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J Thorac Cardiovasc Surg 1994;108:477-486
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

The effects of left heart assist on right ventricular muscle mechanics and ventricular coupling in the injured heart

Rochester, Minn.

From the Division of Cardiovascular and Thoracic Surgery, Mayo Clinic and Foundation, Rochester, Minn.

Received for publication Aug. 10, 1993. Accepted for publication Feb. 4, 1994. Address for reprints: James J. Morris, MD, Division of Cardiovascular and Thoracic Surgery, Mayo Clinic, 200 1st St. S.W. Rochester, MN 55905.

Abstract

So that we could better characterize the effects of left heart assist on right ventricular myocardial muscle mechanics and ventricular mechanical coupling in the injured heart, nine dogs underwent 30 minutes of global cardiac ischemia supported by cardiopulmonary bypass followed by randomly varied levels of left heart assist at 0, 1.0, and 2.0 L/min (0, 37 ± 4, and 74 ± 7 ml/kg per minute). A centrifugal pump with left ventricle-to-aorta bypass was used with the intent to cause left ventricular volume unloading but without complete left ventricular pressure unloading. Right ventricular regional free wall and septal–free wall dimensions were measured by a sonomicrometer and right ventricular pressure by a micromanometer. Pressure and dimension data were acquired over a range of preloads produced by transient vena caval occlusion and at steady state at an initial control point and after ischemia at each level of left heart assist. Right ventricular regional early diastolic function was assessed by percent segmental relaxation during the first third of diastole, end-diastolic compliance by the end-diastolic pressure-dimension relationship, systolic contractile performance by the slope (M_w) and dimension axis intercept (L_w) of the linear preload recruitable stroke work relationship, and right ventricular isovolumic relaxation by the pressure decay time constant. Ischemia reduced M_wof both the free wall (38.3 ± 16.1 to 16.4 ± 4.2 erg·cm ^-3·10³, p< 0.01) and septal free wall (30.2 ± 12.7 to 13.4 ± 4.9 erg·cm^-3·10³, p< 0.01) and shifted L_wrightward (1.3 ± 0.3 to 1.4 ± 0.3 mm, p< 0.01, and 2.8 ± 0.8 to 3.0 ± 0.9 mm, p< 0.01), which confirmed myocardial ischemic injury. There were no effects of left heart assist on free wall or septal–free wall systolic contractile performance assessed by M_wand L_wor on early diastolic relaxation assessed by percent segmental relaxation during the first third of diastole in either right ventricular region (all p= not significant). There were also no observed characteristic alterations of free wall or septal–free wall end-diastolic pressure-dimension relationships with left heart assist. The pressure decay time constant decreased with increasing levels of left heart assist (51 ± 14, 49 ± 16, and 43 ± 11 msec, p< 0.05), which indicated an improvement in right ventricular isovolumic relaxation attributable to left heart assist. These data demonstrate that mechanical ventricular interactive effects during left heart assist are beneficial, but limited to isovolumic relaxation in the injured heart. The likely optimal method of left heart assist for postcardiotomy support should sufficiently augment cardiac output and arterial pressure but maintain left ventricular systolic pressure generation to preserve beneficial ventricular mechanical coupling. (J THORACCARDIOVASCSURG1994;108:477-86)

The use of temporary centrifugal and pulsatile pump devices for left heart assist (LHA) has become an established and increasingly used therapy for acute and chronic refractory cardiac failure. ^1-4 However, the effects of left ventricular (LV) unloading on intrinsic right ventricular (RV) myocardial performance and on RV and LV mechanical coupling remain incompletely defined and poorly understood. Of particular concern is the effect of LHA on performance of the injured or dysfunctional RV.

Because of the arrangement of the RV and LV in series, preload and afterload of the ventricles are interrelated. ^5-8 In addition, because of ventricular arrangement in anatomic contiguity, LV contraction likely contributes to RV pressure generation and ejection. ^9-11 This occurs because reduction of RV chamber volume during systole is accomplished not only by RV free wall contraction and thickening of the interventricular septum, but also by a reduction of the RV free wall–septal dimension. This results from a tethering inward of the RV free wall toward the septum, owing to the RV attachments to the LV.

