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J Thorac Cardiovasc Surg 1999;117:164-171
© 1999 Mosby, Inc.

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

VENTRICULOARTERIAL COUPLING WITH INTRA-AORTIC BALLOON PUMP IN ACUTE ISCHEMIC HEART FAILURE

Osamu Kawaguchi, MDa, Walter E. Pae, MD, FACSa, Bill B. Daily, MD, PhDb, William S. Pierce, MD, FACSa

From the Department of Surgery, Division of Cardiothoracic Surgery, College of Medicine, The Pennsylvania State University, The Milton S. Hershey Medical Center, Hershey, Pa,a and the Department of Surgery, Jewish Hospital, St Louis, Mo.b

Received for publication Feb 19, 1998. Revisions requested March 24, 1998. Revisions received May 20, 1998. Accepted for publication Aug 6, 1998. Address for reprints: William S. Pierce, MD, Director, Office of Surgical Research, Associate Chairman, Department of Surgery, The Milton S. Hershey Medical Center, The Pennsylvania State University, PO Box 850, Hershey, PA 17033.


   Abstract
Top
 Abstract
Introduction
 Materials and methods
 Result
 Discussion
 Appendix
 References
 
Purpose: We analyzed the mechanism of effects of intra-aortic balloon pumping using the pressure-volume relationship and ventriculoarterial coupling in the normal and failing hearts.
Materials: In 12 anesthetized Holstein calves (weight, 94 ± 8 kg), the ventricular end-systolic and arterial elastances, pressure-volume area, and external work were analyzed during steady-state contractions with traditional hemodynamic parameters with intra-aortic balloon pumping–off and –on (1:1 synchronous ratio). An acute ischemic heart failure was induced by injecting 10 µm microspheres (4.2 ± 1.8 x 107 · 100g left ventricular weight–1) into the left main coronary artery; all measurements were repeated.
Results: Intra-aortic balloon pumping did not change hemodynamic parameters in the control. However, during heart failure, intra-aortic balloon pumping decreased the arterial elastance from 3.6 ± 1.3 mm Hg to 2.9 ± 1.2 mm Hg · mL–1 while not affecting the ventricular end-systolic elastance, this resulted in an improvement of the ventriculoarterial coupling ratio from 3.1 ± 0.8 to 2.3 ± 0.8. Intra-aortic balloon pumping decreased not only end-systolic pressure (from 69 ± 16 mm Hg to 64 ± 19 mm Hg) but end-diastolic volume and pressure (from 139 ± 38 mL to 137 ± 37 mL and from 13.9 mm Hg to 12.8 mm Hg, respectively) with the leftward shift of the pressure-volume loop. Pressure-volume area decreased (from 914 ± 284 mm Hg to 849 ± 278 mm Hg · mL) although stroke volume increased (from 21 ± 6 mL to 24 ± 6 mL).
Conclusion: Reduction of the arterial elastance with intra-aortic balloon pumping improved the ventriculoarterial coupling ratio and increased stroke volume. Leftward shift of the pressure-volume loop resulted in the reduction of pressure-volume area, which suggests the conservation of the myocardial oxygen consumption.


   Introduction
Top
 Abstract
 Introduction
Materials and methods
 Result
 Discussion
 Appendix
 References
 
Intra-aortic balloon pumping (IABP) is a common method of circulatory support for acute failing hearts. The major effect of IABP is afterload reduction and a diastolic augmentation. The former indicates a low impedance shunt for the aortic blood during cardiac systole, which provides the mechanical unloading of the left ventricle (LV) by reducing the LV ejection pressure.Go Go 1,2 The latter elevates the perfusion pressure of the coronary artery to increase coronary blood flow,Go 3and the reduction of cardiac work load is expected to reduce the need for oxygen.Go Go 4,5 Patients whose condition requires IABP after the coronary arterial bypass grafting may immediately benefit from increased coronary perfusion and reversal of acute ischemia. On the other hand, the unloading effect of IABP would be more important in patients after the valve operation. However, the data for IABP on the LV work load are limited, especially in the failing heart. The mechanism for the unloading effect with IABP is not completely understood. The purpose of this study was to evaluate the effect of IABP on LV work load by assessing changes in pressure-volume relationship and ventriculoarterial coupling.


