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Ann Thorac Surg 2004;77:158-163
© 2004 The Society of Thoracic Surgeons

Original article: cardiovascular

Hemodynamic unloading of the failing left ventricle using an arterial-to-arterial extracorporeal flow circuit

Benjamin E. Haithcock, MDa,b, Hideaki Morita, MDa,b, Nervin H. Fanous, MDa,b, George Suzuki, MDa,b, Hani N. Sabbah, PhDa,b*

a Division of Cardiovascular Medicine, Department of Medicine, Henry Ford Heart and Vascular Institute, Detroit, Michigan, USA
b Department of Surgery, Henry Ford Health System, Detroit, Michigan, USA

* Address reprint requests to Dr Sabbah, Cardiovascular Research, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI 48202, USA.
e-mail: hsabbah1{at}hfhs.org

Presented at the Forty-ninth Annual Meeting of the Southern Thoracic Surgical Association, Miami Beach, FL, Nov 7–9, 2002.


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 
BACKGROUND: We tested the hypothesis that creation of a constant-flow extracorporeal circuit between the proximal and distal aorta will unload the failing left ventricle.

METHODS: Studies were performed in 14 heart failure dogs produced by intracoronary microembolizations. An extracorporeal circuit incorporating a diagonal pump was placed between a femoral and a carotid artery, with flow directed to the carotid. Hemodynamic measurements were made with the pump delivering 0.25 L/min through the circuit for 4 hours (active group). Measurements obtained from 8 sham-operated heart failure dogs were used for comparison (control group). Heart rate, peak left ventricular systolic pressure, left ventricular end-diastolic pressure, end-diastolic volume, end-systolic volume, and ejection fraction were measured at baseline and at 30, 60, 120, and 240 minutes.

RESULTS: There were no differences in any of the hemodynamic values during the 4 hours of follow-up in the control group. In the active group, there was no effect on heart rate or peak systolic pressure, but reductions between baseline and 240 minutes were observed in left ventricular end-diastolic pressure (15 ± 1 vs 6 ± 1 mm Hg, p < 0.05), end-diastolic volume (61 ± 3 vs 50 ± 3 mL, p < 0.05), and end-systolic volume (44 ± 2 vs 32 ± 2 mL, p < 0.05), and an increase in ejection fraction (28 ± 2 vs 37% ± 2%, p < 0.05).

CONCLUSIONS: Acute use of this artery-to-artery extracorporeal system effectively unloads the failing left ventricle. The potential benefits of this approach on long-term myocardial recovery in heart failure require further investigation.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 

Dr Sabbah discloses a financial relationship with Orqis Medical, Inc.

 

Chronic congestive heart failure (CHF) affects more than 25 million people worldwide. In the United States alone, more than 5 million Americans carry the diagnosis of CHF, with 450,000 new cases diagnosed each year and 250,000 deaths attributed to the disease. It is by far the fastest-growing cardiovascular problem in developed countries and carries an enormous economic burden. One million Americans are hospitalized each year because of heart failure (HF), at a staggering cost of $50 billion. Despite the availability of novel pharmacologic agents and of surgical approaches for the treatment of patients with advanced HF, survival ranges from 80% at 2 years for patients rendered free of congestion to less than 50% at 6 months for patients with refractory symptoms, a dismal survival rate [1].

Heart failure is a progressive disorder whereby the hemodynamic and symptomatic status of the affected patients deteriorates over a period of months or years despite the absence of any clinically apparent intercurrent adverse events. Whereas this process of progressive left ventricular (LV) dysfunction and remodeling can be retarded by drugs such as angiotensin-converting enzyme inhibitors and ß-blockers, many patients go on to develop overt intractable HF. In patients with advanced HF, acute decompensation is frequent and invariably requires hospitalization. This is particularly true for the 500,000 patients worldwide who are refractory to current drug therapy and for whom cardiac transplantation is not an option. Despite individual therapy, many patients continue to develop worsening decompensation resulting in a rehospitalization rate of 30% to 50% [2]. To meet this medical need, LV assist devices (LVADs) have emerged as possible "destination therapies" for this cohort of patients [3, 4]. There is an emerging school of thought that the failing LV, if unloaded and the myocardium allowed to recover, may be able to fully assume the task of providing adequate blood supply to meet the bodily demands without the need for cardiac transplantation [5]. Dennis and associates [6] initially demonstrated this unloading using a left atrial to aorta bypass.

