo depressed myocardium, followed by surgically increased volume to cause heart failure, and subsequent reduction to evaluate how changing architecture affects function. Initial attempts to accomplish initial depression were made by Batista, who produced dilatation in sheep with a large pericardial patch, which remodeled an elliptical to a spherical ventricle, where function worsened [1]. The ventricular incision caused circumflex artery or marginal branch occlusion. Subsequent patch removal allowed sequential analysis of ventriculograms for ejection fraction, but contractile responses to loading or unloading were absent.
Our study in porcine hearts reproduced the Batista protocol. Distended spherical ventricles created a model of heart failure. The hypothesis was tested, i.e. whether surgical reduction of diameter and cavity of spherically distended LV changes geometry towards an ellipse, and whether it improves LV performance and hemodynamics.
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2. Materials and methods |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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The pericardium was incised through a median sternotomy. Intravenous heparin (300 IU/kg) was given. A saline solution cannula inserted into the left atrium (LA) was connected to a pressure-membrane transducer (Gould–Statham, model P 23 XL, Oxnard, CA) to record LA pressure (LAP). A Swan–Ganz catheter placed in the pulmonary artery measured pulmonary artery pressure and cardiac output (CO) by the thermodilution technique. Pressure-transducer tipped catheters (Millar Instruments, Inc., Houston, TX) were inserted into the LV and right carotid artery for continuous determination of LV and aortic pressures, respectively. A saline filled catheter, connected to a pressure-membrane transducer (Gould–Statham, model P 23 XL, Oxnard, CA), was inserted into the jugular vein for continuous recording of the central venous pressure (CVP).
A 16-French-femoral-arterial catheter and 30-French-right-atrial catheter were connected to cardio-pulmonary bypass (CPB; Sarns, Ann Arbor, MI) equipped with a membrane oxygenator (Sarns 1630 membrane oxygenator, Sarns, Ann Arbor, MI). The extracorporal circuit was primed with 1000 ml plasmalyte solution (Baxter Healthcare Corporation), 700 ml stored porcine packed red cells and calcium chloride for normocalcemia. Arterial blood gases were measured to maintain oxygen tension, carbon dioxide, potassium, sodium, calcium, and pH within normal range.
An octipolar impedance catheter (Webster Laboratory, Baldwin Park, CA) was inserted into the LV apex, and an umbilical tape was placed as a loop around the inferior vena cava in order to acquire pressure–volume loops [2].
2.1. Measurements
The global LV function was assessed before and 30 min after discontinuation of CPB by preload recruited Frank–Starling function curves, by pressure–volume analysis and by echocardiograms.
For loading studies with the Frank–Starling curves, the preload was raised by continuously infusing blood intravenously at 4 ml/kg per min, while CO, MAP (mean aortic pressure) and LAP were recorded. CO was determined by duplicate central venous injections of 3 ml of 4 C saline solution. The left ventricular stroke work index (LVSWI) was calculated according to the following formula: LV SWI=(MAP-LAP)xCOx0.0136xHR-1xBW-1 (gxm/kg)where MAP is mean aortic pressure (mmHg), LAP is mean left atrial pressure (mmHg), CO is cardiac output (ml/min), 0.0136 converting (mmHgxml) into (gxm), HR is heart rate (beats/min), and BW is body weight (kg).
For unloading, a triple series of evenly declining pressure–volume loops were generated by transient inferior vena caval occlusion during 10 s of apnea [2]. Analog hemodynamic data were digitized using a 12-bit analog-to-digital converter (DT 2821, Data Translation, Marlboro, MA) and recorded on a microprocessor system (IBM PC486 compatible) that sampled at 250 Hz. Data were analyzed using a video graphic interface computer program (SPECTRUM®, Bowman Gray School of Medicine, Winston–Salem, NC, and Triton Technology, San Diego, CA) [3]. Left ventricular chamber conductance was converted to volume using a Leycom Sigma-5-DF signal conditioner processor (Leycom, Oegstgeest, The Netherlands). Parallel conductance of structures contiguous to the heart was estimated by the hypertonic saline technique [4], and parallel conductance was subtracted from instantaneous left ventricular volume point-by-point to obtain absolute left ventricular volume. The end-systolic point for each loop was identified using the algorithm of Kono [5]. Linear regression was done on the collected end-systolic pressure–volume points to calculate the slope (mmHg/ml) of end-systolic elastance (EES) and its intersection with the volume axis (V0, (ml)) as the mathematically calculated volume at zero pressure.
The diastolic compliance (ß-1) was determined during the same transient caval occlusion from the exponential end-diastolic pressure–volume formula:P=
xe(ßxVed) where is a constant, P is end-diastolic LV pressure, Ved is end-diastolic LV volume, ß is chamber stiffness, or as ß-1 expresses the diastolic compliance.