   Materials and methods
Top
 Abstract
 Introduction
 Materials and methods
Result
 Discussion
 Appendix
 References
 
Experimental preparation
A total of 12 Holstein calves weighing from 86 to 104 kg (average, 94 ± 8 kg) was studied. With the calf under halothane anesthesia, an endotracheal tube was inserted; the ventilation was maintained by a volume respirator with 100% oxygen. A median sternotomy was performed, and the left internal thoracic artery was cannulated for the aortic pressure monitoring. The azygos and hemiazigos veins were ligated. Reversible occluders were placed around the superior and inferior venae cavae.

As shown in Fig. 1, 3 pairs of pulse-transit ultrasonic dimension crystals (4-mm diameter) made of 5 MHz piezoelectric crystals (LTZ-2; Transducer Products, Goshern, Conn) were placed at the endocardial surface (the anteroposterior minor axis, septal-free wall minor axis, and base-apex major axis of the LV).68 Ultrasonic signals were continuously monitored with an ultrasonic dimension system (System 6 chassis with 4 sonomicrometer modules; Triton Technology, San Diego, Calif) with the minimal resolution of 1 mm. LV volume was calculated from the orthogonal endocardial diameters with a modified ellipsoidal shell model.Go Go 6-8



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  		Fig. 1. Experimental preparation. SVC, Superior venae cavae; AO, aorta; PA, pulmonary artery; RA, right atrium; LA, left atrium; IVC, inferior venae cavae; LVP-Fluid, a catheter for fluid-filled LV pressure; LVP-Millar, a manometer-tipped catheter for LV pressure.

 

LV volume = {pi}/6 x DL x DAP x DSL

where DL, DAP, and DSL are base-apex major axis, anteroposterior minor axis, and septal-free wall minor axis orthogonal diameters of the LV, respectively.After anticoagulation with intravenous heparin (300 units/kg), a micromanometer-tipped catheter (model SPC-350; Millar Instruments, Inc, Houston, Texas) with a pressure transducer unit (model TCB-500; Millar Instruments, Inc) was inserted into the LV through the LV free wall. The micromanometer was rechecked in vivo by correlation with the LV end-diastolic pressure signal simultaneously obtained through the fluid-filled polyethylene catheter connected to a pressure transducer (model 041-500-503; Cobe, Lakewood, Colo). An IABP (Kontron model 10; Arrow International, Reading, Pa) was inserted from the left femoral artery to the descending aorta. The position of the balloon pump was assured by pulsation.To prevent arrhythmia during the preparation, digoxin (0.25 mg, intravenously) and lidocaine (2.5 mg/min, intravenously) were administered. To maintain systemic pressure and ventricular filling, adjustments of intravascular blood volume were made by infusion of whole blood. Hematocrit was maintained at 35.2% ± 2.7% during data collection. If needed to prevent systemic hypotension or pulmonary hypertension during the experimental preparation, a constant infusion of epinephrine (0.01 to 0.04 µ/kg per minute, intravenously), phenylephrine (0.3 to 1.0 µ/kg per minute, intravenously) and/or isoproterenol (0.002 to 0.01 µ/kg per minute, intravenously) were used.Go Go 7,8 In all cases, these drugs were successfully weaned before data collection.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).

Experimental protocol
When hemodynamic steady-state was achieved after the calves were weaned from catecholamines, caval and aortic occlusions were applied, and LV unloaded volume and V0 were determined. Then end-systolic and end-diastolic volume and pressure, central venous pressure, mean aortic pressure, and the pressure-volume relationship (which includes end-systolic elastance, pressure-volume area, and external work [EW]) were assessed during steady-state beats. IABP was started with 1:1 synchronous ratio; all measurements were repeated as a control.

