Predictive model to assess risk for cardiac allograft vasculopathy: an intravascular ultrasound study.

OBJECTIVES: This study was performed to assess the influence and interdependence of immunologic and nonimmunologic risk factors in the development of cardiac allograft vasculopathy. Another primary objective was to establish a clinically useful model for risk assessment of cardiac allograft vasculopathy that would facilitate identifying those heart transplant recipients likely to have severe intimal proliferation and thereby at greater risk for adverse clinical events. BACKGROUND: To our knowledge, no comprehensive intravascular ultrasound study has assessed the relative influences of both nonimmunologic and immunologic factors in the development of cardiac allograft vasculopathy, currently the major limitation to long-term cardiac allograft survival. METHODS: Using a computer-assisted model of stepwise logistic regression, immunologic and nonimmunologic risk factors were evaluated to help identify the development of severe intimal thickening in 101 subjects who underwent intravascular ultrasound. Prospective validation of the findings was performed in a separate consecutive cohort of 37 heart transplant recipients, and the accuracy of this model to predict a relative risk > 1 for the development of severe intimal hyperplasia was assessed. RESULTS: Significant independent predictors of severe intimal hyperplasia in this model included a donor age > 35 years, a first-year mean biopsy score > 1 (a measure not only of severity of rejection, but also of frequency of insidious rejection) and hypertriglyceridemia at two incremental levels of risk (150 to 250 mg/dl [1.70 to 2.83 mmol/liter] and > 250 mg/dl [2.83 mmol/liter]). Based on the absence (0) or presence (1) of these factors, 12 individual categories of risk were ascertained with increasing relative risks and predicted probabilities for severe intimal hyperplasia. Prospective validation of this model revealed a sensitivity and specificity of 70% and 90%, respectively, and the positive and negative predictive values were 85% and 80%, respectively. Additionally, subjects with severe intimal thickening had a four-fold higher cardiac event rate than those without severe intimal proliferation on intravascular ultrasound. CONCLUSIONS: This study establishes a clinically useful predictive model that can be applied to individual heart transplant recipients to assess their risk for developing significant cardiac allograft vasculopathy and, thus, aids in the identification of patients at risk for cardiac events in whom closer surveillance and risk factor modification may be warranted.

Heterogeneity of cardiac allograft vasculopathy: clinical insights from coronary angioscopy.

OBJECTIVES: With this study, we sought to examine the heterogeneity of cardiac allograft vasculopathy in vivo using coronary angioscopy as an adjunct to intravascular ultrasound, and we evaluated the clinical relations of immunologic and nonimmunologic risk factors with the different forms of cardiac allograft vasculopathy detected angioscopically. BACKGROUND: Intravascular ultrasound detects vascular intimal proliferation accurately but is limited in its ability to delineate morphologic characteristics. Coronary angioscopy can evaluate intimal surface morphology by direct visualization and can differentiate pathologically distinct forms of plaque topography on the basis of color and contour. METHODS: We studied 107 consecutive heart transplant recipients with intravascular ultrasound and angioscopy at the time of their annual angiogram, and we assessed the relation of nonimmunologic and immunologic risk factors to the development of cardiac allograft vasculopathy distinguished angioscopically into a pigmented (yellow) or nonpigmented (white) intimal thickening. We further evaluated the clinical differences in cardiac events among these two forms of angioscopically heterogeneous forms of cardiac allograft vasculopathy. RESULTS: Significant clinical predictors of nonpigmented intimal thickening were advanced donor age and lower mean cyclosporine levels, whereas hyperlipidemia, cumulative prednisone dose and time since transplantation correlated with pigmented intimal hyperplasia. In addition, comparisons between the two angioscopic groups revealed increased intimal thickening, serum cholesterol, low density lipoprotein cholesterol, acute allograft rejection and time since transplantation in the group with pigmented intimal thickening (p < 0.05). With regard to cardiac events, nonpigmented plaque was more frequently found in the sudden death group (53% vs. 20%, p = 0.05), whereas the nonsudden cardiac event group had a significantly higher prevalence of pigmented plaque (80% vs. 47%, p = 0.07). CONCLUSIONS: These findings indicate that cardiac allograft vasculopathy is a heterogeneous disease with varied morphologic expressions with different clinical implications. Furthermore, this investigation provides insight into the cohesive, yet diverse influences of various factors, particularly immunosuppression, in these forms of cardiac allograft vasculopathy.

