Left ventricular mechanics during synchronous left atrial-aortic bypass

Left ventricular mechanics during synchronous left atrial-aortic bypass The purpose of this study was to analyze left ventricular mechanics during asynchronous, pulsatile left atrial-aortic bypass before and after microsphere injection with the pressure-volume relationship. In 14 anesthetized Holstein calves, left ventricular pressure was measured with a micromanometer and ultrasonic dimension transducers measured left ventricular orthogonal diameters. Ellipsoidal geometry was used to calculate simultaneous left ventricular volume. Contractility index, pressure-volume area, external work, and potential energy were calculated during steady-state contractions. These measurements were repeated during pulsatile left atrial-aortic bypass. To induce heart failure, we injected microspheres into the left main coronary artery, and the protocol for baseline and pulsatile left atrial-aortic bypass was repeated. Despite the significant differences in the baseline contractility index (7.4 ± 0.7 mm Hg/ml versus 4.7 ± 0.5 mm Hg/ml), contractility index remained the same during pulsatile left atrial-aortic bypass in control and heart failure modes, respectively. Pulsatile left atrialaortic bypass significantly decreased end-diastolic volume(22% and 17 %), pressure-volume area (58% and 48 %) and external work (74% and 69 %, all P < 0.05) during control and heart failure measurements, respectively. However, it did not change end-systolic volume or potential energy. In conclusion, asynchronous pulsatile left atrial-aortic bypass did not affect left ventricular contractile state in either the normal or failing heart. Although decreased pressure-volume area accounts for the reduction in myocardial oxygen consumption, unchanged potential energy suggested a limited unloading of the ventricle. (J 'fHORAC CARDIOVASC SURG 1994;107:1503-11)

Osamu Kawaguchi, MD,a John S. Sapirstein, MD,a William B. Daily, MD,b Walter E. Pae, MD, FACS,a and William S. Pierce, MD, FACS,a Hershey, Pa., and St. Louis, Mo.

Left ventricular (LV) bypass increases cardiac output and blood supply to peripheral organs in cases where the native heart has been unable to maintain the peripheral circulation.l-? Additionally, for the heart itself, LV bypass reportedly decreases LV pressure work and oxygen consumption(V02),1,3,4 which results in reduction of infarct expansion in the coronary occlusion model.Y' Recently,a possibleimprovement of natural LV function From the Department ofSurgery, Division ofCardiothoracic Surgery, The Pennsylvania State University, College ofMedicine, The Milton S.Hershey Medical Center, Hershey, Pa., and the Department ofSurgery, Jewish Hospital, St. Louis, Mo. Received for publication March 24, 1993. Accepted for publication Oct. 25, 1993. Address for reprints: WilliamS. Pierce, MD, P.O. Box 850, Department ofSurgery, The Milton S.Hershey Medical Center, The Pennsylvania State University, Hershey, PA 17033. Copyright @ 1994 by Mosby-Year Book, Inc. 0022-5223/94 $3.00 + 12/1/52615

°

was found during nonpulsatileLV bypassby means ofthe end-diastolicvolume-stroke work relation.8 However,the contractility index of the heart has never been studied during asynchronous, pulsatile left atrial-aortic bypass, which is one of the conventionalclinical modalities used. During asynchronous pulsatile left atrial-aortic bypass,loadingconditionsof the heart change during the pumping cycleor variation of the pumping rate. Because traditional hemodynamic parameters are load-dependent, they are not always adequate to assessthe effectsof pulsatile left atrial-aortic bypass on the natural heart function. The end-systolic pressure-volume relationship (ESPVR) has been determined to be a relatively load-independent index of contractile state. 9, 10 The ESPVR is described by a linear relationship with slope (Emax) and volume intercept (VO).9-11 Pressure-volume (P-V) area (PVA) is the area in the P-V diagram circumscribed by the end-systolic and end-diastolic P-V relations and systolic P-V loop.12, 13 PYA correlates with myocardial oxy1503

I 50 4

The Journal of Thoracic and Cardiovascular Surgery June 1994

Kawaguchi et al.

Aortic Occlusion--j~~~";;'...,~

IVC

Occluder'"

LVP-Millar

Fig. 1. Experimental preparation. AO, Aorta; Inlet, inlet cannula ofleft ventricular assist device; IVC, inferior vena cava; LA, left atrium; LVAD, left ventricular assist device; LVP, LV pressure; Outlet, outlet cannula of left ventricular assist device; PA, pulmonary artery; SVC, superior vena cava.

gen consumption in a stable contractile state regardless of changes in loading conditions.U'P The purpose of this study was to analyze whether pulsatile left atrial-aortic bypass affects LV contractility and how pulsatile left atrial-aortic bypass reduces the LV load in both the control and failing heart.