After baseline measurements, to induce heart failure, a 20-gauge Teflon catheter was passed proximally into the left main coronary artery through the left anterior descending coronary artery.79 An average of 4.2 ± 1.8 x 107 per 100 g LV-weight microspheres (10 µ, NEM-001; New England Nuclear, Boston, Mass) was injected. After all tracings reached steady-state, heart failure measurements were performed. 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
All data were sampled simultaneously at 150 Hz and stored on a floppy disk via an on-line data acquisition system. Data were analyzed with interactive computer software that was developed in our laboratory.

LV mechanics
The contractile state of the LV was assessed by the ventricular end-systolic elastance, Emax, which has been recognized as a load-independent index of contractile status (Fig. 2).Go Go 10-12 Practically, Emax of each contraction was defined as the maximal slope relative to the LV unloaded volume, V0, which is the volume intercept of the end-systolic pressure-volume relationship, and normalized for 100 g LV weight. V0 was determined by the repetitive linear regression of end-systolic pressure and volume data at end systole during baseline measurement.



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  		Fig. 2. A, Schematic diagram of the pressure-volume relationship. EDPVR, End-diastolic pressure-volume relationship; PVA, pressure-volume area; PE, potential energy. B, Schematic diagram of the end-systolic ventricular and arterial elastance. The slope of the arterial end-systolic pressure-volume relationship (ESPVR; line A) is Ea with the volume intercept of end-diastolic volume. Line B represents the ventricular ESPVR, with the volume intercept of V0.

 
Pressure-volume area is the area bounded by the end-systolic and end-diastolic pressure-volume relationships and the systolic segment of the pressure-volume trajectory.Go Go Go 10,12,13 Because pressure-volume area linearly correlates with myocardial oxygen consumption in a stable contractile state regardless of changes in loading conditions, pressure-volume area has been recognized as a measure of total mechanical energy.Go Go Go 10,13-15 Pressure-volume area consists of EW within the pressure-volume loop and potential energy, a triangular area next to EW. The ratio of EW to pressure-volume area was calculated as an index of cardiac performance.Go Go 12,16 End-diastole was determined from the R wave of the electrocardiogram. All the parameters were calculated in every cardiac cycle for 12 seconds, and averaged data were subjected to statistical analysis.

Ventriculoarterial coupling
Effective arterial elastance, Ea, is defined as the ratio of end-systolic pressure to stroke volume.1719 Therefore the slope of the arterial end-systolic pressure-volume relationship is Ea with the volume axis intercept of end-diastolic volume although the ventricular end-systolic pressure-volume relationship has a slope of Emax with the volume axis intercept of V0. Because Ea is related to the Windkessel parameters of the arterial system, Ea provides a quick and practical measure of the arterial properties.Go 19Although Ea does not represent the physiologic elastance or compliance of any specific part of the arterial system, Ea represents an "effective" arterial elastance as the ventricle ejects. Therefore Ea suits the assessment of the effect of IABP in the in situ heart. When the ventricle is coupled with the arterial system, the equilibrium is determined graphically as the intersection between the arterial and ventricular end-systolic pressure-volume relationships. In this framework, end-systolic volume is given as the intersection of these 2 lines, and stroke volume is the difference between the end-diastolic and end-systolic volumes.

Statistics
Comparisons of variables among the groups were tested by 2-tailed paired t test. Data are presented as mean ± SD unless otherwise indicated.