Previous investigations have variably reported beneficial, ^1,12-14 detrimental, ^15,16 or negligible ^17-19 effects of LHA on RV performance. However, these investigations have not fully considered significant confounding LHA-induced changes in RV load conditions ^12-15 or have only examined LHA in the normal heart. ^12,14,17,18 RV dysfunction observed during LHA has been speculated to be a result of an adverse effect of LHA on ventricular mechanical coupling and rearrangement of ventricular geometry, particularly of the interventricular septum. ^14,17 However, no prior studies have precisely quantified the effects of LHA on ventricular mechanical coupling in the injured heart.

To better define the optimal method of LHA for postcardiotomy support and to better characterize the effects of LHA on ventricular mechanical interaction in a quantitative manner, we undertook a study to determine the direct effects of LHA on intrinsic systolic and diastolic RV myocardial muscle mechanics independent of alterations in load conditions in an experimental model of postischemic ventricular dysfunction.

MATERIAL AND METHODS

Experimental preparation.
Nine adult dogs (mean weight 27.3 ± 3.1 kg) were studied in the anesthetized state. All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" prepared by the Institute of Laboratory Animal Resources and published by the National Institutes of Health (NIH Publication No. 86-23, revised 1985). The procedures and handling of animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Mayo Foundation.

Each dog received intravenous sodium pentobarbital (30 mg/kg) and the lungs were artificially ventilated. Through a median sternotomy, the pericardium was incised and the heart supported in a pericardial cradle. Pairs of pulse-transit ultrasonic dimension transducers connected to a sonomicrometer (Davis Associates, Durham, N.C.) were positioned to record instantaneous RV, LV, and septal–RV free wall dimensions. Two epicardial transducers (cylinder length 0.16 cm, outer diameter 0.16 cm; Vernitron, Bedford, Ohio) were placed approximately 1 cm apart near the intersection of the long and short axes of the RV free wall to record RV free wall chord dimension. ²⁰ A second pair of epicardial transducers (hemisphere diameter 0.5 cm, Vernitron) was placed to record LV anterior-posterior minor axis dimension. An additional transducer was placed on the epicardial surface of the RV free wall to permit measurement of septal–RV free wall dimension. The septal transducer (cylinder outer diameter 0.16 cm) was placed through the tract of a 19-gauge needle introduced into the septum just to the right of the left anterior descending coronary artery, and the transducer was positioned as near as possible to the RV endocardial surface midway between the anterior and posterior LV transducers. ¹⁸ Instantaneous RV and LV pressures were recorded by micromanometers (model PC-350, Millar Instruments, Inc., Houston, Tex.) passed into the RV chamber via a 0.5 cm incision in the outflow tract and into the LV chamber via a 0.5 cm incision in the apex. Pulmonary artery, left atrial, and central aortic pressures were also measured with micromanometers. Instantaneous pulmonary artery flow was measured with an ultrasonic flow probe (internal diameter 1.6 cm; Transonic Systems Inc., Ithaca, N.Y.).

The sinus node was crushed and the right atrium paced at a rate of 150 beats/min. Each dog received heparin (250 U/kg) and cardiopulmonary bypass was instituted with arterial inflow via the femoral artery and venous outflow from the superior and inferior venae cavae via the right atrium. Mean arterial pressure was maintained at 60 to 70 mm Hg by varying bypass flow. Arterial oxygen tension, carbon dioxide tension, and pH were monitored and adjusted appropriately. Perfusate temperature was maintained at 37° C. After a 15-minute period of equilibration, each dog was subjected to 30 minutes of normothermic global cardiac ischemia produced by aortic crossclamping. The LV was vented. At the end of the ischemic period, the aortic crossclamp was removed and the heart defibrillated. Cardiopulmonary bypass was continued, and the heart was reperfused for 30 minutes in the beating, nonworking state. The dogs were then weaned from bypass without the use of inotropic drugs.