Safety and clinical utility of long-term intravenous milrinone in advanced heart failure.

Few data are available on the long-term safety or clinical utility of the inodilator agent milrinone. We designed a prospective, nonrandomized, observational trial in a cohort of 71 patients who had demonstrated dependence on inotropic therapy, had been clinically stable on an inotropic regimen (milrinone, dobutamine, or both) for > or = 72 hours, and had been given intravenous milrinone for > 72 hours. Group I (n = 22) patients required treatment with both milrinone and dobutamine to achieve stability; group II (n = 49) patients attained stability initially with either milrinone (subgroup IIA) or dobutamine (subgroup IIB), but later required adjunctive therapy with the other inotropic agent for continued hemodynamic support. Of the 71 patients, 38% required mechanical intervention to achieve hemodynamic stability, and 68% were successfully bridged to heart transplantation. Patients were maintained on milrinone therapy for as long as 8 weeks and demonstrated a low incidence of adverse cardiac (7%) or noncardiac (4%) events. Subgroup IIA (28%) had significantly less need than subgroup IIB (52%) for mechanical intervention using an intraaortic balloon pump (p = 0.05), although mortality rates while awaiting transplantation were statistically similar in subgroups IIA (28%) and IIB (35%). Significant improvements from baseline values were noted at the time of transplantation for all aspects of systemic hemodynamics, indicating sustained long-term hemodynamic effects. Long-term intravenous milrinone therapy is safe and well tolerated, and it provides hemodynamic and metabolic support as a pharmacologic bridge to transplantation. The findings also suggest that milrinone as primary inodilator therapy may be associated with less need for mechanical ventricular support.

Management of cardiac allograft vasculopathy by transmyocardial laser revascularization.

Transmyocardial laser revascularization provides a unique and effective intervention for symptomatic relief and improvement of myocardial perfusion in diffuse cardiac allograft vasculopathy.

Usefulness of peak oxygen consumption in predicting outcome of heart failure in women versus men.

This investigation finds that percent of predicted maximum oxygen consumption, an age- and gender-adjusted measurement of exercise, capacity, describes the degree of functional impairment in women more accurately than peak oxygen consumption. This evidence must be considered when cardiopulmonary metabolic parameters are used for prognostic stratification of women with heart failure.

Lipid-lowering therapy and long-term survival in heart transplantation.

The influence of lipid-lowering therapy employing a historic cohort study design was assessed following heart transplantation. Lipid-lowering therapy appears to confer a survival benefit in cardiac transplant recipients who survive beyond the first year.

Assessment of intracoronary morphology in cardiac transplant recipients by angioscopy and intravascular ultrasound.

Percutaneous coronary angioscopy and intravascular ultrasound are sensitive intravascular imaging methods for detecting early changes in coronary morphology in cardiac transplant recipients. To compare the 2 imaging modalities, 29 consecutive cardiac transplant recipients underwent percutaneous coronary angioscopy and intravascular ultrasound during annual coronary angiography. Surface morphology, presence of plaque, and percent area stenosis were determined with each procedure. Percutaneous coronary angioscopy was more sensitive in detecting the presence of plaque and stenosis than was coronary angiography (plaque: 79 vs 10% [p < 0.001]; and stenosis: 24 vs 3% [p < 0.01]). Intravascular ultrasound was also more sensitive in detecting plaque (76 vs 10%; p < 0.001) and stenosis (45 vs 3%; p < 0.001) than was coronary angiography. Although both angioscopy and ultrasound identified atherosclerotic plaque, only percutaneous coronary angioscopy could show luminal surface morphology and pigmentation of the plaque. Conversely, ultrasound could detect calcification and presence of intimal thickening, and was more accurate in assessing the severity of stenosis (45 vs 24%; p < 0.01). In conclusion, percutaneous coronary angioscopy and intravascular ultrasound, in conjunction, provide information not only regarding the appearance of the luminal surface, but also quantitative information regarding the structure and extent of the disease in the coronary artery wall.

Cardiac allograft vasculopathy assessed by intravascular ultrasonography and nonimmunologic risk factors.