   Result
Top
 Abstract
 Introduction
 Materials and methods
 Result
Discussion
 Appendix
 References
 
Fig. 3 shows the pressure-volume loop and the end-systolic pressure-volume relationship in the control and heart failure runs. Acute ischemic heart failure reduced Emax from 2.9 to 1.8 mm Hg · mL · 100 g LV weight1 and resulted in the significant rightward shift of the pressure-volume loop. However, in both runs, IABP did not affect Emax itself. In the control run, although IABP reduced the peak LV pressure and changed the shape of the pressure-volume loop, the effect on the end-systolic pressure-volume data was minimal. On the other hand, IABP in heart failure significantly affected both end-systole and end-diastole, which resulted in a significant leftward shift of the pressure-volume loop. As a result, end-systolic pressure decreased from 86 to 80 mm Hg. Stroke volume increased from 13.7 to 15.9 mL. Effective Ea reduced from 6.3 to 5.5 mm Hg · mL · 100 g LV weight–1. The ratio, Ea/Emax, reduced from 3.5 to 2.9.



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  		Fig. 3. Pressure-volume relationships in the control and heart failure runs. A, Pressure-volume loop shifted to the left with the reduction of the slope of the end-systolic pressure-volume relationship and the increases in volume intercept after microsphere injection. Open circles and triangles represent end-systolic pressure-volume data points during inferior vena cava occlusion. B, Pressure-volume loops of the control run. Closed squares represent the pressure-volume loop without IABP; circles represent the pressure-volume loop with IABP. C, Heart failure run. Open circles and squares represent the end-systolic and end-diastolic pressure-volume data.

 
Table I averages hemodynamic parameters in the control and heart failure model. The heart rate did not change during the experiment. Because we administered whole blood to maintain systemic arterial pressure, both end-systolic volume and end-diastolic volume increased by 76% ± 35% and 44% ± 23%, respectively. Hence, although end-systolic pressure did not significantly change, stroke volume decreased by 22% ± 28%. IABP increased mean aortic pressure in both the control and heart failure runs. However, IABP did not affect these hemodynamic parameters in the controls. On the other hand, during heart failure, IABP increased stroke volume by 15% ± 18% with decreases in end-systolic pressure. IABP also decreased end-diastolic pressure and volume 3% ± 5% and 9% ± 11%, respectively, which indicates that preload of the LV is also reduced although stroke volume increased.


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  		Table I. Hemodynamic parameters during heart failure induction
 
Fig. 4 averages the parameters for LV mechanics and the Ea in all 12 animals.Contractility after microsphere injection was shown by Emax (decreased from 2.7 ± 0.5 mm Hg to 1.3 ± 0.4 mm Hg · mL1 · 100 g LV1). IABP did not change Emax (2.7 ± 0.5 mm Hg to 2.9 ± 0.7 mm Hg · mL1 · 100 g LVl control versus 1.3 ± 0.4 mm Hg to 1.3 ± 0.5 mm Hg · mLl · 100 g LV–1 heart failure). However, IABP significantly decreased Ea in heart failure (2.5 ± 1.3 mm Hg to 2.6 ± 1.6 mm Hg · mL1 · 100 g LV–l in the controls versus 3.6 ± 1.3 mm Hg to 2.9 ± 1.2 mm Hg · mL1 · 100 g LV–1 heart failure). As a result, the ratio, Ea/Emax decreased from 3.1 ± 0.8 to 2.3 ± 0.8. Although pressure-volume area did not change in the controls, in heart failure, pressure-volume area decreased from 951 ± 288 mm Hg · mL · 100 g LV weight–1 to 862 ± 269 mm Hg · mL · 100 g LV weight–1; EW did not change. When work efficiency was assessed by the ratio, EW/pressure-volume area (EW/PVA) improved from 46% ± 6% to 53% ± 7%. This suggested the improvement of the mechanical efficiency from myocardial oxygen consumption to EW as the improved Ea/Emax ratio suggested.



