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Ann Thorac Surg 2000;70:1587-1593
© 2000 The Society of Thoracic Surgeons

Original articles: cardiovascular

Intraaortic balloon pumping for predominantly right ventricular failure after heart transplantation

Osama E. Arafa, MDa, Odd R. Geiran, MD, PhDa, Kai Andersen, MD, PhDb, Erik Fosse, MD, PhDa, Svein Simonsen, MD, PhDb, Jan L. Svennevig, MD, PhDa

a Department of Thoracic and Cardiovascular Surgery, Ny Rikshospitalet, Oslo, Norway
b Department of Cardiology, Rikshospitalet, Oslo, Norway

Address reprint requests to Dr Arafa, Department of Thoracic and Cardiovascular Surgery, Rikshospitalet, N-0027 Oslo, Norway
e-mail: arafa{at}doctor.com


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. Right ventricular failure from elevated pulmonary vascular resistance in the recipient is a main cause of early mortality after heart transplantation. When pharmacologic treatment is insufficient, mechanical circulatory assistance has been used to support the failing right ventricle. Considering right and left ventricular interdependence, we investigated whether intraaortic balloon counterpulsation (IABP) might also alleviate predominantly right ventricular dysfunction after heart transplantation.

Methods. Among 278 cardiac recipients, 12 adult patients underwent mechanical circulatory support for cardiac allograft dysfunction. Five patients were treated with percutaneous IABP for early postoperative low cardiac output syndrome characterized by predominantly right ventricular failure. Clinical data and hemodynamic variables were recorded before and during IABP treatment.

Results. Cardiac index (CI) and mean arterial pressure (MAP) increased (CI 1.7 ± 0.1 to 2.5 ± 0.2, MAP 53 ± 12 to 71 ± 7, p < 0.05) within 1 hour after IABP, whereas central venous pressure (CVP) and pulmonary artery wedge pressure (PAWP) decreased (CVP 21.6 ± 1.7 to 13.8 ± 3.1, p < .05; PAWP 14.8 ± 4.9 to 12.4 ± 3.7, nonsignificant). Within the next 12 hours, CI and mixed venous oxygen saturation increased (p < 0.05) and pulmonary artery pressure decreased (p < 0.05). All 5 patients were weaned successfully and 4 are long-term survivors with adequate cardiac performance at 1 year follow-up.

Conclusions. Intraaortic balloon pumping is a minimally invasive circulatory assist device with proved efficiency in low cardiac output syndromes. This report shows that low output syndrome caused by predominantly right ventricular allograft failure may be an additional indication for IABP.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
Cardiac allograft failure is an important cause of early mortality after heart transplantation. Right ventricular failure (RVF) may be a more prominent problem than left ventricular dysfunction because of failure of the right ventricle to cope with the increased pulmonary vascular resistance in the recipient from long-standing congestive heart failure [1, 2]. Because of the need for right ventricular mechanical assistance after heart transplantation, the early mortality has been reported to exceed 50% [3, 4].

Intraaortic balloon counterpulsation (IABP) is the first choice for mechanical circulatory support for left heart failure. Only a few reports [5, 6] address the use of IABP in RVF and none has reported its use to support the failing right ventricle after human heart transplantation. In graft failure, right ventricular hypertension and distention may both cause reduced coronary blood flow to the right ventricle and in addition impair left ventricular function by reduced filling and altered septal dynamics. IABP is a minimally invasive assist device, which by systolic unloading of the left ventricle reduces myocardial work and oxygen consumption and by diastolic inflation increases coronary artery blood flow and oxygen supply to the myocardium [7, 8]. The aim of the present report is to evaluate the effects of IABP in patients with low output syndrome (LOS) from predominantly RVF shortly after human cardiac allotransplantation.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
Patients
A total of 278 patients underwent 284 orthotopic cardiac transplantations at our center from 1983 through 1997, with a 30-day mortality of 5%. Twelve adult patients were identified to have mechanical circulatory support at any time after heart transplantation (14 treatments). The indications were failure to wean from cardiopulmonary bypass (n = 2), early postoperative RVF (n = 6), and resuscitation after cardiac arrest (n = 6) in the late postoperative period. This report is based on 5 patients who had IABP as the primary and only mechanical assistance for LOS within the first 2 days of heart transplantation.

These patients were accepted for transplantation according to generally accepted selection criteria [9]. The clinical profile of the patients and donor data are shown in Table 1. Patients with severe pulmonary hypertension and high pulmonary vascular resistance (PVR) were only accepted for operation if PVR and pulmonary artery pressures were normalized by sodium nitroprusside infusion (3 to 5 µg · kg-1 · min-1). The 4 long-term survivors have a complete clinical and hemodynamic follow-up.