The genesis of cardiac allograft vasculopathy has been linked to nonimmunologic endothelial injury. Studies evaluating the role of nonimmunologic risk factors have thus far been limited to angiographic assessment. Intravascular ultrasound can detect cardiac allograft vasculopathy before it becomes angiographically evident. To assess the influence of nonimmunologic risk factors in the development of cardiac allograft vasculopathy, we studied 101 consecutive cardiac transplant recipients who underwent intracoronary ultrasound imaging during routine, annual coronary angiography. Based on the severity of intimal thickening, patients were divided into 2 groups: group 1 = minimal, mild, or moderate intimal thickness; and group 2 = severe intimal thickness. Cardiac transplant recipients with severe intimal thickness had higher levels of total cholesterol (267 +/- 70 vs 227 +/- 41 mg/dl, p = 0.0008), low-density lipoprotein cholesterol (187 +/- 47 vs 139 +/- 31 mg/dl, p = 0.0001), and triglycerides (237 +/- 75 vs 182 +/- 88 mg/dl, p = 0.0004), a higher percentage of weight gain (12 +/- 4% vs 8 +/- 5%, p = 0.0001), a larger body mass index (30 +/- 4 vs 25 +/- 3, p = 0.0001), and older donor age (27 +/- 5 vs 23 +/- 7 years, p = 0.005) than recipients with mild or moderate intimal thickness. Multiple regression analysis established that total cholesterol, low-density lipoprotein cholesterol, triglyceride levels, obesity indexes, donor age, and years following cardiac transplantation (p < 0.01) were independent predictors of the severity of intimal thickening, and thus the severity of cardiac allograft vasculopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of caregiver specialty on cost and clinical outcomes following hospitalization for heart failure.

In 614 consecutive hospitalizations with the primary discharge diagnosis of diagnosis-related group (DRG) 127 (heart failure and shock), we sought to assess the effect of caregiver specialty (generalist, n = 217; cardiologist, n = 397) on hospital costs, length of stay, and in-hospital mortality. Patients treated by cardiologists were younger (68 vs 71 years) and less likely to have hypertension (52% vs 61%), but were more likely to be men (61% vs 44%), require an intensive care stay (13% vs 5%), have coronary artery disease (49% vs 23%), have a left ventricular ejection fraction <40% (74% vs 49%), and have lower systolic (132 vs 146 mm Hg) and diastolic (76 vs 81 mm Hg) blood pressures on admission. Predictors of acute disease severity were similarly distributed between the 2 groups. No difference was found between patients treated by cardiologists versus those treated by generalists with respect to crude or adjusted hospital cost, length of stay, and in-hospital mortality. However, in subsets of patients who required intensive care during hospitalization (n = 64), as well as those who did not (n = 550), care by cardiologists was associated with a lower adjusted hospital cost. Any potential cost savings that could have accrued from care by cardiologists was, however, negated by the higher proportion of patients treated by cardiologists who required intensive care during hospitalization. We conclude that when differences in clinical variables are adjusted, care by cardiologists versus generalists is associated with similar or lower hospital cost for patients with DRG 127. Our findings challenge the notion that in-patient care provided by specialists is more expensive than that provided by generalists.

Home inotropic therapy in advanced heart failure: cost analysis and clinical outcomes.

STUDY OBJECTIVES: This study was conducted to assess cost savings and clinical outcomes associated with the use of home i.v. inotropic therapy in patients with advanced (New York Heart Association [NYHA] class IV) heart failure. DESIGN: Retrospective analysis. SETTING: Tertiary care referral center. PATIENTS AND INTERVENTIONS: Twenty-four patients (13 men, 11 women; age, 61+/-12 years) with left ventricular ejection fraction <30% and heart failure refractory to oral agents required home i.v. inotropic therapy for at least 4 consecutive weeks between May 1994 and April 1996. Inotropic agents used included dobutamine (n=20; dose, 5.0+/-2.2 microg/kg/min) or milrinone (n=7; dose, 0.53+/-0.05 microg/kg/min). MEASUREMENTS AND RESULTS: Cost of care and clinical outcomes (hospital admissions, length of hospital stay, NYHA functional class) were compared during the period of inotropic therapy (study period) and the immediate preceding period of equal duration (control period). In comparison to the control period, the study period (3.9+/-2.7 months) was associated with a 16% reduction in cost, amounting to a calculated savings of $5,700 per patient or $1,465 per patient per month. Concomitantly, a decrease in the number of hospital admissions from 2.7+/-2.6 to 1.3+/-1.3 (p=0.056) and length of hospital stay from 20.9+/-12.7 to 5.5+/-5.4 days (p=0.0004) was observed with improvement in NYHA functional class from 4.0+/-0.0 to 2.7+/-0.9 (p<0.0001). Eight patients (38%) died after 2.8+/-1.7 months of home i.v. inotropic therapy. CONCLUSIONS: Home i.v. inotropic therapy reduces hospital admissions, length of stay, and cost of care and improves functional class in patients with advanced (NYHA class IV) heart failure.