Materials and methods Experimental preparation. A total of 14 Holstein calves weighing from 89 to 112kg (mean 96 ± 7 kg) were studied. All animals involved in this study 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 Research and published by the National Institutes of Health (NIH Publication No. 86-23, revised 1985). While animals were under halothane anesthesia, endotracheal intubation was performed and ventilation was maintained by a volume respirator with 100% oxygen. The electrocardiogram was continuously monitored. A Swan-Ganz catheter (Baxter Healthcare Corporation, Edwards Div., Santa Ana, Calif.) was inserted to measure cardiac output by the thermodilution method. A median sternotomy was performed, and the heart was suspended in a pericardial cradle. The left internal thoracic artery was cannulated for monitoring aortic pressure. The azygous and hemizygous veins were ligated, and reversible occluders were placed around the superior and inferior venae cavae. Pulse-transit ultrasonic dimension crystals (4 mm diameter),

which were made of 5 MHz piezoelectric crystals (L TZ-2; Transducer Products, Goshen, Conn.) and coated with epoxy in our laboratory, were placed at the endocardial surface across the anteroposterior minor axis, septal-free wall minor axis, and base-apex major axis of the LV. 14• 15 The septal transducer was placed into the septum just to the right of the left anterior descending coronary artery and positioned as near as possibleto the LV endocardial surface midway between the anterior and posterior transducers. 14. 15 A micromanometer-tipped catheter (Model SPC-350, Millar Instruments, Inc., Houston, Tex.) was inserted into the LV through the LV free wall to measure LV pressure. A fluid-filled polyethylene catheter was inserted into the LV in the same manner and connected to a pressure transducer (Model 041-500-503; Cobe, Lakewood, Colo.). The micromanometer was rechecked in vivo by correlation with the LV end-diastolic pressure signal obtained simultaneously through the fluid-filled catheter. After successful anticoagulation with intravenous heparin (300 U/kg), an 18 mm Dacron-segmented polurethane composite outflow graft was sutured to the ascending aorta, and a 51F lighthouse-tipped cannula was inserted through a pursestring suture into the left atrium. The cannulas were connected to the inlet and outlet ports of a Pierce-Donachy pump to establish LV bypass (Fig. 1). To prevent arrhythmia during the preparation, digoxin (0.25 mg, intravenously) and lidocaine (2.5 mg/rnin, intravenously) were administered. If needed, a constant infusion of epinephrine (0.01 to 0.04 Jlg/kg per minute, intravenously), phenylephrine (0.3 to 1.0 Jlg/kg per minute, intravenously), isoproterenol (0.002 to 0.01 Jlg/kg per minute, intravenously), or any combination thereof were used to prevent systemic hypotension or pulmonary hypertension during the experimental preparation. In all of the cases except one, the catecholamines were discontinued before data collection. In one case, we could not wean the animal from catecholamines, and these were maintained at an unchanged rate during all measurements. To assure ventricular filling, we made minor adjustments of intravascular blood volume by infusion of whole blood. Experimental protocol. For control measurements, measurements before pulsatile left atrial-aortic bypass were performed during steady-state contractions. The ESPVR was generated to determine the LV unloaded volume, Yo, by changing preload and afterload conditions by gradually occluding superior and inferior venae cavae and then the aortic root with a vascular clamp. Pulsatile left atrial-aortic bypass was established at a maximal rate termed 100%, as limited by the pump fillingfrom the left atrial cannula, and measurements were then repeated (control measurements of pulsatile left atrial-aortic bypass). A 20-gauge Teflon catheter was passed proximally into the left main coronary artery through the left anterior descending coronary artery to induce heart failure. An average of 3.6 X 107 ± 2.3 X 107 microspheres (10 Jlm, NEM-ooI; New England Nuclear, Boston, Mass.) per 100 gm LV were injected. After reassessment of the ESPVR and V0 after induction of heart failure, the protocols before pulsatile left atrial-aortic bypass and for pulsatile left atrial-aortic bypass were repeated during steady-state conditions as they were in the control mode. At the conclusion of the experimental protocol, the animal was killed, and the heart was excised to verify the proper positioning of the crystals and transducers. Data analysis. Data were recorded on both a multichannel thermal-pen recorder (Gould 3000 Series thermal chart record-

The Journal of Thoracic and

Kawaguchi et ai.

Cardiovascular Surgery Volume 107, Number 6

Table I.