Whereas very reliable in fully assuming the pumping function of the failing LV and potentially effective as unloading and recovery devices, LVADs require major surgery for implantation, to say nothing of the associated costs of both device and surgery. If one adopts the principle that long-term unloading of the failing LV can indeed lead to biochemical, molecular, and functional recovery of the failing myocardium, it would then be rational to develop simpler and possibly less costly devices that specifically address this therapeutic concept. In the present study, we describe the early, preclinical evaluation of such a device specifically, the Cancion short-term Cardiac Recovery System (CRS; Orqis Medical, Lake Forest, CA). The CRS is an extracorporeal device that incorporates a constant-flow pump. The circuit is established between a femoral artery and a carotid artery, with flow directed from the femoral to the carotid (Fig 1). Unlike an LVAD, the CRS does not take over support of the failing LV but rather is intended to unload and ultimately allow for recovery of the failing heart while maintaining appropriate physiologic perfusion to all organs. This study specifically tested the hypothesis that, in dogs with HF, the creation of a constant-flow extracorporeal circuit from the femoral artery to the carotid artery can result in acute reduction of the LV size and improved hemodynamics. The carotid artery was chosen because of the limited size of the axillary artery in the dog.



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  		Fig 1. The placement of the Cancion Cardiac Recovery System as was used in the present study.

 

   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 Acknowledgments
 Discussion
 References
 
Animal model
The canine model of CHF used in this present study was previously described in detail [7]. In this study, chronic LV dysfunction and failure were induced by multiple sequential intracoronary embolizations with polystyrene latex microspheres (70 to 102 µm in diameter). This results in loss of viable myocardium, as seen in myocardial infarction. This model manifests many of the sequelae of HF seen in humans, including marked and sustained depression of LV systolic and diastolic function, reduced cardiac output, and increased LV [7]. In the present study, 14 healthy mongrel dogs, weighing between 20 and 30 kg, underwent serial coronary microembolizations to produce HF. Embolizations were performed 1 week apart and were discontinued when the LV ejection fraction, determined angiographically, was less than 35%. Microembolizations were performed during cardiac catherization under general anesthesia and with sterile conditions. The anesthesia used consisted of a combination of intravenous hydromorphone (0.1 mg/kg) and diazepam (0.075 mg/kg), and isoflorane (1% to 2%) to maintain a plane of anesthesia. The study was approved by the Henry Ford Health System Institutional Animal Care and Use Committee and conformed to the "Position of the American Heart Association on Research Animal Use" and the Guiding Principles of the American Physiologic Society.

Study protocol
Two weeks after the last microembolization and after the targeted ejection fraction was achieved, the dogs were anesthetized as described above. Each animal received heparin to achieve an activated clotting time (ACT) of approximately 300 seconds. The femoral and carotid arteries were cannulated with 12F pediatric arterial cannulas. The CRS was placed between the femoral artery and the carotid artery. In 6 of 14 dogs (active CRS group), the system was primed and the pump was activated to deliver 0.25 L/min through the circuit for 4 hours. Hemodynamic and angiographic measurements were made at baseline, before activation of the CRS, and were repeated at 30, 60, 120, and 240 minutes after pump activation. Blood samples for electrolytes, blood urea nitrogen (BUN), creatinine, hematocrit, and liver enzymes were also collected at the same study time points. An identical sham procedure was performed in the remaining 8 HF dogs that served as controls (sham-operated controls). In this sham-operated group of HF dogs, the CRS was not activated for the 4 hours duration of the study. The total volume of fluids (saline) administered and the total volume of urine produced over the course of the 4-hour study was measured. The bladder was emptied before starting each study and at the end of the study.