The prognostic impact of immunosuppression and cellular rejection on cardiac allograft vasculopathy: time for a reappraisal.

BACKGROUND: Our current immunosuppressive strategies have made little impact on the development of cardiac allograft vasculopathy, the leading cause of long-term allograft loss. This study sought to evaluate the relationship of cellular rejection and immunosuppressive therapy with the development of morbid events resulting from cardiac allograft vasculopathy. METHODS: The study population consisted of 163 consecutive patients who received heart transplants between January 1990 and May 1994. Data regarding nonimmunologic risk factors (lipids, obesity indexes, hypertension, donor age and sex, cytomegalovirus infection, diabetes mellitus, time after transplantation, and cold ischemic time), immunologic factors (histocompatibility, episodes of treated rejection, and average first-year biopsy rejection score), and immunosuppressive regimens (cumulative prednisone dose, average daily prednisone dose, mean cyclosporine level, average cyclosporine daily dose, cumulative azathioprine dose, and average daily azathioprine dose) were collected and analyzed in all patients. The diagnosis of cardiac allograft vasculopathy was established in all patients by a combination of necropsy, angiography, and intravascular ultrasound examination of the allograft vasculature. Cardiac events were defined as sudden death, myocardial infarction, and need for revascularization. RESULTS: Of all variables assembled, stepwise logistic regression recognized cumulative prednisone dose > 15 gm (relative risk [RR] 5.7; p = 0.01), donor age > 35 years (RR 3.73; p < 0.05), and average biopsy rejection score > 1 (RR 2.77; p < 0.05) as independent adverse predictors of cardiac events. In distinction, average daily cyclosporine dose > 4.5 mg/kg/day was found to confer a protective effect (RR 0.16; p = 0.03). CONCLUSIONS: The development of cardiac events as a result of cardiac allograft vasculopathy is influenced by the interdependence of allograft rejection and the balance of immunosuppression. The clinical implications of these findings point to the need for a reappraisal of our traditional approach to using corticosteroids (acute and maintenance) and cyclosporine (maintenance) in heart transplantation.

Presence of severe intimal thickening by intravascular ultrasonography predicts cardiac events in cardiac allograft vasculopathy.

BACKGROUND: The clinical utility of intimal hyperplasia detected by intravascular ultrasonography in predicting cardiac events in heart transplant recipients with cardiac allograft vasculopathy has not been previously investigated. METHODS: Intravascular ultrasonographic examination of 74 consecutive heart transplant recipients, including 62 men and 12 women with a mean age of 51 +/- 10 years (range 22 to 68 years), was performed at the time of annual angiography. Two groups of study patients were identified: group I consisted of patients with minimal, mild, or moderate intimal thickness by intravascular ultrasonography, whereas group II patients had severe intimal thickness. RESULTS: Patient characteristics were similar in both groups except for higher serum triglycerides (220 +/- 95 versus 165 +/- 79 mg/dl), more advanced donor age (28 +/- 11 versus 23 +/- 6 years) and greater duration of follow-up after transplantation (3.3 +/- 1.4 versus 1.8 +/- 1.2 years) in group II patients with severe intimal thickening (p < 0.01). Cardiac events were defined as the occurrence of sudden death, myocardial infarction, or the need for coronary revascularization via percutaneous or surgical intervention. One cardiac event occurred in group I patients (sudden death), whereas seven events were noted in the group II patients (p = 0.006). Cardiac events in the group of patients with severe intimal thickening included four patients with sudden cardiac death and three patients who underwent percutaneous revascularization procedures involving directional coronary atherectomy. Angiograms were normal in 62% of patients who had cardiac events. CONCLUSIONS: This study represents one of the first reports that provides evidence that severe intimal hyperplasia predicts the development of cardiac events even in the presence of a normal coronary angiogram.