Dogs then underwent LV-to-aorta LHA with a centrifugal pump (Bio-Pump, Biomedicus Inc., Eden Prairie, Minn.). LV outflow was via a 20F cannula (C.R. Bard, Inc., Billerica, Mass.) inserted into the LV apex and aortic inflow via an 18F cannula (C.R. Bard, Inc.) inserted into the femoral artery. LHA flow levels were varied at 0, 1.0, and 2.0 L/min in random order. Each level of LHA flow was maintained for 15 minutes. Assist levels of 1.0 L/min (37 ml/kg/min) and 2.0 L/min (75 ml/kg/min) were selected to represent partial and complete LHA inasmuch as 2.0 L/min represents the typical resting cardiac output in anesthetized dogs of this size. The intent was not complete pressure unloading of the LV, but rather volume unloading. In all cases, comparison of LV and central aortic pressure waveforms confirmed minimal LV ejection at maximal LHA flows.

At the conclusion of each study, the dogs were killed by deep barbiturate anesthesia. The hearts were excised and proper position of the dimension transducers verified.

Data acquisition and analysis.
Pressure, dimension, and flow data were acquired at a control point before ischemia and after ischemia at each level of LHA after steady state was achieved. At each data acquisition point, static data were recorded and data were recorded over a range of RV end-diastolic volumes produced by transient (5 to 10 second) vena caval occlusion for 10 to 25 cardiac cycles.

Physiologic data were filtered with a 50 Hz low-pass analog filter and digitized at an 8-channel sweep speed of 200 Hz by an analog-to-digital converter (model 5025MF, ADAC, Woburn, Mass.). The analog-to-digital conversion time per channel was 30 microseconds, which created a phase delay between channels of less than 4.5 degrees. After data were collected and stored on hard disk by personnel computer (Reason Technology Inc., Minneapolis, Minn.), data analysis was accomplished on a microcomputer (DEC, Vaxstation 3100, Maynard, Mass.) with the use of interactive software (Davis Associates, Durham, N.C.) and software developed in our laboratory. The first derivatives of both RV and LV pressures (dP/dt) were determined from a running five-point polyorthogonal transformation of the digitized ventricular pressure waveform. RV and LV cardiac cycles were defined automatically with the use of dP/dt criteria previously described. ^20,21

Regional RV free wall, septal–free wall, and LV systolic contractile performance were each assessed by the preload recruitable stroke work relationship, an analysis of ventricular ability to generate stroke work as a function of end-diastolic length (EDL). This analysis has been previously described in detail. ^22-24 In brief, regional RV and LV stroke work (SW) values were calculated from instantaneous pressure (P) and dimension (L) data for each cardiac cycle as

SW = P · dL (1)

Data from each vena caval occlusion were fitted to the equation

SW = M_w(EDL - L_w) (2)

which relates stroke work to end-diastolic length, where M_w is the slope and L_w is the dimension axis intercept. Previous work has shown this relationship between stroke work and end-diastolic length to be a highly linear, load-independent descriptor of ventricular contractile performance. ^22-24 Changes in intrinsic contractile functionare reflected as changes in M_w and L_w. For each dog, M_w and L_w were determined for equation 2 for each vena caval occlusion. Mean values were calculated for three to five vena caval occlusions done during the control period before ischemia and after ischemia at each level of LHA.

RV regional diastolic function during the early phase of diastole was assessed by determining percent segmental relaxation (%RELAX) during the first as follows:

% RELAX is an index of active ventricular dilation that occurs during early diastole before atrial contraction. ^25,26

RV regional end-diastolic compliance was assessed by the end-diastolic pressure–end-diastolic dimension relationship.

RV chamber isovolumic relaxation was assessed by the decay of RV isovolumic pressure, where the rate of relaxation was defined by the time constant T. T was calculated as the slope of ln(P) against time as previously described. ^27,28 Instantaneous RV pressure points from the point of peak negative dP/dt to the point at which RV pressure declined to the level of end-diastolic pressure from the prior cardiac cycle were fitted to the exponential equation

P(t) = A · e^bt (4)

where

In P(t) = A + bt (5)

and

T = - 1/b(6)

T is independent of systolic pressure and end-systolic fiber length ²⁷ and an increase in T indicates a decrease in the speed of ventricular chamber relaxation.

RV stroke volume (SV) was measured from instantaneous pulmonary artery flow (Q) data for each cardiac cycle as

SV = Q · dt (7)

All values are presented as the mean plus or minus the standard deviation. Statistical analyses were done with t tests for paired data and analysis of variance for repeated measures with the Newman-Keuls test used to localize differences. Statistical significance was accepted at p < 0.05.