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  		Fig. 4. Left ventricular mechanics and ventriculoarterial coupling. Circles and squares indicate the individual data. Comparison of left ventricular mechanics and ventriculoarterial coupling with IABP. Means ± SD indicated. C, Control; C-I, control with IABP; HF, heart failure; HF-I, heart failure with IABP.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and methods
 Result
 Discussion
Appendix
 References
 
The mechanism of IABP for cardiac support has been recognized as a reduction of LV work load achieved by afterload reductionGo Go 1,2 and an enhancement of coronary blood flow secondary to a diastolic augmentation.Go 3This would result in an improvement of oxygen supply/ demand ratio of the heart. Therefore IABP has been recognized to have an important role in the treatment of the patient with acute heart failure. However, the effect of IABP on LV mechanics assessed with the ventricular elastance, Emax, and/or arterial elastance, Ea, is limited.20

Bavaria and colleaguesGo 20 assessed Emax with circulatory assist devices on stunned myocardium. Despite a similar leftward shift of the pressure-volume loop, they observed a significant increase in Emax with IABP although we found no improvements. This may depend on the difference of the coronary perfusion pressure. In our experiment, "mean" aortic pressure was maintained at 57 ± 16 mm Hg to maintain the coronary perfusion although LV "peak" pressure was 57 ± 12 mm Hg in their experiment.Go 20Therefore there is a possibility that the coronary perfusion pressure was not high enough to maintain coronary blood flow, which would result in deterioration of LV contractility, Emax. Emax is more coronary perfusion pressure dependent when perfusion pressure becomes less than 50 mm Hg.Go 21 When the coronary perfusion pressure is maintained above the physiologic range where coronary autoregulation exists, LV contractility may not necessarily be enhanced by IABP.

The effect of IABP on LV mechanics is well understood when Ea is taken into account.1719 The artery is characterized as an elastic chamber with a volume elastance, similar to the ventricle, which has the end-systolic pressure-volume relationship. The coupling between the ventricle and arterial afterload is characterized in terms of the slope of the end-systolic pressure-volume relationship, Emax, and the slope of the arterial end-systolic pressure-stroke volume relationship, Ea.Go 19Both of these relationships are superimposed in the same pressure-volume plane where the stroke volume that the ventricle can eject from a given end-diastolic volume is represented as the intersection of these 2 relationships. IABP decreased Ea, which suggested reduction of aortic impedance especially in heart failure.Go 2When Ea decreases without affecting Emax, the intersection point shifts down and to the left, resulting in an increase in stroke volume as shown in Fig. 5, A.This has been considered one of the major mechanisms to increase stroke volume with afterload reduction.22



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  		Fig. 5. Schematic diagram of changes in pressure-volume loops with IABP. IABP induced changes in Ea (arrows). Shadowed areas represent the pressure-volume area preserved when the pressure-volume loop changed by IABP. Reduction of the pressure-volume area is larger with the preload reduction (shaded area). ESPVR, End-systolic pressure-volume relationship; EDPVR, end-diastolic pressure-volume relationship.

 
The ventricle transfers the mechanical energy of contraction to the intracavitary blood as an adequate flow to the arterial system. When the energy source and its load are matched, a maximal amount of energy is transferred from the source to the load.Go l8 This is important because, for any given state of preload, contractility, and afterload, there is a unique combination of ventricular and arterial elastances that will maximize ventricular stroke work, or EW.Go Go 17,18 The optimality of afterload is defined as the ratio of EW to its maximal value (appendix).Go 23

Over 1.0 of Ea/Emax, the optimality proportionally decreases as Ea/Emax increases (Fig. 6).Ratios outside of the range of 0.5 to 1.0 are said to reflect varying degrees of ventriculoarterial uncoupling and changes in the ratio of Ea to ventricular contractility. The deterioration of the optimality in the ventricle with poor contractility has been demonstrated in animals and in patients.Go Go 24,25 In our experiment, the significant reduction (Fig. 6Go) of optimality suggested severe uncoupling after heart failure induction.Go 26To improve the optimality, enhancement of Emax and/or reduction of Ea is necessary. Our result showed that IABP effectively reduces Ea without affecting Emax and improving Ea/Emax. The afterload reduction with other methods would result in the decrease of the end-systolic pressure and hence mean pressure, which is disadvantageous to maintain coronary perfusion pressure. On the other hand, with diastolic augmentation, IABP improves the relationship by reducing Ea without compromising coronary perfusion pressure. By changing the Ea/Emax ratio to the normal side, IABP improves afterload particularly in heart failure by decreasing myocardial oxygen consumption and/or increasing EW.