Case Case Case Case Case Case Case

I 50 5

Effect of LV bypass on Vo

1 2 3 4 5 6 7 Mean ± SEM

VOD (ml)

VOL (ml)

r

ESP(mmHg)

ESV(ml)

53.8 28.6 60.1 39.9 21.7 38.3 23.1 37.9 ± 5.2

48.5 28.4 57.2 31.8 21.7 4\.9 23.1 36.1 ± 4.7

0.969 0.934 0.926 0.953 0.943 0.770 0.969

44-120 39-122 25-93 31-153 34-129 27-82 25-79 32 ± 3-111 ± 10

59.6-79.6 35.3-59.4 86.4-126.1 39.3-74.3 3\.9-62.4 5 1.3-7\.2 50.8-100.6 50.7 ± 6.5-8 \.9 ± 8.3

Von, Directly measured VO ; VOL, Vo determined by linear regression; r, correlation coefficient; ESP, end-systolic pressure; ESV, end-systolic volume. SEM, standard error of the mean.

er; Gould Inc., Cleveland, Ohio) and a floppy disk by means of an on-line data acquisition system. Data were analyzed with interactive computer software developed in our laboratory. Ultrasonic signals were continuously monitored with a ultrasonic dimension system (System 6 chassis with four sonomicrometer modules; Triton Technology, San Diego, Calif.) with a sampling rate of 1302 Hz and a practical frequency response of 0 to 64 Hz. Minimal resolution was I mm. The instantaneous distance between the crystals was calculated electronically on the basisofthevelocityofsound in blood (1.58 X 105 cm/s), LV volume (L VV) was calculated from the orthogonal endocardial diameters with a modified ellipsoidal shell model: LVV = rr/6 . DL' DAP' DSL where D L, D AP , and DSL are base-apex major axis, anteroposterior minor axis, and septal-free wall minor axis orthogonal diameters of the LV, respectively.lv" LV mechanics. The contractile state of the LV was assessed by the ventricular end-systolic elastance, E max.9 E max was defined as the maximal slope relative to Vo and normalized for 100gm LV weight. The LV unloaded volume, Yo, was defined as the volume intercept of the baseline ESPVR and calculated by linear regression analysis of end-systolic pressure and volume data.!? Both of the transitional parts of 8 to 10 seconds of data during aortic and caval occlusions were subjected to the linear regression to achieve a wide range of pressure and volume data for linear regression analysis to determine ESPVR. Therefore, end-systolic pressure and volume data ranged from 36 ± 7 (mean ± SD) to 129 ± 26 mm Hg, and from 61 ± 21 to 94 ± 34 ml, respectively. We determined provisional end-systole at the timing of minimal L V compliance, V/P, where V and P are LV volume and pressure, respectively. We then used repetitive linear regressions in which the first linear estimation of V o was used in a second linear regression of end-systolic data points defined by the maximal P/(V-V o) ratio in each cardiac cycle. I 8 This process resulted in a new estimate of'Vs, which was then used to determine end-systole. All the second ESPVR showed highly linear relation (median correlation coefficient = 0.934; V o = 54.5 ± 20.3 ml in the controls; median r = 0.96; Vo = 64.8 ± 26.6 ml in the heart failure measurements). During pulsatile left atrial-aortic bypass, it is difficult to achieve a wide range of pressure and volume data by caval or aortic occlusion. Linear regression analysis from narrow range of pressure and volume data might then result in an inappropriate estimation of ESPVR and Yo. In seven animals, we temporarily inserted the left atrial cannula through the mitral valve into the LV to directly measure Vo by totally unloading the LV.

As shown in Table I, no statistical difference was found between V o and that derived from linear regression. We, therefore, assumed the same Vo in pulsatile left atrial-aortic bypass condition as in conditions before pulsatile left atrial-aortic bypass in each control and heart failure measurements. Fig. 2 illustrates PV A as the area bounded by the end-systolic and end-diastolic P- V relations and the systolic segment of the P-V trajectory. 10, II, 19 PYA, which correlates linearly with Yo, represents the total mechanical energy generated by ventricular contraction.'? It consists of external work within the P- V loop and potential energy on the original side of the loop. Potential energy is generated during contraction and has been assumed to dissipate as heat during relaxation. PYA of the beating LV was calculated by summing all small triangular areas swept by the lines connecting Vo and instantaneous P-V data points during systole." The crescent area between the actual end-diastolic P- V curve and the straight line connecting V 0 and the end-diastolic P- V point was approximated with a third power function." This area was added to the sum of the small triangular areas to complete PV A. End diastole was determined from the electrocardiogram. All the parameters were calculated in every cardiac cycle for 12 seconds, and average data were subjected to statistical analysis. Statistics. Comparisons of variables among the groups were tested by two-way analysis of variance. When analysis of variance showed statistical significance by F test, mean values were compared by the least significance method. Probability values smaller than 0.05 were considered statistically significant. Data are presented as mean ± standard deviation unless otherwise indicated. Results

Hemodynamic parameters before and during pulsatile left atrial-aortic bypass in the control and heart failure groups are shown in Table II. Microsphere injected heart failure significantly decreased Emax, approximately 37% (7.4 ± 0.2 mm Hgjml to 4.7 ± 0.1 mm Hgjml) and cardiac output by 16% ± 11% from controls. Although end-systolic pressure did not change, both end-systolic volume and end-diastolic volume significantly increased by 29% ± 18% and 27% ± 20%, respectively. End-diastolic pressure increased by 20% ± 16%. The heart rate and central venous pressure was unchanged between the control and heart failure groups. In each experiment, heart rate and central venous and

I 50 6

The Journal of Thorac ic and Cardiovascular Surgery June 1994

Kawaguchi et al.