Hemodynamic and angiographic measurements
All hemodynamic measurements were made during left and right heart catheterization. Aortic and LV pressures were measured with catheter-tipped micrometers (Millar Instruments, Houston, TX). Left ventricular end-diastolic pressure was measured from the phasic LV pressure waveform. Pulmonary artery wedge pressure was measured using a Swan-Ganz catheter. Left ventriculograms were obtained after completing the hemodynamic measurements with the dog placed on its right side. Ventriculograms were recorded on 35-mm cine film at 30 frames per second during the ejection of 20 mL of contrast material (iothalamate meglumine injection USP 60%, Mallinckrodt, Inc., St. Louis, MO). Correction for image magnification was made using a radiopaque calibrated grid placed at the level of the LV. Left ventricle end-systolic volume (ESV) and end-diastolic volume (EDV) were calculated using the area-length method [8]. Extrasystolic and postextrasystolic beats were excluded from all angiographic analyses. Ejection fraction was calculated as [(EDV - ESV)/EDV]x100. Left ventricle stroke volume was calculated as EDV - ESV. At the end of each study, gross examination of the kidneys, liver, and lungs was performed to identify potential sites of thromboembolic injury in dogs in which the pump was activated. The entire circuit as well as the pump itself was also closely examined for possible thrombus formation.

Data analysis
All hemodynamic, angiographic, and hematological measures within each study group were examined using repeated-measures analysis of variance (ANOVA), with {alpha} set at 0.05. If significance was achieved, pairwise comparisons between the various time points were made using the Student's Neuman-Keuls test. For this test, a probability value of less than 0.05 was considered significant. All data are reported as the means ± SEM.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 Acknowledgments
 Discussion
 References
 
Findings in sham-operated controls
The hemodynamic, angiographic, and hematological findings in the sham-operated control group are shown in Table 1. Repeated-measures ANOVA showed no significant temporal differences in heart rate, peak LV systolic pressure, LV end-diastolic pressure, and mean pulmonary artery wedge pressure. Similarly, there were no significant temporal differences in EDV, ESV, stroke volume, or LV ejection fraction, or any differences with respect to any of the hematologic measures (Table 1). In this group, the average ACT was 294 ± 3 seconds. The total volume of fluid administered over the course of 4 hours was 883 ± 29 mL, and the total volume of urine output was 286 ± 15 mL.


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  		Table 1. Hemodynamic, Angiographic, and Hematologic Measurements in Sham-Operated Controls

 
Findings in the active CRS group of dogs
The hemodynamic, angiographic and hematological findings in the sham-operated control group are shown in Table 2. Activation of the CRS for 4 hours had no significant effects on heart rate of peak LV systolic pressure. Left ventricular end-diastolic pressure decreased significantly in a time-dependent manner (Fig 2), as did mean pulmonary artery wedge pressure. Left ventriculography showed a time-dependent reduction of LV EDV (Fig 2) and ESV (Fig 2) and a time-dependent increase of LV ejection fraction (Fig 2), whereas stroke volume was unchanged. At the end of 4 hours of pumping, there was no evidence of any hematological abnormalities (Table 2) and no evidence of any thrombosis within the extracorporeal circuit or the pump itself. There also was no gross evidence of thromboembolic injury in any of the organs examined. There was also no evidence of hemolysis in any of the dogs studied. In this group, the average ACT was 328 ± 6 seconds. The total volume of fluid administered over the course of 4 hours was 936 ± 43 mL and the total volume of urine output was 308 ± 20 mL, which were not significantly different from the sham-operated group.


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  		Table 2. Hemodynamic, Angiographic, and Hematologic Measurements in Active Cardiac Recovery System Dogs

 


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  		Fig 2. Temporal changes in left ventricular (LV) end-diastolic pressure (EDP) (A), end-diastolic volume (EDV) (B), end-systolic volume (ESV) (C), and ejection fraction (EF) (D) in sham-operated control dogs and in a group of dogs that underwent active operation of the Cardiac Recovery System (CRS). *p less than 0.05 versus time 0.