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  		Fig. 6. Changes in the optimality of the afterload with IABP after heart failure as a function of the ventriculoarterial ratio, Ea/Emax. The optimality of the afterload becomes unity when Ea/Emax is unity. When Ea/Emax changes from 3.0 to 2.4, the optimality increases from 0.75 to 0.83. The open square indicates the average data for the heart failure with IABP. The open circle indicates the average data for the heart failure.

 
In addition, our data suggested that IABP also has the unloading effect of the LV as shown in reduced end-diastolic volume and pressure. As IABP reduced preload and afterload of the heart in the heart failure run, it resulted in the significant reduction of pressure-volume area. Fig. 5, GoB, shows the schematic diagram of pressure-volume loops with the preload reduction. With decrease in end-diastolic volume, the intersection between the ventricular and arterial end-systolic pressure-volume relationship further shifts to the left. Therefore, with a given change in Ea as shown, the reduction of the pressure-volume area is much greater with the preload reduction. As pressure-volume area linearly correlates with myocardial oxygen consumption, our result suggests that IABP has the effect of myocardial oxygen conservation because of the preload reduction, especially in the damaged heart.

Despite the significant increase in stroke volume with IABP in heart failure, IABP did not increase EW, which is presumably due to the afterload reduction. However, it resulted in a significant reduction in potential energy and pressure-volume area. Because of the reduction of pressure-volume area with unchanged EW, there is a significant improvement in work efficiency of the heart. Work efficiency does not change with mechanical efficiency (EW/myocardial oxygen consumption) in a parallel manner because mechanical efficiency is the product of work efficiency and efficiency from myocardial oxygen consumption to pressure-volume area. However, this suggests the possibility that mechanical efficiency is effectively improved with the preload reduction and the correction of the ventriculoarterial coupling toward the normal side although mechanical efficiency might not improve to the same extent as work efficiency improved.

The same extent of changes in ventriculoarterial coupling in vasodilator therapy has been observed in the heart failure patient.Go 16Others have measured the same parameters (such as Emax, Ea, Ea/Emax, EW/PVA) and concluded that the reduction of afterload with nitroprusside plays an important role in restoring optimal ventricular load, in which work efficiency is improved by changing the ratio, Ea/Emax. Therefore the reduction of end-diastolic volume, Ea/Emax, and improvement of work efficiency is consistent with afterload reduction regardless of the mechanism to reduce the afterload.

The primary limitation of this study that could affect its applicability to clinical IABP is that we used a microsphere-induced heart failure model. In the patients with postcardiotomy after coronary artery bypass graft, the damage to the heart may be different from our model even though the hemodynamic change is similar. The conservation of myocardial oxygen consumption with IABP is strongly suggested from the pressure-volume diagram. In addition, although pressure-volume area linearly correlates with myocardial oxygen consumption, EW/PVA does not always represent the changes in the mechanical efficiency when the relation between pressure-volume area and myocardial oxygen consumption changes with the intervention. Because we did not measure myocardial oxygen consumption, the direct measurement of myocardial oxygen consumption will be necessary to characterize fully the effect of IABP on LV energetics.

To calculate the optimality, we used the same equation as Sunagawa's group.Go 22 They ignored the diastolic compliance on EW area to simplify the equation. However, especially in heart failure, this part may not be small enough to be negligible. In that case, the optimal relationship becomes preload dependent of the LV because the diastolic compliance is exponentially preload dependent. Therefore the optimal relationship might not improve to the same extent as shown in this article.