Q)

1.-

::J

C/) C/) Q)

1.-

o,

Pressure-Volume area (PVA) End-diastolic P-V Relation (EDPVR)

Slope of the ESPVR (Emax)

Volume

Fig. 2. Schematic diagram of P-V relationship. Pressure, Left ventricular pressure; Volume, left ventricular volume.

Table II. H emodynamic parameters bef ore and during left atrial-aortic bypass pre-PLAAB-Ctr Pump ra te HR (beats/ min) EDV (rnl) ESV (ml) EDP (rnrn Hg) ESP ( mm Hg ) CV P (mm Hg) mAoP (mrn Hg) CO (Lj'min)

NA 99 ± 13 116 ± 10 87 ± 8 13.4 ± 1.6 66 :t 4 6.8 ± 0.6 57.4 ± 4 6.8 ± 0.5

PLAAB-Ctr

71 ± 104 ± 91 ± 76 ± 6.4 ± 48 ± 6.7 ± 58 ± 6.7 ±

9 9 9* 7 1.3* 6* 0.1 4 0.7

pre-PLA AB-Hf N/A 99 ± 5 135 ± 9t 108 ± st 14.6 ± l.l 69 ± 6 8.0 ± 0.8 58 ± 6 6.0 ± 0.5t

PLAA B-Hf

71 ± 99 ± 110 ± 97 ± 8.4 ± 53 ± 8.4 ± 62 ± 7.0 ±

9 4 10* 9 1.0* 7* 0.7 6 0.5*

PLAAB. Pulsatile left atri al- aort ic bypass; Ctr, control mode; Hf, heart failure mode; NA. not applicable; HR. heart rate ; EDV. end-dia stolic volume; ESV. end-systolic volume; EDP. end-diastolic pressure; ESP, end-systolic pressure ; CVP. central venous pressur e; m AoP, mean aortic pressure; CO, cardiac output. •p < 0.05 compared with values before pulsati le left atrial- a ortic bypass. tp < 0.05 comp ared with the normal.

mean aortic pressure s before pulsatile left atrial-aortic bypass did not change during pulsatile left atrial- aortic bypass. In the control s, pulsatile left atrial-aortic bypass did not change the cardiac output. However, pulsatile left atrial-aortic bypass did significantly reduce end-diastolic pressure and volume by 51% ± 42% and 22% ± II %, respectively. In spite of the fact that end-systolic pressure was significantly decreased by 29 ± 30 mm Hg , end-systolic volumes were similar . In the heart failure model, although both end-diastolic volume and end-diastolic pressure were significantly decreased by 22% ± 15% and 42% ± 19%, respectively, with pulsatile left atrial-aortic bypass, pumping did not affect end-systolic volume. Pulsatile left atrial- aortic bypass significantly increased cardiac output in the heart failure preparations.

Fig. 3 shows representative P-V loops in the control. PVA, external work, and potential energy were 1050 mm Hg/rnl, 878 mm Hg/rnl, and 172 mm Hg/rnl in the period before pulsat ile left atrial-aort ic bypass in the control mode, respectively (Fig. 3, A ). When the pumping was maximized at 60 beats/min, pulsatile left atrialaortic bypass decreased end-diastolic volume from 92.1 ml to 65.4 ml but did not affect end-systolic volume. Because pulsat ile left atrial-aortic bypass was not synchronized with the heart rate , LV P-V tracings vary beat by beat , depending on the random timing of pumping (Fig . 3, B). Although PVA and extern al work decreased by 33% and 25%, respectively, potential energy did not change. When the loops in the control mode before and durin g pulsatile left atrial-aortic bypass are plotted on

The Journal of Thoracic and Cardiovascular Surgery Volume 107, Number 6

Kawaguchi et al.

A

B

C

Il'l

Il'l

Il'l

a

a

a

E a01

a

a

a

a

a

aI")

a

r-...