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  		Table 1. Demographic and Hemodynamic Variables in 5 Cardiac Recipients and Their Organ Donors

 
Heart transplantation
Allograft preservation was obtained with 1 L of St. Thomas cardioplegic solution infused in the aortic root during harvesting, topical cooling (4°C) by normal saline, and application of cold sponges and slushed ice during transplantation. Orthotopic heart transplantation was performed by the standard technique. Ischemic time was 148 ± 50 minutes (range 65 to 196 minutes) and extracorporeal bypass time was 87 ± 17 minutes (range 63 to 107 minutes). A standard drug protocol (ie, isoprenaline 0.02 to 0.1 µg · kg-1 · min-1, dopamine 2.5 to 5 µg · kg-1 · min-1, and sodium nitroprusside 0.5 to 1.0 µg · kg-1 · min-1) was used to wean patients from the heart-lung machine and to achieve hemodynamic stability in the first postoperative days.

Hemodynamics
In addition to an arterial and central venous pressure (CVP) line, all patients had a thermodilution catheter inserted in the pulmonary artery when circulatory failure became clinically evident. Hemodynamic variables were registered and calculations were done according to common practice.

IABP
Low output syndrome was diagnosed by invasive monitoring when corrective measures by judicious volume loading and pharmacotherapy had failed. In all patients a 40 cc balloon catheter was inserted percutaneously through the common femoral artery by the Seldinger technique. Anticoagulation was achieved by low dose heparin or low molecular weight dextran. The patients were weaned from IABP if hemodynamic stability was maintained after decreasing the balloon inflation or the rate of counterpulsation. The balloon was removed by direct extraction in all patients and bleeding was prevented by a local compression device.

Statistical analysis
Data were analyzed using the SPSS software program (SPSS, Inc, Chicago, IL). Analysis of variance (test for repeated measurements) and parametric test (two-tailed t test for paired samples to compare means) were used to analyze the effect of IABP if appropriate: before and 1 and 12 hours after IABP insertion. The same statistical methods were used to compare hemodynamic variables during IABP treatment with long-term observations.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
Clinical observations
A donor heart became available a median of 10 days (range, 2 to 85 days) after listing. Lymphocyte crossmatch was negative in all patients. There was no apparent mismatch between donor and recipient size. All 5 recipients were weaned from cardiopulmonary bypass without particular problems. However, low cardiac output syndrome refractory to inotropic support and afterload reduction occurred within the first 2 postoperative days (2 to 34 hours) and IABP was inserted in the intensive care unit to improve hemodynamics. The clinical profile of the patients and data of their organ donors are shown in Table 1.

Hemodynamic changes
Observations obtained before and 1 and 12 hours after IABP insertion are presented in Table 2. At the time of IABP insertion, LOS with a predominantly RVF was evident by decreased cardiac index (CI), high CVP, moderately elevated mean pulmonary artery pressure (MPAP) and transpulmonary gradient (TPG), reduction of right ventricular stroke work index (RVSWI), stroke index (SI), and left ventricular stroke work index (LVSWI) with variable levels of left ventricular filling pressure. In addition, there was indirect evidence that right ventricular end-diastolic pressure exceeded left ventricular end-diastolic pressure by reversal of the atrial transseptal gradient (ATSP = pulmonary artery wedge pressure [PAWP] - CVP). The hemodynamic improvement was significant immediately after the application of IABP in all 5 patients (Fig 1). Both left and right ventricular performance improved. The hemodynamic variables, except for PAWP, normalized after the first hour of IABP. Twelve hours after IABP insertion a slight further hemodynamic improvement could be observed, with statistically significant differences for SI, MPAP, and PVR 1 and 12 hours after IABP insertion. The values of PAWP measured before and after (1 and 12 hours) IABP insertion were not significantly different.


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  		Table 2. Hemodynamic Variables Before and During IABP Treatmenta

 



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  		Fig 1. Hemodynamic measurements before and 1 and 12 hours after intraaortic balloon counterpulsation (IABP) insertion. (A) Cardiac index (CI) improved in all patients. (B) Central venous pressure (CVP) decreased significantly within the first hour after IABP insertion. (C) Pulmonary artery wedge pressure (PAWP) remained unchanged after IABP insertion. (D) Mean pulmonary artery pressure (PAP) decreased significantly over the first 12 hours after IABP insertion. (E) Transpulmonary gradient (TPG = mean PAP - PAWP) normalized over the first 12 hours after IABP insertion. (F) Atrial transseptal pressure gradient (ATSP = PAWP - CVP) gradually reversed to normal during the first 12 hours of IABP treatment. (G) Pulmonary vascular resistance (PVR) decreased significantly over the first 12 hours after IABP insertion. Each symbol represents 1 of 5 patients.

 
Metabolic variables and drug treatment
The hemodynamic improvement after IABP was accompanied by a progressive decrease in the need for inotropic drugs concomitant with a significant increase in mixed venous oxygen saturation and reversal of metabolic acidosis (p < 0.05).