A 3.5 MHz sonographic transducer, connected to a Hewlett Packard Sonos 1500 echocardiographic machine, was placed on the epicardium. Two-chamber, short and long axis views of the LV were recorded. The LV EF was calculated from a modified Simpson's rule [6] from biplane projections. The mitral valve was checked for regurgitation, and the LV outflow tract for obstruction.
The LV performance determined as SWI (stroke work index), EES, ß-1, and EF (ejection fraction) was expressed post-CPB as percent recovery from pre-CPB values.
2.2. Experimental design
Control group, ‘Controls’: five pigs were placed on CPB for 1 h without surgical alteration of the heart. Post-CPB hemodynamics served to evaluate the influence of extracorporal circulation (Fig. 1).
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Group with patch, ‘sphericalization’ and ‘elliptical modeling’: an additional seven hearts were incised as described above. A pericardial patch (8x6 cm; Hancock Pericardial Patch, Medtronic, Minneapolis, MN) enlarged the LV cavity and LV diameter. It was sutured over the ventriculotomy with 3–0 prolene in an over and over manner. This maneuver produced an enlargement and sphericalization of the previously elliptical ventricle. Air was evacuated from the apex before closing the circumferential patch suture. Post-CPB hemodynamics served as value to evaluate cardiac capacities in the condition of sphericalization (Fig. 1).
After recording sphericalization-related hemodynamics CPB was restored in these pigs. The suture line was incised and the patch withdrawn. Again, LV was closed as described above after evacuation of air. Post-CPB hemodynamics served to evaluate the effects of LV diameter reduction and elliptical modeling of a formerly enlarged spherical LV.
The aorta of the pigs was not cross-clamped. For myocardial protection during the surgical procedure of the experimental groups ‘LV incision’, ‘sphericalization’ and ‘elliptical modeling’ the method of beating empty open hearts was applied, i.e. the left ventricular cavity was vented by the LV incision and the blood shed to the pericardium was drained to the venous reservoir of the CPB. Avoiding cross-clamping of the aorta prevented ubiquitous myocardial ischemia. Local ischemia of the LV was intended when the marginal branch was occluded on LV incision.
2.3. Statistics
Statistical analyses were performed using the Statview II software package v2.0 (Abacus Concepts, Berkeley, CA) on an Apple-Macintosh II ci computer (Apple Inc., Cupertino, CA). All data are given as mean±standard error of the mean. Comparable variance of the groups’ results was checked with the F-test; a Gaussian curve distribution of the results was validated by the method of David, Pearson and Stephens before parametric comparison. The unpaired Student's t-test was applied for comparison between the groups. For internal group comparison of those hearts that underwent sphericalization and subsequent elliptical modeling the paired Student's t-test was used. Statistical significance was accepted at P<0.05 for unpaired and paired data (see abstract).
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3. Results |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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The incision and subsequent direct suture of the LV wound impaired the stroke work index and the diastolic compliance (Figs. 2 and 3). The end-systolic elastance was only slightly reduced (Fig. 4).
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Incision and final suture of the LV led in two cases to papillary trauma with subsequent mitral regurgitation; these pigs were excluded from the statistical analysis. LV outflow tract obstruction following surgical alteration of the hearts was not observed.
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4. Discussion |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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In our present study, the pericardial patch accentuated heart failure in damaged hearts by altering an elliptical ventricle to a distended sphere. This cardiac failure is relieved by patch removal to restore the elliptical ventricle. Immediate hemodynamic recovery followed these geometric changes. This in vivo model circumvented several problems with theoretical concepts, and demonstrated that reducing LV size in enlarged and failing hearts improves cardiac function. With regard to distended ventricles, this may explain hemodynamic benefits following cardio-reduction for severe left ventricular failure.
This current model with an intraventricular patch enabled the evaluation of changes in the radius, thickness and ventricular shape that are difficult to simulate in conceptual mathematical models. We caused a damaged myocardium by marginal branch infarction before evaluating circulatory changes. Actual aortic pressure perfuses the coronary artery rather than artificially establishing a mean aortic pressure, which does not naturally occur. Therefore, the in vivo ventricle generates both the cardiac output for systemic perfusion and the systolic/diastolic pressure for coronary perfusion.
LV incision, respective excision, marginal branch ischemia and subsequent direct LV suture without patch are substantial parts of the Batista operation. In our experiments this procedure impaired the diastolic stiffness and contractility during Frank–Starling curve inscription. EES did not change before dilatation by patch placement. Similar observations were made previously by Bogen after small LV scaring after coronary ligation [8], and by Tyson who interposed a segment of rigid Teflon graft [9]. Sunagawa characterized comparable changes of ESPVR in the physiological range by coronary ligation [10]. He separated this from global ischemic changes that we avoided when placing the patch.