In conclusion, IABP unloads the LV by reducing preload and afterload especially in the failing heart. IABP decreases afterload by improving ventriculoarterial coupling. Data suggested that IABP improves mechanical efficiency of the LV.


   Appendix
Top
 Abstract
 Introduction
 Materials and methods
 Result
 Discussion
 Appendix
References
 
On the pressure-volume diagram, end-systolic pressure, Pes, is determined with either Emax or Ea as follows:

Pes = Emax x (Ves – V0)

Pes = –Ea x (Ves – Ved)

where Ves and Ved are end-systolic and end-diastolic volume, respectively. Then, end-systolic volume is calculated as:


Ves = Ea x (Ved – V0)/Emax + Ea

Because stroke volume is calculated as (Ved – Ves), assuming a constant LV pressure during ejection, EW is approximated as:


Therefore EW is a function of Emax and Ea. From Equation 1, maximal EW (EWmax) will be obtained when Emax equals Ea:


Then maximal EW generated by the ventricle is determined by the ratio Ea/Emax as shown in Fig 6. The optimal ratio is achieved when the Ea/Emax is 1.Go 23


   Acknowledgments
 
We thank G. Allen Prophet, Cindy Miller, and David N. Katz for their help and Mark Schwartz for the experimental preparation.


   References
Top
 Abstract
 Introduction
 Materials and methods
 Result
 Discussion
 Appendix
 References
 