I

01

a

~

L-

::J

(f) (f)

Q)

L-

0..

a

CD

en

CD

a

".,

a

~

en

'-' Q)

a

~

E

CD

".,

0

30

60

90

Volume (rnl)

120

a

150

I 507

0

30

60

90

120

Volume (ml)

a

150

0

30

60

90

120

150

Volume (rnl )

Fig. 3. P-V loops of the normal heart run. A, P-V loops before pulsatile left atrial-aortic bypass (open circle); B, P-V loops during pulsatile left atrial-aortic bypass (closed circle); C, superimposition of the loops before and during pulsatile left atrial-aortic bypass demonstrating similarESPVRs. Dashed lines represent the ESPVR (Emax = 12.9 mm Hgjml).

the same axis, the ESPVRs are superimposable (Fig. 3, C). Fig. 4 averages E max, PV A, external work, and potential energy in all 14 experiments, pulsatile left atrial-aortic bypass did not affect E max but significantly decreased PVA and EW by 54% ± 21% and 72% ± 14%, respectively. The decreases in PVA are mostly attributable to decreases external work because potential energy was unchanged. Fig. 5 shows representative P-V loops after inducing the heart failure in the same heart shown in Fig. 3. Microsphere injection significantly decreased E max from 12.9 mm Hgjml to 6.5 mm Hgjml and increased both end-systolic volume and end-diastolic volume; that is, the P-V loop shifted to the right. PVA, external work, and potential energy were 1192 mm Hgjml, 853 mm Hgjml, and 439 mm Hgjml in the heart failure mode before pulsatile left atrial-aortic bypass, respectively. Fig. 5, B shows the P-V loops and ESPVR during pulsatile left atrial-aortic bypass. Pumping rate was at the same rate as in the control measurements. In the heart failure experiment, pulsatile left atrial-aortic bypass decreased end-diastolic volume, but the shape of P-V loop changed. Fig. 5, C shows the plotting of the P-V loops in the heart failure mode before and during pulsatile left atrial-aortic bypass. Pulsatile left atrial-aortic bypass did not affect Emax. As in the control experiment, the ESPVRs are superimposable. Fig. 6 shows the means in E max, PVA, external work and potential energy in the heart failure measurements of a1114 experiments. Despite the significant difference in

the baseline Emax, the measurements before pulsatile left atrial-aortic bypass did not change during pulsatile left atrial-aortic bypass in the heart failure mode. The lack of change implies that heart failure decreased LV contractility, whereas pulsatile left atrial-aortic bypass did not affect LV contractility. In the heart failure mode, although pulsatile left atrial-aortic bypass significantly decreased PVA and external work by 47% ± 30% and 65% ± 34%, respectively, pulsatile left atrial-aortic bypass did not change potential energy. Discussion

Recently, Ratcliffe and associates'' suggested that an immediate improvement in contractile state could be achieved in the ischemic heart failure model during nonpulsatile LV bypass.f They showed a negative end-diastolic volume-stroke work relationship by changing afterload in the failing heart and pointed out that data points shifted to the normal, positive relation during nonpulsatile LV bypass. The "preload" recruitable stroke work relation, which is the relation between end-diastolic volume and stroke work in different "preload", has been reported as an index of LV contractility.20, 21 Although Feneley and associates-" showed preload recruitable stroke work relationship is independent of afterload, the interpretation of this negative slope of end-diastolic volume-stroke work relation in different settings of "afterload" during aortic occlusion is still unproven. Because stroke work is afterload-dependent, stroke work decreases in proportion to increases in afterload in high afterload range,23 which would result in a negative end-

I 508

The Journal of Thoracic and Cardiovascular Surgery June 1994

Kawaguchi et al.

A ~

'"

0 0

<,

B

-


:;-

-

a'"

('oj

--'

NS

C1

:::,.

E :::: eo

'" E

.E

r

E

...

w

a

C s--'

'"

a a

a a a ~

a

'"

,....

:::,. a E

0>

:r: E E ~

w

a

'" a '"

a a

-'"

*

a a 0

~

E

0>

:r: E E ';{

> 0-

D :;--'

*

0

a

'"

0

E

N

:r: '" E E

a

0-

W

prePLAAB-Ctr

~

PLAAB-Ctr

* P < 0.05

0

0 0 0

-

a '" '"

a

<,

D

r-,

NS

a 0

'" 0

'"

N

0

Fig. 4. Comparison of LV mechanics in the control mode. Values are mean ± SEM standarderrorof the mean. EW, External work; PE, Potential energy; pre-PLAAB-Ctr, control contractions before pulsatile left atrial-aortic bypass; PLAAB-Ctr, asynchronous, pulsatile left atrial-aortic bypass; NS, statistically insignificant; *statistically significant (p < 0.05).

A Irl

,....... I

C

B 0

0

0 io

Irl

0

0

0

0'1

N

E E

O'l

O'l

O'l

0

CD

0 CD

0 CD

0 ""l

0 ""l

0 ""l

"-"

N

0

N

0

0

Q)

.....

:J CIl CIl Q)

.....

Cl...