Echocardiography
Bedside echocardiography was performed before IABP in the last 2 patients and disclosed right ventricular dilatation, reduced systolic motion of the right ventricular free wall, and systolic movement of the interventricular septum to the right. These findings are demonstrated by the recordings in patient 4, which also showed lack of systolic thickening of the interventricular septum (Fig 2, left panels). An investigation 2 weeks later showed normalized right ventricular free wall motion as well as normalized septal thickening (Fig 2, right panels).



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  		Fig 2. (Patient 4.) Echocardiographic recordings. Two-dimensional recordings of the right ventricle (RV) and left ventricle (LV) obtained from the apical position with schematic depiction of RV end-diastolic (–) and end-systolic () silhouettes. The M-mode recordings (bottom panels) were made from the parasternal position. Note the inverse systolic motion of the RV free wall and the concomitant lack of interventricular septal (IVS) thickening before intraaortic balloon counterpulsation (Pre-IABP). Subsequently, RV free wall motion and IVS systolic thickening normalized as shown by the recordings performed 2 weeks later (Post-IABP). (PW = left ventricular posterior wall).

 
Outcome
All 5 patients were weaned successfully from IABP; mean treatment time was 44 ± 16 hours (range, 28 to 70 hours). One patient developed lower limb ischemia and compartment syndrome; IABP could be removed and fasciotomy was performed after 36 hours of treatment. One patient died in hospital 10 days after transplantation from recurrent cardiac arrests from acute rejection, 8 days after weaning from IABP, in spite of open resuscitation, reinsertion of IABP, and cardiac pacing. The remaining 4 patients are alive and well at a mean of 36.8 months (range, 10 to 56 months) after transplantation. The central hemodynamics observed after 12 hours of IABP treatment were maintained 6 and 12 months posttransplantation (Table 3). The 4 surviving patients are in New York Heart Association class I or II 1 year after transplantation.


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  		Table 3. Hemodynamic Variables After Cardiac Transplantation and IABP (n = 4)a

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
Our results support the hypothesis that IABP may alleviate RVF in allograft dysfunction by improving coronary artery perfusion and left ventricular mechanics when the underlying problem is suddenly increased right ventricular afterload caused by increased pulmonary vascular resistance. There is limited experience of IABP in patients with RVF [6]. As the main effects of IABP are left ventricular afterload reduction and improvement of coronary perfusion, our success with IABP in the management of early graft failure from right ventricular dysfunction is remarkable. In the reported patients, the ability of IABP to improve hemodynamics was evident within minutes after insertion. The improvement was significant during the first hour; thereafter the rate of improvement slowed down. Although increasing inotropic support did not maintain acceptable cardiac function and peripheral tissue perfusion, IABP treatment also improved peripheral tissue perfusion and reduced the need for inotropic drugs. The most likely explanation for the improvement obtained by IABP is enhanced coronary artery filling. The improved myocardial perfusion will relieve right and left ventricular dysfunction, thereby also improving right ventricular function both directly and indirectly. Afterload reduction of the left ventricle also may play a part in the apparent effect of IABP.

The early mortality after orthotopic heart transplantation has remained almost unchanged at 10% for the past 5 years with nonspecific graft failure as the most important cause [1]. As graft failure is commonly precipitated by elevated pulmonary vascular resistance of the recipient and often combined with myocardial dysfunction of the allograft [4, 10], right ventricular dysfunction may be more evident than left ventricular dysfunction [11]. Right ventricular allograft dysfunction has been attributed mainly to failure of the donor right ventricle to adapt to the sudden increase in afterload [2]. Pulmonary hypertension more than doubles the risk of death associated with transplantation [12]. Thus, severe pulmonary hypertension and increased PVR unresponsive to vasodilators are contraindications for orthotopic heart transplantation [3, 13].

In addition to right ventricular pressure overload, several factors have been offered to account for RVF after cardiac transplantation, namely right ventricular subendocardial ischemia, left ventricular free wall ischemia, and right ventricular dysfunction secondary to compromised left-to-right ventricular systolic interaction [14, 15]. In animal experiments it has been shown that widespread ischemia of the right ventricular free wall was followed by only a modest reduction in stroke volume, but there was always a reduction or even reversal in transseptal diastolic pressure with gradual and possible leftward diastolic movement of the interventricular septum [16]. In contrast, when the left ventricular free wall is rendered ischemic, not only the left ventricular function curve, but also the right ventricular function curve are impaired [17].

It has been shown experimentally that brain death may precipitate significant biventricular dysfunction, with contractility of the right ventricle being more depressed than the left ventricle [18]. If brain death was followed by cardiac harvesting and prolonged graft preservation before heart transplantation, brain death contributed significantly to allograft failure [19]. The donor heart is injured during the hyperdynamic and hypertensive phase of the donor’s brain death. In spite of myocardial preservation techniques, the global ischemia during the harvesting, transport, and transplantation procedure may add to the graft dysfunction. Cardiopulmonary bypass per se leads to increased inflammatory reaction and neutrophil infiltration of the lungs with associated increase in PVR and right ventricular strain [20].

