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Ann Thorac Surg 2007;83:62-67
© 2007 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Multivariate Predictors of Heart Transplantation Outcomes in the Era of Chronic Mechanical Circulatory Support

Stavros G. Drakos, MD, PhDa,b, Abdallah G. Kfoury, MDa,*, Edward M. Gilbert, MDb,c, James W. Long, MD, PhDa, James C. Stringham, MDb,c, Elizabeth H. Hammond, MDa, Kent W. Jones, MDa, David A. Bull, MDb,c, MaryBeth E. Hagan, NPc, Jan W. Folsom, RNa, Benjamin D. Horne, MPH, PhDa, Dale G. Renlund, MDa,b

a LDS Hospital, Utah Transplantation Affiliated Hospitals (U.T.A.H.) Cardiac Transplant Program, Salt Lake City, Utah
b University of Utah School of Medicine, Utah Transplantation Affiliated Hospitals (U.T.A.H.) Cardiac Transplant Program, Salt Lake City, Utah
c George E. Wahlen Veterans Affairs Medical Centre, Utah Transplantation Affiliated Hospitals (U.T.A.H.) Cardiac Transplant Program, Salt Lake City, Utah

Accepted for publication July 21, 2006.

* Address correspondence to Dr Kfoury, Cardiac Transplant Program, LDS Hospital, 8th Ave and C St, Salt Lake City, UT 84143 (Email: akfoury{at}intermountainmail.org).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
BACKGROUND: Determining which pretransplantation (TX) characteristics predict the development of chronic renal dysfunction (CRD) or death after heart TX would enable more accurate risk assessment at the time of candidate evaluation.

METHODS: A cohort of 278 patients underwent TX in three hospitals between 1993 and 2002. Predictive models for CRD (serum creatinine consistently above 2 mg/dL) and allograft loss (death or re-TX) were constructed using logistic and Cox regression, respectively.

RESULTS: Using logistic regression, CRD was more likely to develop in TX patients if they had a larger body surface area (odds ratio [OR] = 5.8 per m2, 95% confidence interval [CI] = 1.04 to 31.9, p = 0.04) or were inotrope dependent (OR = 1.8, 95% CI = 0.90 to 3.7, p = 0.09). Notably, the implementation of mechanical circulatory support as bridge to transplantation decreased the risk of CRD (OR = 0.30, 95% CI = 0.12 to 0.72, p = 0.007). Cox analysis demonstrated independent predictive ability of improved survival for males (hazard ratio [HR] = 0.42, 95% CI = 0.21 to 0.83, p = 0.01). Worse survival was observed with prior sternotomy (HR = 3.5, 95% CI = 2.0 to 6.0, p < 0.001), diabetes mellitus (HR = 1.9, 95% CI = 0.98 to 3.9, p = 0.06), and elevated serum creatinine (HR = 2.8 per mg/dL, 95% CI = 1.3 to 5.8, p = 0.007).

CONCLUSIONS: Certain pretransplant characteristics clearly predispose a patient to the development of CRD or increased mortality after heart transplantation. Interestingly, the risk of CRD after heart transplantation is greater for patients bridged to transplant with inotropes than with mechanical circulatory support. When hemodynamically indicated, timely implementation of pretransplant mechanical circulatory support should be considered.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 References
 
Heart transplantation is the procedure of choice for patients with refractory heart failure. The introduction of cyclosporine for immunosuppression therapy after heart transplantation 20 years ago has led to marked improvement in survival. Unfortunately, calcineurin inhibitors, such as cyclosporine, are also associated with nephrotoxicity. In fact, posttransplantation chronic renal dysfunction (CRD) is well recognized as one of the main problems that confronts heart transplant recipients in the long term [1–3].

Heart failure management generally and care before transplantation specifically have become increasingly complex. Specialized heart failure units with inpatient and outpatient branches, electrophysiologic devices such as implantable cardioverter-defibrillators and cardiac resynchronization therapies, and ventricular assist devices are frequently used. Often, severely compromised transplant candidates need to be stabilized before heart transplantation.

Given the increased complexities in end-stage heart failure management, the objective of this report was to determine which pretransplantation characteristics predict the development of CRD or death after heart transplantation. More accurate risk assessments at the time of candidate evaluation would provide patients and providers with more realistic expectations in posttransplant outcomes.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
Data Collection
We retrospectively reviewed the records of 278 patients who underwent cardiac transplantation between 1993 and 2002 in Utah. We collected data from heart transplantation recipients and donors using flow sheet–like tables prepared for each patient, medical charts, and data from the centers’ electronic databases. Our Institutional Review Board approved this study, and individual consent for the study was waived.