0

0

30

60

90

Volume (rnl)

120

0

150 0

30

60

90

Volume (rnl)

120

0

150 0

30

60

90

120

150

Volume (rnl)

Fig. 5. P-V loops after induced heart failure. A, P-V loops before pulsatile left atrial-aortic bypass (open circles), B,P-V loops duringpulsatile leftatrial-aorticbypass (closedcircle); C,superimposition of the loops illustrating similar ESPVR. Dashed lines represent the ESPVR. diastolic volume-stroke work relation. A negative relation of end-diastolic volume-stroke work relation under different settings of afterload might represent this afterload dependency rather than LV contractility itself. We, on the other hand, could find neither improvement nor depression in the LV contractility index, E max, during pulsatile left atrial-aortic bypass of the control and failing heart. The assessment of native heart function is fundamental to the determination of when to wean a patient

from LV bypass. IfLV bypass were to immediately affect LV contractility, it would be difficult to estimate native heart function without cessation of LV bypass. However, because pulsatile left atrial-aortic bypass does not affect the LV contractile state, the underlying native LV systolic function could be estimated with Emax without discontinuing circulatory support. Increases in contractility of the LV are accompanied by increases in LV oxygendemand for excitation contraction

The Journal of Thoracic and Cardiovascular Surgery Volume 107. Number 6

I 509

Kawaguchi et al.

A >' ...J

;;;...J

~

'" '"

0 0

B


'"

~

<,

E ec

NS

~:t:

E

~

C ;;;...J

'"

I

E E

~

W

0

0 0 0

;;;...J

~

'" ,...0 "'

E C.

> 0..

0

0 0

*

"' ~

0 0 0 ~

E E E ';(

+

0 0

~

<,

I

0

E

!oJ

0 0

0 0

'"

0 0

<,

0 0

"'

prePLAAB-Hf

a

PLAAB-Hf

0 0

~ 0

r-, "' 0 0

N

E E

"'

0

0..

0

•

* p < 0.05

0

E

"' "'

*

NS

'" "'

I

W

0

N

0

Fig. 6. Comparison of LV mechanics during heart failure. For abbreviations, see Fig. 4. coupling. 10, 19 With regard to LV energetics, this results in the parallel upward shift of the Vo 2-PVA relationship as shown in Fig. 7.1 9 Parallel shift of Vo 2-PVA relationshipinducedby changes in LV contractility indicatesthat myocardial oxygen consumption increases as LV contractility increases when LV work is constant. 19, 24 In addition, as LV was totally decompressed during LV bypass, the effectsof LV contractility change in LV work would be minimal. It is reasonable to postulate that immediate increases in LV contractility induced LV myocardial oxygen consumption without increasing LV work. However, even though nonpulsati1e LV assist may decrease LV PVA by unloading the LV, leftward shift of a V02-PVAdata point does not necessarily decrease V02 (Fig. 7). Pulsatile LV bypass did not affect LV contractility, thus the Vo2-PVA relationship did not shift upward. Therefore, pulsatile assist can always conserve V02by reducing PYA (Fig. 7). Ifnonpulsatile LV bypass inducesan immediate increase in LV contractility, then, for any given magnitude of LV unloading, nonpulsatile LV bypass should result in less V0 2 conservation than occurs with pulsatile LV bypass. The goalof LV bypassisto decompressthe LV as much as possible. In such a situation, an immediate increase in LV contractility does not impart any increase in LV performance. The useof an assistdeviceimpliesthat the need for immediate improvement of contractility is unnecessary becausethe primary goal is to maximally unload the failing heart and to conserveV02.5-7 The unchanged LV contractilityduring pulsatile left atrial-aortic bypassand its inherent sparing of V0 2 should help the LV to ultimately recover from damage. LV bypass did not affect end-systolic volume in the

..

'

C\J

o

>

PVA Fig. 7. Schematic diagram of LV energetics. Dashed line represents the Voz-PVA relationship during control contractions. Dotted line represents theelevated Voz-PVA relationship byincreases inventricular contractility. Open square represents the Voz-PVA data point before pumping. Closed circle represents the Voz-PVA data point during pulsatile leftatrial-aortic bypass. Open circle represents the Voz-PV A data point with increased ventricular contractility with LV bypass. normal heart (Fig. 8, A). We hypothesized that if LV bypassof the failing heart could achieve the same degree of LV unloading as in the normal heart (i.e., have the same end-systolic and end-diastolic volumes; Fig. 8, A), then decreases in PVA and PE would be much greater in the failing heart than in the normal heart. In the P-V diagram, LV bypass could achieve the greater reduction of

I5I0

The Journal of Thoracic and Cardiovascular Surgery June 1994

Kawaguchi et al.