RESULTS

Regional RV contractile performance.
The 30- minute period of ischemia followed by reperfusion resulted in significant RV injury and impairment of regional contractile performance assessed by changes in slope, M_w, and dimension axis intercept, L_w, of the linear preload recruitable stroke work relationship. The characteristic effect of ischemia and reperfusion on contractile performance of both the RV free wall and septal–free wall segments is depicted in Fig. 1 for a single representative dog. For both the free wall and septal–free wall regions, ischemia resulted in a decrease in M_w and rightward shift of L_w, which indicated decreased ability of the RV free wall and septal–free wall muscle segments to generate work as a function of end-diastolic length.

View larger version (18K): [in this window] [in a new window]   Fig. 1. Representative data from single dog demonstrating effect of global ischemic injury on RV free wall (FW) and septal-free wall (S-FW) regional preload recruitable stroke work relationships.

Table I

Table I

Table I

View larger version (20K): [in this window] [in a new window]   Fig. 2. Representative data from single dog demonstrating effect of increasing levels of LHA (0 L/min, 1.0 L/min, and 2.0 L/min) on RV free wall (FW) and septal–free wall (S-FW) regional preload recruitable stroke work relationships.

Table II

View larger version (35K): [in this window] [in a new window]   Fig. 3. Effect of increasing levels of LHA (0 L/min, 1.0 L/min, 2.0 L/min) on RV free wall (FW) regional end-diastolic pressure-dimension relationships for all dogs. EDP, End-diastolic pressure.

View larger version (35K): [in this window] [in a new window]   Fig. 4. Effect of increasing levels of LHA (0 L/min, 1.0 L/min, 2.0 L/min) on RV septal-free wall (SFW) regional end-diastolic pressure-dimension relationships for all dogs. EDP, End-diastolic pressure.

Table III

Table IV

This study demonstrates that with use of a centrifugal LHA device to attain complete volume unloading of the LV but not complete pressure unloading of the LV, there are minimal effects of LHA on intrinsic RV diastolic and systolic contractile muscle mechanics in the injured heart. Direct mechanical ventricular interactive effects during LHA are beneficial but are limited to the isovolumic relaxation phase in the open-chest dog.

To characterize most accurately the effects of LHA on RV performance, we used an experimental model of biventricular myocardial ischemic injury that has previously been well characterized. ²⁴ This model approximates clinical postcardiotomy myocardial ischemic injury and also closely simulates cardiogenic shock resulting from dysfunctional but presumed viable stunned myocardium, which is the most frequent clinical indication for the use of LHA. ⁴ This experimental model of ventricular injury resulted in a greater than 40% reduction in both RV and LV systolic contractile performance assessed by the preload recruitable stroke work relationship and resulted in a significant, yet nonfatal degree of myocardial injury in that all dogs could be weaned, though marginally, from cardiopulmonary bypass.

With the use of this model of acute ventricular dysfunction, we demonstrated that LHA had no significant effect on intrinsic RV myocardial systolic contractile performance as indicated by no change in either slope, M_w, or x-axis intercept, L_w, of the linear, load-independent regional preload recruitable stroke work relationship in either the RV free wall or septal–free wall muscle segments. In addition, at matched RV free wall and septal– free wall end-diastolic dimensions, which indicated matched RV end-diastolic volumes, parameters of global RV pump performance, such as peak RV dP/dt and RV stroke volume, were also not affected by LHA. LV volume unloading with LHA did not appear to result in any rearrangement of RV three-dimensional geometry or transfer of mechanical energy that adversely influenced intrinsic regional or global RV contractile mechanics in any detectable manner.