Chronic renal dysfunction was defined as a serum creatinine measuring consistently greater than 2 mg/dL for at least 6 months. Allograft loss was defined as death or retransplantation. Several patient characteristics that could influence allograft loss and the development of CRD were examined. For both heart donors and heart transplant recipients, sex, age, ethnicity, height, weight, body surface area, and cytomegalovirus (CMV) status were evaluated. The heart transplant recipients’ etiology of heart failure, transplant waiting time, ischemic time, United Network for Organ Sharing (UNOS) status, the presence or absence of diabetes mellitus, whether the patients were bridged to transplantation with intravenous inotropic agents (inotrope-dependent patients), or mechanical circulatory support or intraaortic balloon counterpulsation, and whether they underwent prior median sternotomy were noted. Pretransplant data from right-side heart catheterization, cardiac ultrasonography, radionuclide ventriculography, and cardiopulmonary exercise test, along with pretransplant New York Heart Association functional class, creatinine, bilirubin, hemoglobin, sodium, and the degree of human leukocyte antigen (HLA) allosensitization as expressed by the panel reactive antibody measured by either the antiglobulin-augmented, complement-dependent lymphocytotoxicity assay, or flow cytometry were evaluated.

Operative Techniques
Cardiectomy from the brain-dead donor and orthotopic heart transplantation were performed using standard surgical technique, as previously described [4].

Immunosuppression Therapy
Immunosuppression therapy consisted of a calcineurin inhibitor (cyclosporine or tacrolimus), an antiproliferative agent (mycophenolate mofetil or azathioprine), and corticosteroids. The dosage of calcineurin inhibitor was adjusted according to blood levels, serum creatinine, other toxicity, and frequency and severity of rejection episodes. In general, if the serum creatinine in the week preceding transplant was less than 1.8 or creatinine clearance greater than 45 mL/min early rejection prophylaxis was standard triple therapy. Early rejection prophylaxis was modified in patients with serum creatinine less than 1.8 or creatinine clearance greater than 45 mL/min and one of the following risk factors: left ventricular assist device, multiple sternotomies, severe pulmonary hypertension, or inotrope dependency. In such patients, early rejection prophylaxis included interleukin-2 receptor antagonist (ie, basiliximab or daclizumab) on top of standard triple therapy to adjust calcineurin inhibitors to a lower serum level. Finally, for patients with renal insufficiency (serum creatinine >1.8 or creatinine clearance <45 mL/min), no preoperative calcineurin inhibitor was utilized, and its institution was delayed for 72 hours. In such patients, either OKT3-based therapy or antithymocyte globulin were utilized as early rejection prophylaxis.

Mechanical Support
Mechanical circulatory support (MCS) as a bridge to transplantation was defined as any cardiac assist device used in a UNOS status I patient. The devices used were the IP (pneumatic) or VE (vented electric) HeartMate LVAS (Thoratec, Pleasanton, California) and the CardioWest Total Artificial Heart (SynCardia Systems, Tucson, Arizona). Intraaortic balloon pump counterpulsation was not counted as part of MCS.

The following two main criteria were used to select patients for MCS: (1) end-stage chronic heart failure patients who were clinically and hemodynamically deteriorating while waiting for cardiac transplantation despite maximal pharmacologic support; and (2) acute heart failure patients who could not be weaned from short-term MCS if these patients were found to be eligible for cardiac transplantation.

Statistical Analysis
Initial comparisons of the study covariates by CRD were performed by {chi}2 (for discrete variables) or Student’s t test (for continuous variables), while comparison of study covariates by allograft loss (death or retransplantation) was performed by Wald’s likelihood approximation to the {chi}2 test in Cox regression. Predictive models for CRD and allograft loss during the entire follow-up period were constructed using logistic and Cox regression analyses, respectively. Follow-up for CRD and allograft loss was 100% complete. Initial regression models entered groups of variables to evaluate associations with the CRD or allograft loss endpoints. Variables included in the modeling were all those described above. Further modeling evaluated significant variables, and those with important confounding effects on inotrope-dependent versus MCS status. Variables were entered through backward and forward step-wise analysis, and the final models were fit using forced variable entry. Nominal statistical significance was set at p value of 0.05 or less.