A B

\!IIIIII!III\

B

Vo

D

~E

A

~

::J

en en

.... Q)

n,

c ~

::J

en en Q)

....

o,

Volume Fig. 8. Schematic diagrams of the changes in the P-V loops during pulsatile left atrial-aortic bypass in the normal and failing heart. A, P-V loops before and after pulsatile left atrial-aortic bypass in the normal heart. Because left heart bypass does not affect the end-systolic parameters, the P-V loop changes from ABCD to EFCD. B, Hypothetical P-V loops before and after pulsatile left atrial-aortic bypass in the failing heart. P-V loops of the failing heart (GHIJ) are larger than those of the normal heart (ABCD). If LV unloading were achieved as the same magnitude in the normal heart, P-V loop shifts to the left along the ESPVR as shown (dotted line). C, P-V loops before and after pulsatile left atrial-aortic bypass in the failing heart. Hashed area represents the P-V loop during pulsatile left atrial-aortic bypass. Dotted area represents the reduction of PVA area during pulsatile left atrial-aortic bypass.

LV PYA (Fig. 8, B). However, pulsatile left atrial-aortic bypass did not affect end-systolic volume and potential energy as much as anticipated, even in the heart failure model in Fig. 8, C. Nonetheless, pulsatile left atrial-aortic bypass did significantly decrease external work and PYA. Asynchronous pulsatile left atrial-aortic bypass cannot continuously unload the LV because the time required for the pump's ejection of blood allows the LV to fill with blood. The magnitude of LV unloading varies beat by beat as the assist pump competes with the native LV for the blood volume (preload). In addition, pulsatile aortic

pressure generated by pulsatile left atrial-aortic bypass occasionally increased LV pressure (afterload) during simultaneous pump and native LV ejections. The overall result was limited pressure and volume unloading of the LV. Nonpulsatile LV bypass, by contrast, has been shown to decrease both end-systolic and end-diastolic volumes in the postischemic heart, resulting in a leftward shift of the P-V loop." On the other hand, asynchronous pulsatile left atrial-aortic bypass did not affect the end-systolic volume and resulted in unchanged potential energy in both the normal and failed hearts, which indicates the limited unloading effect in asynchronous pulsatile left atrialaortic bypass. Although potential energy did not change, pulsatile left atrial-aortic bypass significantly reduced PVA mainly by reducing external work. Because PVA closely correlates with V0 2 in a stable contractile state, this reduction in PVA reasonably accounts for the reduction in V02. The heart failure model used in our experiment is a 10 urn microsphere injection into the main left coronary artery. The heart failure model produced by this size of microsphere has outstanding features which resembles myocardial stunning: (I) absence of myocardial necrosis in the histologic examination strongly suggests that there is almost complete recovery from acute ischemia in the chronic phase, and (2) myocardial contractile and metabolic dysfunctions were significantly attenuated after treatments with recombinant human superoxide dismutase. 24-26 Therefore, heart failure induced by microsphere injection of this size is more likely to be related to chemical reaction than the other ischemic processes obtained by coronary ligation and would be able to simulate myocardial stunning. However, further study should be needed to characterize a true effect of pulsatile left atrial-aortic bypass on the failing heart in clinical settings. Microsphere injection into the left main coronary artery resulted in decreases in LV contractility (Emax) and increases in the LV size. Although microspheres promoted significant decreases in cardiac output, the absolute changes were fairly small, which is understandable in that control hearts had relatively low cardiac output after the experimental preparation. During the experimental heart preparation, pulmonary hypertension or systemic hypotension occurred, which would result in mild damage of the heart. Thus, the myocardium could tolerate only small decrements in cardiac output without compromising coronary blood flow. Although this model might not represent all clinical situations, it would simulate the damage of the heart in shock after cardiotomy. In conclusion, pulsatile left atrial-aortic bypass did not change the LV contractility index, E max, but did decrease