The marginal branch infarction ventricle became spherical after a pericardial patch was placed, and thereby simulated more closely the initially depressed myocardium that ultimately fails. Comparison of improvement after cardio-reduction was made to both a damaged heart and a normal myocardium before ventriculotomy for patch insertion. Reducing LV volume by patch removal raised stroke volume as LV size was reduced. Compliance improves as normal ventricular elliptical shape is restored. LV end-diastolic pressure falls and stroke volume rises. The surgical trauma, which is a prerequisite of the Batista procedure, impairs the cardiac function. However, the distended spherical ventricle, which is already highly impaired, benefits from the cardio-reduction surgery by elliptical modeling. This benefit overcame surgical trauma in our experiments.
Direct knowledge about how cardio-reduction alters heart failure was obtained without reliance upon computer defined changes. Dickstein's coworkers recently used a multiple compartment elastic model and found improved systolic function offset by changes in diastole [11]. He assumed no changes in baseline wall thickness, and observed increased left ventricular diastolic pressure with increased stroke volume by loading during Starling curves. We observed an opposite effect in vivo as stroke volume and EES increased, while left ventricular end-diastolic pressure fell during augmented cardiac output. This may occur because the dilated heart has reduced thickness due to stretch, and is at the ascending limb of a compliance curve (i.e. large change in pressure for small change in volume). The distension of a thicker muscle wall is more elastic than that of a thinner one, so that it reaches a more horizontal site on the diastolic pressure–volume compliance curve (i.e. less pressure increase for a large change in volume). This raised end-diastolic volume at lower pressure has the expected Frank–Starling effect in geometrically normal hearts.
Geometric rearrangement to reduce wall stress is accomplished by surgically altering the dysfunctional segment, i.e. removing the patch in this study, or reducing ventricular volume by excluding parts of the septum and lateral wall by the Dor procedure [12], or excising viable muscle as done by Batista. This reduces the LV radius so that the numerator of the stress equation of Laplace (wall tension=PxR/2H) is decreased, where P is pressure, R is radius, and H is wall thickness. The spherical shape of the distended heart becomes more elliptical to augment performance [13–15], and simultaneously the thin muscle wall of dilated hearts will start to become thicker when wall tension decreases. This self-enforcing circle will again reduce wall tension by the augmented denominator (wall thickness) of the Laplace equation.
Increased muscle tension at larger ventricular volumes compensates for reduced shortening rates [16]. In one sense, increased fiber tension tries to compensate for decreased fiber shortening. More importantly, a dilated heart cannot reduce its wall tension during diastole as efficiently as a normal sized heart. Katz reported a 40% reduction in wall tension at normal stroke volume in normal hearts vs. 7% with dilation [17]. This reduced contractility and subsequent decreased unloading of the dilated spherical ventricle is changed by geometric restoration to an elliptical shape. Li and Chiu used a spherical model and found that reducing ventricular radius by 30% increased the mass/volume relationship by 32% and decreased wall stress by 29% [7]. They estimated that an additional unloading benefit occurred by restoring the elliptical shape. It is unlikely that the specific ventricular site excluded or excised to reduce radius is important, since desphericalization can occur by Batista's excision of viable muscle, by Dor's exclusion of non-contracting scarred muscle or by our removal of the patch.
Avoidance of impaired myocardial protection during patch placement is of central importance to assess the immediate benefits of cardio-reduction. We observed immediate hemodynamic impairment of function after large patch placement as the Frank–Starling curve, EES and EF were reduced. Conversely, complete return of all hemodynamic measurements to pre-patch placement levels followed patch removal. Similar changes may also follow clinical cardio-reduction. Our cardio-protective approach used the beating open heart described by Batista [1] and Jatene [18].
The in vivo model has limitations because the patch incision itself disrupts ventricular muscle fiber architecture. Furthermore, there is an absence of the pro-inflammatory responses of remodeling during chronic dilatation due to up-regulation of sympathetic tone, cytokines and the renin–angiotensin–aldosteron system. The ventricular wall thickness is not altered from chronic dilatation. Direct intramyocyte changes, such as the formation of Aschoff bodies, apoptosis, or collagen formation, do not develop. The absence of chronic studies does not offset what happens with acute cardio-reduction; robust hemodynamic improvement follows patch removal and restoration of the normal ellipsoid shape with an apex. Systolic and diastolic function improved immediately with the beating open technique of myocardial protection; this occurs clinically following the Batista procedure. The experimental and clinical benefits of beating open method in dilated hearts makes this approach the standard to which cardioplegic techniques must be compared.
We conclude that cardio-depression occurs after the ventricular radius is increased by patch dilatation. The marginal branch occlusion model exhibits limited deteriorating hemodynamic alterations before and after patch placement causes cardiac failure. Consequently, patch removal restored contractility and hemodynamics, but did not produce normality. This immediate improvement in acute function may reflect what is seen clinically after de-sphericalization. This early value of cardiac improvement suggests that the surgically re-re-modeled geometry is a major reason that Batista's cardio-reduction is useful.
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Acknowledgments |
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Footnotes |
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References |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionReferences |
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