Unadjusted time-to-event estimates were calculated using the Kaplan-Meier method, and probability values were computed using the log-rank test.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
The mean follow-up period was 4.9 years, with a range between 6 months and 10 years. Seventy-two patients were bridged to transplantation with MCS, and 64 patients were bridged with inotropes (inotrope-dependent patients). Chronic renal dysfunction during the follow-up period occurred in 70 patients (25.2%) and did not occur in 208 patients (74.8%). In the univariate analysis comparing these two groups of patients, the CRD group was found to be older, have larger body surface area, included a larger proportion of males, and had lower pretransplant cardiac output (Table 1). Notably, the proportion of patients bridged to transplantation with MCS was significantly lower in the CRD group (p < 0.001), whereas the proportion of inotrope-dependent patients was higher in the CRD group but did not reach statistical significance (p = 0.12).


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  		Table 1. Study Variables by CRD Status
 
However, in the multivariate analysis, as shown in Table 2, logistic regression revealed that inotrope dependency was associated with increased likelihood of developing CRD (p = 0.09). Larger body surface area was also identified as independent prognostic indicator of increased likelihood of CRD, whereas the implementation of MCS as bridge for transplantation significantly decreased the risk of CRD (Table 2).


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  		Table 2. Multivariate Predictors of Chronic Renal Dysfunction
 
Comparing the survivors (n = 209) with the group of patients who an allograft loss occur during the follow-up period (n = 69), we found that the incidence of prior sternotomy along with the donor CMV positive status were significantly higher in the allograft loss group (Table 3). In addition, the pretransplant serum creatinine was also found to be significantly higher in the allograft loss group (Table 3).


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  		Table 3. Study Variables by Allograft Loss Endpoint
 
Multiple pretransplant characteristics were evaluated as to their impact on posttransplant mortality (Table 4). Cox regression analysis demonstrated independent predictive ability of improved survival for males. Worse survival was observed with prior sternotomy, diabetes mellitus, and elevated serum creatinine.


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  		Table 4. Multivariate Predictors of Allograft Loss
 
As shown above, CRD after heart transplantation was found to be more likely in inotrope-dependent than in MCS-requiring recipients. In order to elucidate whether this difference could affect the long-term mortality rate of these patients, the posttransplant survival of these two groups of patients was directly compared. As shown in Figure 1, the actuarial survival of the MCS-requiring recipients tended to be better than the inotrope-dependent recipients (p = 0.47).


Figure 1
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  		Fig 1. Actuarial survival (p = 0.33) for mechanical circulatory support (dashed line) versus inotrope dependent (solid line) in multivariable Cox regression.

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
Heart transplantation is the best treatment for selected patients with end-stage heart failure. Chronic renal dysfunction is a major complication of cardiac transplantation that is mainly attributed to therapy with calcineurin inhibitors [1]. Many reports in the literature have described the extent of this problem and the long-term morbidity and mortality that ensues from the development of posttransplant CRD [5–12]. One of the aims of this study was to evaluate the posttransplant renal function of patients having undergone cardiac transplantation and to identify the risk factors for the development of CRD.

As found in the multivariate analysis, transplant recipients were more likely to have CRD develop if they had a larger body surface area or were inotrope dependent. Interestingly, the patients who were bridged to transplantation with MCS had a decreased risk of CRD. In addition to these, in the univariate analysis, the CRD group compared with the no-CRD group was found to be older and with lower pretransplant cardiac output. Notably, the pretransplant renal function, as expressed by the serum creatinine, was not associated with increased posttransplant development of CRD.

The corresponding data in the literature are controversial. Zietse and colleagues [7] showed that no relationship could be found between the age at transplantation and the decline in renal function after transplant. On the other hand, Greenberg and colleagues [5] and Lindelöw and associates [10] reported that high recipient age was an independent predictor of postoperative renal dysfunction. Regarding the impact of pretransplant renal insufficiency most of the studies failed to show any correlation between this parameter and the decline in renal function after transplantation [5–10]. On the contrary, according to the study by Sehgal and associates [13], patients with renal insufficiency before transplant and those with a more pronounced depression of renal function at 6 months after transplant had a high risk for progressive kidney failure after heart transplantation.

Regarding patients with larger body surface area, the increased likelihood of developing CRD in this population could be a manifestation of the utilization of higher calcineurin antagonist dosages. Notably, even this issue raises controversy since most studies have been unable to show a correlation between cyclosporine level and renal function after heart transplantation [1]. However, it is generally accepted that close monitoring of cyclosporine blood levels is critically important in preventing or limiting progressive decline in renal function [1].