The Journal of Thoracic and Cardiovascular Surgery Volume 107, Number 6

PVA and external work without changing potential energy. These results suggest a limited unloading of the ventricle during pulsatile left atrial-aortic bypass. The first author (O.K.) acknowledges the continuous encouragement by Professor Hiroyuki Suga of the Second Department of Physiology of Okayama University Medical School. REFERENCES I. Pantalos GM, Marks JD, Riebman JB, et al. Left ventricular oxygen consumption and organ blood flowdistribution during pulsatile ventricular assist. Trans Am Soc Artif Organs 1988;34:356-60. 2. Sukehiro S, Flameng W. Effects ofleft ventricular assist for cardiogenic shock on cardiac function and organ blood flow distribution. Ann Thorac Surg 1990;50:374-83. 3. Dennis C, Hall DP, Moreno JR, Senning A. Reduction of the oxygen utilization ofthe heart by left heart bypass. Circ Res 1962;10:298-305. 4. Pennock JL, Pierce WS, Prophet GA, Waldhausen JA. Myocardial oxygen utilization during left heart bypass: effect of varying percentage of bypass flow rate. Arch Surg 1974;109:635-41. 5. Laschinger J C, Cunningham IN, Catinella FP, Knopp EA, Glassman E, Spencer Fe. "Pulsatile" left atrial-femoral artery bypass: a new method of preventing extension of myocardial infarction. Arch Surg 1983;118:965-9. 6. Axelrod JL, Galloway AC, Murphy MS, et al. A comparison of methods for limiting myocardial infarct expansion during acute reperfusion: primary role of unloading. Circulation 1987;76 (Suppi):V28-32. 7. Grossi EA, Krieger KH, Cunningham IN Jr, et al. Time course of effective interventionalleft heart assist for limitation of evolvingmyocardial infarction. J THORAC CARDIOVASC SURG 1986;91:624-9. 8. Ratcliffe MB, Bavaria JE, Wenger RK, Bogen DK, Edmunds LH Jr. Left ventricular mechanics of ejecting postischemic hearts during left ventricular circulatory assistance. J THORAC CARDIOVASC SURG 1991;101:24555. 9. Suga H, Sagawa K. Instantaneous pressure-volume relationships and their ratio in the excised,supported canine left ventricle. Circ Res 1974;35:117-26. 10. Suga H, Sagawa K, Shoukas AA. Load independence of the instantaneous pressure volume ratio of the canine left ventricle and effects of epinephrine and heart rate on the ratio. Circ Res 1973;32:314-22. II. Suga H, Hisano R, Goto Y, Yamada 0, Igarashi Y. Effect of positive inotropic agents on the relation between oxygen consumption and systolic pressure volume area in canine left ventricle. Circ Res 1983;53:306-18. 12. Suga H, Hayashi T, Suehiro S, Hisano R, Shirahata M, Ninomiya 1. Equal oxygen consumption rates of isovolumic and ejection contractions with equal systolic pressure volume areas in canine left ventricle. Circ Res 1981; 49:I082-91.

Kawaguchi et ai.

15 11

13. Suga H, Hisano R, Hirata S, Hayashi T, Ninomiya 1. Mechanism of higher oxygen consumption rate: pressureloaded versus volume-loaded heart. Am J Physiol I982;242:H942-8. 14. Goto Y, Yamamoto J, Saito M, et al. Effects of right ventricular ischemia on left ventricular geometry and the enddiastolic pressure-volume relationship in the dog. Circulation 1985;72:II 04-14. 15. Little WC, O'Rourke RA. Effect of regional ischemia on the left ventricular end systolic pressure-volume relation in chronically instrumented dog 120. J Am Coll Cardiol 1985;5:297-302. 16. Nakamura T,HayashiK,SekiJ,etal. Effect of drive model of left ventricular assist device on the left ventricular mechanics. Artif Organs 1988;12:56-66. 17. Kass DA, Yamazaki T, BurkhoffD, Maughan WL, Sagawa K. Determination of left ventricular end-systolic pressure-volume relationships by the conductance (volume) catheter technique. Circulation 1986;73:586-95. 18. Kass DA, Midei M, Graves W, Brinker JA, Maughan WL. Use of a conductance (volume) catheter and transient inferior venacaval occlusion for rapid determination of pressure-volume relationship in man. Cathet Cardiovasc Diagn 1988;15:192-202. 19. Suga H. Ventricular energetics. Physiol Rev 1990;70:24777. 20. Feneley MP, Gaynor JW, Glower DD, BurkhoffD, Rankin JS. Comparison of the relationship between left ventricular preload recruitable stroke work and systolic elastance during increased afterload in isolated canine hearts and in conscious dogs. Automedica 1987;9:240. 21. Glower DD, Spratt JA, Snow ND, et al. Linearity of the Frank-Staring relationship in the intact heart: the concept of preload recruitable stroke work. Circulation 1985; 71:994-1009. 22. Glower DD, Spratt JA, Kabas JS, Davis JW. Quantification of regional myocardial dysfunction after acute ischemic injury. Am J Physiol 1988;255:H85-93. 23. Sunagawa K, Maughan WL, Sagawa K. Optimal arterial resistance for the maximal stroke work studied in isolated canine left ventricle. Circ Res 1985;56:586-95. 24. Hori M, Koretsune Y, Iwai K, et al. A possible model of the anginal syndrome with normal coronary arteriograms: microembolization of canine coronary arteries. Heart Vessels 1987;3:7-13. 25. Hori M, Gotoh K, Kitakaze M, et al. Role of oxygen-derived free radicals in myocardial edema and ischemia in coronary microvascular embolization. Circulation 1991; 84:828-40. 26. Takashima S, Hori M, Kitakaze M, Sato H, Inoue M, Kumada T. Superoxide dismutase restores contractile and metabolic dysfunction through augmentation of adenosine release in coronary microembolization. Circulation 1993; 87:982-95.