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
Acknowledgments
 Discussion
 References
 
The results of this study indicate that an extracorporeal circuit that allows blood flow from the distal aorta (femoral artery) to the proximal aorta (carotid artery) can acutely unload the failing LV in dogs. The effectiveness of this approach is evident based upon a marked reduction of preload, marked reduction of LV chamber size, and an improvement of LV ejection fraction. Use of the Cancion short-term CRS elicited these benefits without having any significant impact on heart rate of organ perfusion pressure.

Unlike an LVAD, the Cancion CRS does not take over support of the failing LV, but rather is intended to unload and ultimately allow for recovery of the failing LV while maintaining appropriate physiologic organ perfusion pressure. The principle of operation, whereas not fully understood, is based on the fact that when activated, the CRS increases blood velocity in the descending thoracic and abdominal aorta during systole and diastole (Fig 3). Thus, forward momentum in the aorta is preserved. This leads to reduced impedance, which, in turn, allows for unloading of the failing LV. In simpler terms, one can view the theory of operation of the CRS as being reflective of Ohm's Law, where resistance or impedance is the ratio of voltage to current, or in physiologic terms, pressure to velocity. Because pressure does not change in the aorta but velocity increases when the CRS is activated, impedance or resistance decreases. Other attributes, as of yet not fully understood, may also contribute to the acute benefits derived from the CRS. One possibility is that having forward flow velocity in the aorta may have a direct influence on reflective waves from the periphery, which, in turn, can also lead to reduced impedance. The exact mechanism by which the CRS elicits its short-term beneficial effects, nonetheless, remains to be fully elucidated.



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  		Fig 3. Pulsatile blood velocity measurements in the descending aorta 10 cm above the renal arteries made with a Doppler flow wire before (OFF) and after (ON) activation of the Cardiac Recovery System (CRS). Note the increase in blood velocity during both systole and diastole when the CRS is on.

 
From the perspective of ventricular unloading with an eye toward long-term myocardial recovery, the CRS, unlike an LVAD, does not augment stroke volume but produces the same stroke volume from a smaller, more efficient LV ventricular chamber. Reducing LV size along with a reduction of preload invariably leads to a reduction in LV wall stress and stretch and, accordingly, to a reduction in myocardial oxygen consumption, a highly desired end point in the long-term management of patients with HF. Unlike an LVAD, the Cancion CRS was developed to allow for unloading of the LV and, in doing so, elicit myocardial recovery. Whereas the CRS approach to ventricular unloading has not been tested in the long term with an eye toward myocardial recovery, there is every reason to believe that long-term unloading of the failing LV elicits beneficial effects. By unloading the failing LV, LVADs have been shown to induce reverse LV remodeling [9] and improve myocardial blood flow and metabolism, and increase exercise capacity [10]. These global benefits of chronic LV unloading are also accompanied by cellular and biochemical changes that include regression of LV hypertrophy and fibrosis [11], down-regulation of matrix metalloproteinases [12], down-regulation of regulators of apoptosis [13], and decrease in cytokines such as tumor necrosis factor-{alpha}. Additional studies are clearly needed to establish the safety and efficacy of the CRS approach for chronic LV unloading beyond what is described in the present study for acute intervention.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
Discussion
 References
 
The study was supported in part by grants from Orqis Medical, Inc, and the National Heart, Lung, and Blood Institute (HL 49090-08).


   Discussion
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
References
 
DR CONSTANTINE MAVROUDIS (Chicago, IL): I have a simple question. How and why does this work?

DR HAITHCOCK: It is through Ohm's law that we have created an extra circuit for the dog; we have actually created another circuit in parallel. We have increased the velocity through the descending aorta, augmented the flow through the circuit itself, and placed it back up in the axillary artery. With the increase in the velocity through the aorta, it actually decreases resistance, improving the workload on the heart so that it does not have to work as much.