Our data suggest that variables like the pretransplant preservation of adequate cardiac output, and as a consequence of this, adequate renal blood flow, might be important in preventing posttransplantation CRD. This mechanism could explain the protective role we found for MCS as bridge for transplantation as opposed to bridging marginal heart failure patients to transplant with inotropes.

Another aim of our study was to identify certain pretransplant characteristics as predictors of long-term allograft loss. We found that pretransplant elevated serum creatinine, diabetes, and prior median sternotomy were independent predictors of allograft loss whereas male recipient sex was associated with decreased likelihood of long-term allograft loss.

Elevated serum creatinine and diabetes are considered to be risk factors associated with increased long-term posttransplant morbidity and mortality [14–16]. However, diabetes is not uniformly accepted as a cardiac transplantation risk factor [17, 18]. The impact of prior sternotomy and sex on the survival of heart transplant recipients raises controversy. Regarding prior sternotomy, some reports showed no adverse effect on the posttransplant survival [14, 19, 20], whereas other studies revealed increased posttransplant morbidity and mortality [21–23]. The influence of recipient sex on the posttransplantation survival is also a matter of debate. In the 2004 International Society for Heart and Lung Transplantation Registry report, female recipient sex appeared to be associated with decreased long-term mortality [14]. However, in that multi-institutional report, the absolute mortality difference was found to be small (5% at 14 years); the difference did not become evident until after 7 to 8 years, and prior pregnancy was identified as an independent adverse predictor of long-term survival [14]. In our report, we found a protective effect of male sex on survival that remains unexplained.

Univariate analysis surprisingly revealed lower incidence of positive CMV grafts in the allograft loss group. In the multivariate analysis, this finding was not confirmed, and donor CMV status was not identified as an independent predictor of posttransplantation survival.

In our study, we also tried to clarify whether the decreased likelihood of CRD found in the MCS-requiring recipients as opposed to their inotrope-dependent counterparts affected the long-term posttransplant survival of these two subgroups of patients. Although we found that the actuarial posttransplant survival of the patients bridged to transplantation with MCS is higher than those bridged with inotropes, this difference did not reach statistical significance. Nevertheless, it is in accordance with previously published data [24].

The limitations of this study include those related to a retrospectively performed analysis. Data were obtained by means of chart and electronic database review, which has inherent limitations, such as access and accuracy of the data. Additionally, although we demonstrated no statistically significant difference in survival between inotrope-dependent and MCS-requiring recipients, the increased long-term survival in the MCS-requiring cohort raises the possibility that if a larger population was studied, a statistically significant difference might be observed. An additional limitation of this study is that the timing of CRD diagnosis (ie, the exact time-point after transplantation that a high creatinine was observed) was not evaluated. Differential CRD onset might have biased the study results and deserves further study and validation. Finally, we have not investigated whether the number or frequency of rejection episodes and immunosuppressive management were important factors in either the univariate or multivariate analysis of allograft loss or development of CRD.

In conclusion, certain pretransplant characteristics clearly predispose patients to the development of CRD or increased mortality risk after heart transplantation. Interestingly, the risk of CRD after heart transplant is greater for patients bridged to transplantation with inotropes than with MCS; and thus, when hemodynamically indicated, timely implementation of pretransplant MCS should be considered and inordinate deferral avoided.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