These observations regarding LHA effects on RV systolic function are in agreement with several prior observations in the normal noninjured heart in open-chest animals in which LHA also did not affect global RV contractile performance assessed by the preload recruitable stroke work relationship. ^17,18 In a porcine model of chronic tachycardia-induced heart failure, Chow and Farrar, ¹⁶ with the use of a valved sac-type assist device with complete systolic pressure unloading of the LV to near 0 mm Hg, observed a significant reduction in slope and a rightward shift of the dimension axis intercept of the preload recruitable stroke work relationship of the septal–free wall segment with LHA. In addition, they reported a reduction in global RV stroke work as a function of RV end-diastolic pressure, indicative of an impairment in global systolic contractile performance attributable to LHA in the failing heart. That method of LHA with complete LV pressure unloading with the intent of reducing peak LV pressure to near 0 mm Hg differed substantially from the method of LHA that we and others ¹⁸ used, which uses a centrifugal pump with the intent of LV volume unloading. This mode of LHA was capable of providing levels of circulatory assist equivalent to an effective total cardiac output of greater than or equal to 70 ml/kg per minute, yet it maintained a nonejecting, essentially isovolumic LV systolic contraction pattern with LV peak pressure generation of 70 to 80 mm Hg. In contrast to LHA with complete LV pressure unloading, ^16,17 this method of LHA does not result in a completely decompressed and collapsed LV chamber.

Normally, LV contraction augments RV contraction and generation of RV pressure by transmission of myocardial wall tension during LV systole to the RV free wall and by simultaneous generation of a left-to-right transseptal pressure gradient that maintains septal convexity and augments the effectiveness of both RV free wall contraction and LV mechanical interaction with the RV free wall. ¹¹ Leftward displacement of the interventricular septum during ventricular systole tends to increase RV systolic chamber volume and results in reduction of RV pressure generated by contraction of the RV free wall. ²⁹ Leftward shifting of the interventricular septum and loss of septal convexity occurs with LHA. ^13,18,30 Complete decompression and collapse of the LV chamber during LHA would further reduce and, in fact, reverse the normal left-to-right transseptal pressure gradient and would potentially profoundly distort the RV three-dimensional geometry and contraction pattern.

Other investigators have demonstrated that complete pressure unloading of the LV has a detrimental effect on RV systolic performance. ^12,29 Elzinga, Piene, and deJong, ²⁹ in an isolated heart model, used a rapid synchronized reduction in aortic pressure induced for a single cardiac cycle to assess the beat-to-beat influence of LV developed pressure on RV performance. During an isovolumic contraction on the left side, RV generated pressure and RV stroke volume were greater than those indices during LV contraction against a very low afterload and with a reduced left-to-right transseptal pressure gradient. Miyamoto, Tanaka, and Matloff ¹² likewise noted that, in an open-chest canine model of left heart bypass with a roller pump, incremental increases in left heart bypass flows from 60% to 100% of total cardiac output with reduction of peak LV pressure from near 100 mm Hg to 0 mm Hg were associated with increased mean right atrial pressure and decreased RV peak dP/dt, which suggested an impairment in global RV performance. The findings of our present study confirm these observations that LV volume unloading with maintenance of a near isovolumic LV contraction pattern and LV systolic pressure generation preserve beneficial RV to LV mechanical coupling. ^12,18,29 Our data also indirectly support other observations that maximal LV decompression impairs RV contractile performance by impairing effective ventricular systolic mechanical coupling. ^12,16,29

We observed that increasing levels of LHA significantly reduced T, which indicated an increase in the rate of fall of isovolumic RV pressure and an improvement in RV relaxation with LHA. Isovolumic relaxation measured by T is known to be prolonged in a number of pathophysiologic states including myocardial hypoxemia and ischemia, ^31,32 hypertrophy, ³³ and heart failure. ³⁴ Conversely, the time course of isovolumic relaxation is shortened by infusion of catecholamines. ^35,36 In the LV, T is independent of peak ventricular systolic pressure and end-systolic volume or fiber length. ²⁷ T is presumed to be one index of the activity of the active myocardial relaxation system and, to a lesser extent, of myocardial viscoelastic properties. ²⁷ Although characteristics of RV isovolumic relaxation have not been as extensively investigated, the accelerated time course of RV isovolumic pressure decay with LHA indicates that LV volume unloading by LHA effectively reduces LV tension transmitted to the RV free wall after the completion of RV ejection and enhances intrinsic RV myocardial muscle isometric relaxation.