Vibrio vulnificus sepsis in solid organ transplantation: a medical nemesis.

We report two cases of Vibrio vulnificus wound infection leading to fulminant sepsis syndrome in immunocompromised solid organ transplant recipients. Features of clinical presentation in each of these cases suggest that host immune factors are of great importance in the virulence of this organism and that immunocompromised recipients of solid organ transplants are particularly vulnerable to life-threatening consequences from infection with Vibrio vulnificus. Prompt institution of antibiotic therapy and early consideration for surgical wound debridement are the mainstay of successful management. Heart and other organ transplant recipients should be educated and warned about the hazards associated with raw oysters and shellfish consumption and asked to exercise caution when exposed to a salt water environment.

Adenovirus-mediated in vivo gene transfer in a rabbit model of allograft vasculopathy.

BACKGROUND: The long-term success of heart transplantation continues to be in jeopardy because of the development of accelerated vascular myointimal proliferation. Transfer of genes encoding products that can modulate the adverse consequences of phenomena that cause myointimal proliferation, into the allograft vessel wall, may modify these pathologic processes. The purpose of this study was to assess the feasibility of gene transfer and to evaluate the duration of gene expression in a rabbit heterotopic aortic transplant model of allograft vasculopathy. METHODS: The abdominal aortas of 32 outbred New Zealand rabbits were harvested and cross-sectionally bisected (n = 64). Six donor and recipient animals were used in a preliminary study to examine neointimal proliferation without accompanying gene transfer. Of the remaining 26 rabbits (52 allografts), one half of each allograft aorta was administered a control solution, while the other half was incubated with a replication-defective, recombinant, adenoviral vector-encoding, cytomegalovirus promoter-regulated beta-galactosidase. After a 20-minute incubation period, bilateral aorto-carotid transplantations were performed in 26 recipient rabbits. All animals received cyclosporine immunosuppression (10 mg/kg/day subcutaneously). The allografts were harvested at 3, 7, 10, 21, and 28 days after transplantation and assayed for beta-galactosidase activity. RESULTS: Neointimal areas showed an initially slow increase for the first 10 days, followed by a rapid increase up to 21 days, and tended to plateau thereafter. Significant beta-galactosidase was apparent in aortic sections dissected from host rabbits for all time points, except at 28 days. At the 21-day time point, the aortic section from one rabbit was positive, whereas the other two remained negative. However, the one positive section showed intense beta-galactosidase activity, suggesting variability in the experimental model. At 28 days, all aortic sections were negative. CONCLUSIONS: Our findings confirm that genes delivered by this method are expressed for the duration of early rapid intimal proliferation in this heterotopic rabbit model of aortic allograft vasculopathy. These findings suggest that this animal model can be used to assess the therapeutic potential of gene transfer at the time of vascular transplantation and may provide a novel therapeutic approach to prevent or ameliorate the genesis of allograft vasculopathy.

Current issues in advanced heart failure.

In the past 50 years, an increased understanding of the pathophysiologic mechanisms associated with the development of heart failure has produced a more precise treatment of this syndrome. The effects of the agents used for the treatment of patients with advanced heart failure have been summarized in this article and demonstrate the importance of vasodilatory drugs on the survival and progression of dilated cardiomyopathy.

Cardiac transplantation: clinical aspects of recipient selection.

The improved outcome following cardiac transplantation has produced changes in the traditional criteria for potential candidates. We have analyzed these changes and the clinical aspects involved in the selection process, which are of critical importance to assure an excellent result of cardiac transplantation in patients with advanced heart failure.

Cyclosporine-induced hypertension in cardiac transplantation.

Cyclosporine-induced hypertension occurs in more than 90% of patients following cardiac transplantation. This article underlines the clinical characteristics as well as the mechanisms that can be associated with the development of cyclosporine-induced hypertension. In addition, the clinical trials up to date for the treatment of hypertension following cardiac transplantation are discussed. However, in view of the possible long-term sequelae associated with cyclosporine-induced hypertension, further studies to evaluate the long-term efficacy and safety of antihypertensive agents and finally the long-term effects of hypertension on the cardiac allograft are needed.

Cardiovascular adaptation to cyclosporine-induced hypertension.