DR MAVROUDIS: As far as I can see from this, this is the first time this has been thought about or presented. Is that accurate?

DR HAITHCOCK: Yes, it is.

DR MAVROUDIS: Congratulations on this.

DR THORALF SUNDT (St. Louis, MO): How did you come up with the flow rate that you chose? The logic would be the higher you crank the pump the better, right?

DR HAITHCOCK: That would make sense and I agree with you, but we were trying to find actually the minimum amount of flow that is necessary in order to see any kind of hemodynamic improvement in heart failure dogs or patients.

DR NEAL D. KON (Winston-Salem, NC): I still do not understand how it works. It seems to me the faster you jack this pump up, the more pressure you are going to put backwards. Is there a valve in it or something?

DR HAITHCOCK: No, there is not a valve, sir. It is a constant-flow system that we have. We increase the velocity through the native aorta. And actually, if you think about it, as you increase the velocity through the native aorta, you are pulling blood from the femoral artery, placing it back up into the axillary artery. As you are pulling that blood, you are increasing the velocity. As you are increasing velocity, you decrease resistance.

The other thing that could be involved with this is also maybe the release of nitric oxide, because that could also help with the decrease in resistance, in addition to the increase in the velocity through the native aorta.

DR W. STEVES RING (Dallas, TX): Could this be a venturi effect and thus related to the angle at which the axillary artery comes into the descending aorta, creating a venturi effect on the distal arch and thus reducing the resistance of the descending aorta?

DR HAITHCOCK: That is a possible theory, yes.

DR RING: I am just guessing. I have no idea.

DR HAITHCOCK: That is possible, that is possible.

DR JOHN M. KRATZ (Charleston, SC): Tell us more exactly how the carotid artery is cannulated. We are all sitting here trying to figure out why you just do not pump the blood back against the aortic valve. Is the carotid cannula aimed cephalad and does it partially obstruct so the blood only flows from your cannula up to the brain and not back to the aorta?

DR HAITHCOCK: Yes, it goes up to the brain. It is angled cephalad away from the heart going up to the brain.

DR MAVROUDIS: Now, that is a dog's heart, so the distal artery on the arch is the subclavian artery all the time, because the proximal artery is the common brachiocephalic vessel. So if that is the subclavian artery, then it makes sense that a venturi effect might occur.

DR HAITHCOCK: But we directly cannulate only the common carotid.

DR LOUIS A. BRUNSTING III (Nashville, TN): I want to congratulate you on providing this group an interesting intellectual challenge, and for presenting a very clean set of data. My question is, did you measure cardiac output, and if so, did you present that data and I just missed it?

DR HAITHCOCK: No, sir, I did not present the data, and actually, there was no significant change in cardiac output.

DR BRUNSTING: Because your echo data documented heart rate and stroke volume did not change.

DR HAITHCOCK: Exactly. So, no. Cardiac output actually did not change. What you saw was that there was a same stroke volume but a smaller left ventricle so it makes it more optimal for the heart to pump.

DR BRYAN F. MEYERS (St. Louis, MO): If you did not change the cardiac output and you do not change the cross-sectional area of the ascending aorta, then the velocity in the ascending aorta does not change. Therefore, the only aortic velocity that you are changing is that just downstream from your cannulation site in the axillary artery. It is possible that the axillary or the subclavian flow might even reverse. It appears that the average velocity in the system has not changed at all, you have just changed the velocity in the descending aorta, and in order to do that, you have to create kind of a pressure sump downstream, below the mesenterics and below the renals. So I would challenge you that you might even be decreasing the gut perfusion by doing this because you are sucking that blood down into your pump and then recharging the system upstream.

DR HAITHCOCK: That is true, but the only point that I would have to disagree with that is that, yes, we did increase the velocity, but it was not such that it did affect mesenteric organ perfusion, because we did not see a significant change in the electrolytes or LFTs.

DR MEYERS: But my point is mainly that the only velocity you have changed is regional: the velocity between your distal takeoff point and your proximal recharging point.