We observed that LHA had no detectable effect on RV regional early diastolic relaxation as measured by %RELAX nor was there any consistent effect of LHA on RV end-diastolic compliance assessed by the regional end-diastolic pressure-dimension relationship. During the early, rapid phase of ventricular diastolic filling, a negative pressure gradient across the atrioventricular valve is known to be generated by active energy-dependent ventricular dilation before atrial contraction. ^25,26 Ventricular relaxation during this first third of diastole is reportedly impaired during regional LV myocardial ischemia ²⁶; however, in our present study, %RELAX did not appear to be a sensitive indicator of a more severe RV global ischemic injury. %RELAX was also not significantly influenced by LV unloading with LHA.

One important potential implication of the findings of this study is that the preferred mode of LHA for postcardiotomy support should be carefully considered with regard to avoiding complete LV pressure unloading, enhancing beneficial direct mechanical systolic ventricular interactive effects, and optimizing overall cardiac performance during LHA. The intent of LHA for postcardiotomy support is to augment effective cardiac output and arterial pressure sufficient to meet whole body metabolic needs. A secondary goal of LHA is to reduce myocardial workload demand and oxygen consumption of the injured, dysfunctional LV by LV decompression. Although reduction of LV work, wall stress, and myocardial oxygen consumption with LHA have been shown experimentally to limit infarct size in ischemic myocardial regions, ^37-39 no data yet support the supposition that the extent of LV pressure unloading with LHA influences either recovery or the rate of recovery of viable but dysfunctional postischemic stunned myocardium. Our data suggest that, in terms of overall cardiac performance, RV-LV interactive effects may be enhanced and impairment of intrinsic RV myocardial muscle mechanics minimized in the postischemic heart during LHA with the use of a mode of LHA that sufficiently augments cardiac output and arterial pressure while preserving a near isovolumic LV contraction pattern.

There are several potential criticisms of this study. First, we examined only the effect of LHA on RV performance in the anesthetized open-chest state. The pericardium was not intact. Constraining effects of the intact pericardium may potentiate direct mechanical ventricular coupling and interaction of ventricular diastolic compliance. ^7,40 If so, then the effect of LHA on RV performance may also be influenced to some extent by an intact pericardium. Opening of the pericardium, instrumentation of the heart, and placement of LHA cannulas followed by reclosure of the pericardium was not undertaken in this study because of the perceived high likelihood of some degree of artifactual pericardial restriction. The question of pericardial influences on the effects of LHA on RV performance therefore remains unanswered. However, this point does not represent a significant weakness in the clinical relevance of this study in that LHA is used in virtually all patients without an intact pericardium after cardiotomy.

A second potential criticism of this investigation is that a nonpulsatile centrifugal pump device rather than a pneumatic sac-type device was used exclusively. The use of a different type of device possibly might have yielded different results. The principal differences in devices, however, are limited to the timing of LV unloading with regard to the cardiac cycle and the attainable degree of LV pressure unloading. Pulsatile, valved sac-type devices typically fill during LV systole, eject during diastole, ^16,19 and maximally reduce LV systolic pressure. Flow through centrifugal devices is nearly continuous during the cardiac cycle. Although LHA flow is greater during LV systole, complete LV pressure unloading is not usually attained with centrifugal pumps. The design of our experimental model was intended to simulate the clinical conduct of LHA to draw conclusions applicable to clinical decision-making. Compared with pulsatile sac-type devices, centrifugal pumps are less costly and complex, are readily available, do not require an investigational device exemption to be obtained, and, as a result, are much more widely used in current practice. ⁴

In summary, with the use of an experimental model of moderately severe biventricular ischemic injury and incorporating the use of a centrifugal LHA device to progressively volume unload the LV in the ischemically injured heart, we demonstrated that there are minimal effects of LHA on intrinsic RV diastolic and systolic myocardial muscle mechanics. Direct mechanical interactive effects between the RV and LV during LHA are beneficial, but are limited to isovolumic relaxation in the open-chest state. These observations suggest that in the clinical use of LHA, the theoretic but unproved benefits of maximal LV pressure unloading and decompression should be balanced against the demonstrated beneficial effects of LV volume unloading and maintenance of LV pressure generation on ventricular mechanical coupling and overall cardiac performance. A better appreciation of mechanical ventricular interaction during LHA will, it is hoped, enhance the clinical utility of short- and long-term circulatory support.

The secretarial assistance of Alice J. Laudon is gratefully acknowledged.

Footnotes

*NS = Not significant.

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