Although the consequences of right ventricular pressure overload failure have been attributed to inadequate right ventricular myocardial blood flow [21], many studies have demonstrated that both the diastolic and systolic functions of the right ventricle are more dependent on the left ventricle, which may contribute to more than 50% of right ventricular function through ventricular interdependence mechanisms [15, 22]. Thus, it is more likely that impaired left ventricular systolic function decreases right ventricular function, evidenced by reduced right ventricular systolic pressure and stroke volume, with a subsequent decrease in left ventricular filling and function. Ventricular interdependence has also been suggested as an important factor in circulatory failure after human heart transplantation [5].

In a sheep model of RVF induced by pulmonary artery constriction [5], IABP provided immediate improvement in global cardiac function and hemodynamics. The significant improvement in coronary perfusion after IABP could account for the improvement in both left and right ventricular function. These experiments strongly support our experience that predominantly right ventricular allograft dysfunction may be treated by intraaortic counterpulsation.

We have used IABP in the management of early graft failure at least partly caused by increased recipient PVR and pulmonary artery pressure. When attempts to reduce right ventricular afterload by vasodilators (sodium nitroprusside, prostaglandins) are insufficient, other adjuncts like nitric oxide (NO) inhalation may be attempted [23]. We had no personal experience with NO at the time when our first patients were treated, but we are certainly aware of this treatment strategy [24], although to date we have not used it in heart transplantation patients. The relative efficacy of NO inhalation versus IABP in this setting remains to be determined.

When IABP insertion does not improve global cardiac function in right RVF, a more invasive circulatory support with a centrifugal pump with or without extracorporeal membrane oxygenation (ECMO) [25, 26], or right ventricular assist devices, have been successful [4].

We conclude that IABP is a minimally invasive, readily available surgical tool that may be useful in the management of early graft failure, even when caused by increased right ventricular afterload. IABP may thus alleviate the need for more invasive methods of cardiac assistance, eg, right ventricular assist pumps or ECMO.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

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  2. Kirklin J.K., Naftel D.C., McGiffin D.C., et al. Analysis of morbid events and risk factors for death after cardiac transplantation. J Am Coll Cardiol 1988;11:917-924.[Abstract]
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  4. Chen J.M., Levin H.R., Rose E.A., et al. Experience with right ventricular assist devices for perioperative right sided circulatory failure. Ann Thorac Surg 1996;61:305-310.[Abstract/Free Full Text]
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  6. Kopman E.A., Ramirez-Inawat R.C. Intra-aortic balloon counterpulsation for right heart failure. Anesth Analg 1980;59:74-76.[Free Full Text]
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  9. Mudge G.H., Goldstein S., Addonizio L.J., et al. Task force 3. J Am Coll Cardiol 1993;22:21-31.[Medline]
  10. Wahlers T.H., Beer C., Fieguth H.G., et al. Right heart failure following orthotopic cardiac transplantation. Clinical Transplantation 1988;2:252-256.
  11. Bourge R.C., Naftal D.C., Costanzo-Nordin M.R., Kirklin J.K., Young J.B., Kubo S.H. Pretransplantation risk factors for death after heart transplantation. J Heart Lung Transplant 1993;12:549-562.[Medline]
  12. Heck C.F., Shumway S.J., Kaye M.P. The Registry of the International Society for Heart Transplantation. J Heart Transplant 1989;8:271-276.[Medline]
  13. Simonsen S., Mølstad P., Geiran O., Frøysaker T. Heart transplantation in patients with severe pulmonary hypertension and increased pulmonary vascular resistance. Scand J Thorac Cardiovasc Surg 1990;24:161-164.[Medline]
  14. Calvin J.E., Quinn B. Right ventricular pressure overload during acute lung injury. J Crit Care 1989;4:271-276.
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  18. Van Trigt P., Bittner H.B., Kendall S.W., Milano C.A. Mechanisms of transplant right ventricular dysfunction. Ann Surg 1995;221:666-676.[Medline]
  19. Bittner H.B., Kendall S.W.H., Chen E.P., et al. Myocardial performance after graft preservation and cardiac transplantation from brain dead donors. Ann Thorac Surg 1995;60:47-54.[Abstract/Free Full Text]
  20. Dreyer W.G., Michael L.H., Millman E.E., et al. Neutrophil sequestration and pulmonary dysfunction in a canine model of open heart surgery with cardiopulmonary bypass. Circulation 1995;92:2276-2283.[Abstract/Free Full Text]
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Accepted for publication June 14, 2000.




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