DR HAITHCOCK: That is true.

DR MEYERS: And you have not changed anything about the velocity of the blood leaving the heart.

DR HAITHCOCK: That part is true. I am not sure exactly of the velocity through the descending thoracic aorta. We did not actually measure that value. So you may be right.

DR MICHAEL H. HINES (Winston-Salem, NC): This is very similar to the closed system we use for venovenous ECMO: no net volume change, no real effect on anything other than oxygenation. An arterial-arterial closed shunt circuit is all you have. If it does not affect cardiac output, it does not affect preload, I am going to accept your argument that it affects resistance. How is this any better than Milrinone or Nipride, or just medical afterload reduction?

DR HAITHCOCK: It does actually decrease preload; we saw a decrease in the pulmonary artery wedge pressure. How this is different from medication is that this could actually help take off pressure from the failing left ventricle, and from that decrease in the pressure of the left ventricle, it can actually probably promote cardiac recovery in these failing myocytes and help the patient long term.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 Discussion
 References
 

  1. Nohria A., Lewis E., Stevenson L.W. Medical management of advanced heart failure. JAMA 2002;287:628-640.[Abstract/Free Full Text]
  2. Tsuchihashi M., Tsutsui H., Kodama K., et al. Medical and socioenvironmental predictors of hospital readmission in patients with congestive heart failure. Am Heart J 2001;142:E7.[Medline]
  3. El-Banayosy A., Fey O., Sarnowski P., et al. Midterm follow-up of patients discharged from hospital under left ventricular assistance. J Heart Lung Transplant 2001;20:53-58.[Medline]
  4. Morales D.L.S., Argenziano M., Oz M.C. Outpatient left ventricular assist device support: a safe economical therapeutic option for heart failure. Prog Cardiovasc Dis 2000;43:55-66.[Medline]
  5. Frazier O.H., Benedict C.R., Radovancevic B., et al. Improved left ventricular function after chronic left ventricular unloading. Ann Thorac Surg 1996;62:675-681.[Abstract/Free Full Text]
  6. Dennis C., Hall D.P., Moreno J.R., Senning A. Reduction of the oxygen utilization of the heart by left heart bypass. Circ Res 1962;10:298-330.[Abstract/Free Full Text]
  7. Sabbah H.N., Stein P.D., Kono T., et al. A canine model of chronic heart failure produced by multiple sequential coronary microembolizations. Am J Physiol 1991;260:H1379-1384.
  8. Dodge H.T., Sandler H., Baxley W.A., Hawley R.R. Usefulness and limitations of radiographic methods for determining left ventricular volume. Am J Cardiol 1966;18:10-24.[Medline]
  9. Burkoff D., Holmes J.W., Madigan J., et al. Left ventricular assist device-induced reverse ventricular remodeling. Prog Cardiovasc Dis 2000;43:19-26.[Medline]
  10. Maybaum S., Epstein S., Beniaminovitz A., et al. Partial loading of the left ventricle during mechanical assist device support is associated with improved myocardial function, blood flow, metabolism and increased exercise capacity. J Heart Lung Transplant 2002;21:446-454.[Medline]
  11. Bruckner B.A., Stetson S.J., Perez-Verdia A., et al. Regression of fibrosis and hypertrophy in failing myocardium following mechanical circulatory support. J Heart Lung Transplant 2001;20:457-464.[Medline]
  12. Bartling B., Milting H., Schumann H., et al. Myocardial gene expression of regulators of myocyte apoptosis and myocyte calcium homeostasis during hemodynamic unloading by ventricular assist devices in patients with end-stage heart failure. Circulation 1999;100(Suppl):216-223.[Free Full Text]
  13. Torre-Amione G., Stetson S.J., Youker K.A., et al. Decreased expression of tumor necrosis factor-alpha in failing human myocardium after mechanical circulatory support: a potential mechanism for cardiac recovery. Circulation 1999;100:1189-1193.[Abstract/Free Full Text]



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