  1. Herlitz H, Lindelow B. Renal failure following cardiac transplantation Nephrol Dial Transplant 2000;15:311-314.[Free Full Text]
  2. Shiba N, Chan M, Kwok B, Valantine H, Robbins R, Hunt S. Analysis of survivors more than 10 years after heart transplantation in the cyclosporine era: Stanford experience J Heart Lung Transplant 2004;23:155-164.[Medline]
  3. Satchithananda D, Parameshwar J, Sharples L, et al. The incidence of end-stage renal failure in 17 years of heart transplantation: a single center experience J Heart Lung Transplant 2002;21:651-657.[Medline]
  4. McCarthy PM, Smith JA, Siegel LC, et al. Cardiac transplant admission, anesthesia, and operative proceduresIn: Smith JA, McCarthy PM, Sarris GE, Stinson EB, Reitz BA, editors. The Stanford manual of cardiopulmonary transplantation. New York: Futura Publishing; 1996. pp. 31-61.
  5. Greenberg A, Thompson ME, Griffith BJ, et al. Cyclosporine nephrotoxicity in cardiac allograft patients—a seven-year follow-up Transplantation 1990;50:589-593.[Medline]
  6. Gonwa TA, Mai ML, Pilcher J, et al. Stability of long-term renal function in heart transplant patients treated with induction therapy and low-dose cyclosporine J Heart Lung Transplant 1992;11:926-928.[Medline]
  7. Zietse R, Balk AH, Dorpel MA, Meeter K, Bos E, Weimar W. Time course of the decline in renal function in cyclosporine-treated heart transplant recipients Am J Nephrol 1994;14:1-5.[Medline]
  8. Tinawi M, Miller L, Bastani B. Renal function in cardiac transplant recipients: retrospective analysis of 133 consecutive patients in a single center Clin Transplant 1997;11:1-8.[Medline]
  9. Goral S, Ynares C, Shyr Y, Yeoh TK, Johnson HK. Long-term renal function in heart transplant recipients receiving cyclosporine therapy J Heart Lung Transplant 1997;16:1106-1112.[Medline]
  10. Lindelow B, Bergh CH, Herlitz H, Waagstein F. Predictors and evolution of renal function during 9 years following heart transplantation J Am Soc Nephrol 2000;11:951-957.[Abstract/Free Full Text]
  11. Senechal M, Dorent R, du Montcel ST, et al. End-stage renal failure and cardiac mortality after heart transplantation Clin Transplant 2004;18:1-6.[Medline]
  12. Veillon S, Caillard S, Epailly E, Eisenmann B, Hannedouche T, Moulin B. Chronic renal failure after cardiac transplantation: predictive factors and influence on mortality-results of a monocenter study in 141 patients Transplant Proc 2002;34:2819-2820.[Medline]
  13. Sehgal V, Radhakrishnan J, Appel GB, et al. Progressive renal insufficiency following cardiac transplantation: cyclosporine, lipids, and hypertension Am J Kidney Dis 1995;26:193-201.[Medline]
  14. Taylor DO, Edwards LB, Boucek MM, Trulock EP, Keck BM, Hertz MI. The Registry of the International Society for Heart and Lung Transplantation: twenty-first official adult heart transplant report—2004 J Heart Lung Transplant 2004;23:796-803.[Medline]
  15. Radovancevic B, Konuralp C, Vrtovec B, et al. Factors predicting 10-year survival after heart transplantation J Heart Lung Transplant 2005;24:156-159.[Medline]
  16. Kirklin J, Miller LW, Brown RN, et al. Who is most likely to enjoy long term survival after cardiac transplantation?Risk stratification in a 10 year multi-institutional experience. J Heart Lung Transplant 2001;20:168.[Medline]
  17. Munoz E, Lonquist JL, Radovancevic B, et al. Long-term results in diabetic patients undergoing heart transplantation J Heart Lung Transplant 1992;11:943-949.[Medline]
  18. Morgan JA, John R, Weinberg AD, Colletti NJ, Mancini DM, Edwards NM. Heart transplantation in diabetic recipients: a decade review of 161 patients at Columbia Presbyterian J Thorac Cardiovasc Surg 2004;127:1486-1492.[Abstract/Free Full Text]
  19. Lammermeier DE, Nakatani T, Sweeney MS, et al. Effect of prior cardiac surgery on survival after heart transplantation Ann Thorac Surg 1989;48:168-172.[Abstract]
  20. Ott GY, Norman DJ, Hosenpud JD, Hershberger RE, Ratkovec RM, Cobanoglu A. Heart transplantation in patients with previous cardiac operationsExcellent clinical results. J Thorac Cardiovasc Surg 1994;107:203-209.[Abstract/Free Full Text]
  21. Vijayanagar RR, Chan GL, Weinstein SS, Sears NJ, Cardiac Transplant Team Effect of prior sternotomy on mortality and morbidity after heart transplantation Cardiovasc Surg 1995;3:325-329.[Medline]
  22. De Maria R, Minoli L, Parolini M, et al. Prognostic determinants of six month morbidity and mortality in heart transplant recipients J Heart Lung Transplant 1996;15:124-135.[Medline]
  23. Uthoff K, Wahlers T, Cremer J, Borst HG. Previous open heart operations: a contribution to impaired outcome after cardiac transplantation? Ann Thorac Surg 1997;63:117-123.[Abstract/Free Full Text]
  24. Jaski BE, Kim JC, Naftel DC, et al. Cardiac transplant outcome of patients supported on left ventricular assist device vs. intravenous inotropic therapy J Heart Lung Transplant 2001;20:449-456.[Medline]



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