  1. Urschel CW, Eber L, Forrester J, et al. Alteration of mechanical performance of the ventricle by intraaortic balloon counterpulsation. Am J Cardiol 1970;25:546-51. [Medline]
  2. Kim SY, Euler DE, Jacobs WR, et al. Arterial impedance in patients during intraaortic balloon counterpulsation. Ann Thorac Surg 1996;61:888-94. [Abstract/Free Full Text]
  3. Brown BG, Goldfarb D, Topaz SP, Gott VL. Diastolic augmentation by intra-aortic balloon. J Thorac Cardiovasc Surg 1967;53:789-804. [Medline]
  4. McDonnell MA, Kralios AC, Tsagaris TJ, Kuida H. Comparative effect of counterpulsation and bypass on left ventricular myocardial oxygen consumption and dynamics before and after coronary occlusion. Am Heart J 1976;97:78-88.
  5. Williams DO, Korr KS, Gewirtz H, Most AS. The effect of intraaortic balloon counterpulsation on regional myocardial blood flow and oxygen consumption in the presence of coronary artery stenosis in patients with unstable angina. Circulation 1982;66:593-7. [Abstract/Free Full Text]
  6. Little WC, O'Rourke RA. Effect of regional ischemia on the left ventricular end-systolic pressure-volume relation in chronically instrumented dog. J Am Coll Cardiol 1985;5:297-302. [Abstract]
  7. Kawaguchi O, Sapirstein JS, Daily WB, et al. Left ventricular mechanics during synchronous left atrial-aortic bypass. J Thorac Cardiovasc Surg 1994;107:1503-11. [Abstract/Free Full Text]
  8. Kawaguchi O, Pae WE, Daily WB, et al. Left ventricular mechanoenergetics during asynchronous left atrial-to-aortic bypass: effects of pumping rate on cardiac workload and myocardial oxygen consumption. J Thorac Cardiovasc Surg 1995;110:793-9. [Abstract/Free Full Text]
  9. Hori M, Gotoh K, Kitakaze M, et al. Role of oxygen-derived free radicals in myocardial edema and ischemia in coronary microvascular embolization [see comments]. Circulation 1991;84:828-40. [Abstract/Free Full Text]
  10. Suga H, Hisano R, Goto Y, et al. 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. [Abstract/Free Full Text]
  11. Suga H, Sagawa K. Instantaneous pressure-volume relationships and their ratio in the excised, supported canine left ventricle. Circ Res 1974;35:117-26. [Abstract/Free Full Text]
  12. 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. [Abstract/Free Full Text]
  13. Suga H. Ventricular energetics. Physiol Rev 1990;70:247-77. [Free Full Text]
  14. Suga H, Hayashi T, Suehiro S, et al. Equal oxygen consumption rates of isovolumic and ejecting contractions with equal systolic pressure-volume areas in canine left ventricle. Circ Res 1981;49:1082-91. [Abstract/Free Full Text]
  15. Suga H, Hisano R, Hirata S, et al. Mechanism of higher oxygen consumption rate: pressure-loaded vs volume-loaded heart. Am J Physiol 1982;242:H942-8.
  16. Kameyama T, Asanoi H, Ishizaka S, Sasayama S. Ventricular load optimization by unloading therapy in patients with heart failure. J Am Coll Cardiol 1991;17:199-207. [Abstract]
  17. Sunagawa K, Maughan W, Burkhoff D, Sagawa K. Left ventricular interaction with arterial load studied in isolated canine ventricle. Am J Physiol 1983;242:H154-60.
  18. Sunagawa K, Maughan W, Sagawa K. Optimal arterial resistance for the maximal stroke work studied in isolated canine ventricle. Circ Res 1985;56:586-95. [Abstract/Free Full Text]
  19. Sagawa K, Maughan WL, Suga H, Sunagawa K. Cardiac contraction and the pressure-volume relationship. New York: Oxford Press; 1988. p. 232-98.
  20. Bavaria JE, Furukawa S, Kreiner G, et al. Effect of circulatory assist devices on stunned myocardium. Ann Thorac Surg 1990;49:123-8. [Abstract]
  21. Sunagawa K, Maughan WL, Friesinger G, et al. Effects of coronary arterial pressure on left ventricular end-systolic pressure-volume relation of isolated canine heart. Circ Res 1982;50:727-34. [Abstract/Free Full Text]
  22. Sunagawa K, Sagawa K, Maughan WL. Ventricular interaction with the vascular system. In: Yin FCP, editor. Ventricular interaction. New York: Springer; 1986. p. 210-39.
  23. Kubota T, Alexander J Jr, Itaya R, et al. Dynamic effects of carotid sinus baroreflex on ventricular coupling studied in anesthetized dogs. Circ Res 1992;70:1044-53. [Abstract/Free Full Text]
  24. Myhre E, Johansen A, Bjomstad, Piene H. The effect of contractility and preload on matching between the canine left ventricle and afterload. Circulation 1986;73:161-71. [Abstract/Free Full Text]
  25. Asanoi H, Sasayama S, Kameyama T. Ventriculoarterial coupling in normal and failing heart in humans. Circ Res 1989;65:483-93. [Abstract/Free Full Text]
  26. Sunagawa K, Hayashida K, Sugimachi M, et al. Optimal left ventricle versus optimal afterload. In: Sasayama S, Suga H, editors. Recent progress in failing heart syndrome. New York: Springer; 1991. p. 161-85.



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J. J. Schreuder, F. Maisano, A. Donelli, J. R.C. Jansen, P. Hanlon, J. Bovelander, and O. Alfieri
Beat-to-Beat Effects of Intraaortic Balloon Pump Timing on Left Ventricular Performance in Patients With Low Ejection Fraction
Ann. Thorac. Surg., March 1, 2005; 79(3): 872 - 880.
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D. Nordhaug, T. Steensrud, S. Muller, K. V. Husnes, and T. Myrmel
Intraaortic Balloon Pumping Improves Hemodynamics and Right Ventricular Efficiency in Acute Ischemic Right Ventricular Failure
Ann. Thorac. Surg., October 1, 2004; 78(4): 1426 - 1432.
[Abstract] [Full Text] [PDF]

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