Arterial hypertension is a complication of cyclosporine therapy in heart transplant recipients. We studied cardiovascular adaptation to cyclosporine-induced hypertension by determining haemodynamic and echocardiographic indexes in 25 cardiac transplant recipients matched by mean arterial pressure, age, sex, height and weight to 25 patients with established essential hypertension. Twenty-five normotensive subjects matched by age, sex and body habitus were used as controls. Systemic vascular resistance was 15% higher (P = 0.07) and cardiac and stroke volume indices were 20% and 25% lower (P < 0.01), respectively, in the hypertensive cardiac transplant recipients compared with patients with essential hypertension. Patients with essential hypertension and hypertensive cardiac transplant recipients had greater posterior wall thickness and left ventricular mass index than normotensive subjects (P < 0.01); however, hypertensive cardiac transplant recipients had a greater left ventricular mass (245 +/- 7 vs. 223 +/- 8 g, P < 0.05) than patients with markedly established essential hypertension. Left ventricular ejection fraction was significantly lower in hypertensive cardiac transplant recipients when compared with either normotensives or patients with established essential hypertension. These results indicate that established essential and cardiac transplant hypertension are associated with markedly increased systemic vascular resistance. However, after heart transplantation, hypertension is associated with higher systemic vascular resistance, lower cardiac output, stroke volume and stroke work compared with patients with established essential hypertension at the same level of mean arterial pressure. The cardiac adaptation to cyclosporine-induced hypertension has more severe concentric left ventricular hypertrophy and impaired left ventricular systolic performance.(ABSTRACT TRUNCATED AT 250 WORDS)

Rhabdomyolysis and acute renal failure in a cardiac transplant recipient due to multiple drug interactions.

BACKGROUND: The 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors lovastatin and simvastatin have been associated with rhabdomyolysis in cardiac transplant recipients. Herein, we report a case of a 52-year-old male recipient of a cardiac transplant who developed rhabdomyolysis and acute renal failure caused by simvastatin precipitated by multiple drug interactions. METHODS: The patient had a history of cardiac transplantation (5 years before) and presented with a 2-day history of dark urine preceded by 2 weeks of diffuse myalgias. He had been maintained on cyclosporine throughout the entire post-transplant period. Simvastatin was added and pravastatin was discontinued 2 months before admission. Two weeks before the onset of muscle symptoms, digoxin and verapamil were started for new-onset atrial fibrillation. Creatinine phosphokinase levels peaked at 950,000 IU with serum creatinine of 3.3 mg/dL (baseline, 1.8 mg/dL). RESULTS: Review of the medication history indicates a temporal association between the addition of 3 drugs (simvastatin, verapamil, and digoxin) to the medication regimen already containing cyclosporine and the episode of rhabdomyolysis. All of these drugs are cytochrome P450 3A4 and/or P-glycoprotein substrates that are known from previous pharmacokinetic studies to individually produce substantial increases in levels of simvastatin. CONCLUSION: We believe this case illustrates that avoiding the use of drugs that are cytochrome P450 3A4 and/or P-glycoprotein substrates reduces the risk of rhabdomyolysis caused by 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors.

Induction immunosuppression with the monoclonal antibody OKT3 after cardiac transplantation.

The routine use of monoclonal induction immunosuppression with OKT3 after orthotopic heart transplantation remains controversial. This study examined the clinical response of prophylactic monoclonal induction immunosuppression versus standard triple-drug immunosuppression in 41 patients who underwent orthotopic heart transplantation from January 1989 to December 1990 at this institution. Of these, eight received monoclonal induction immunosuppression for a period of 10 to 14 days. All patients received identical triple-drug immunosuppression with the exception of cyclosporine starting on the fifth postoperative day in those who received OKT3. At 6 months the duration of hospitalization, freedom from rejection, incidence of infection requiring hospitalization, and serum creatinine in the monoclonal induction immunosuppression and triple-drug groups were compared. It was found that the length of hospital stay in the OKT3 group was 14.3 +/- 4.5 days, compared with 14.7 +/- 4.7 days in the triple-drug group and that freedom from rejection was 66% in the OKT3 group compared with 75% in the triple-drug group. In addition, it was found that the incidence of infection was 36% in the OKT3 group compared with 38% in the triple-drug group and that serum creatinine at 6 months was 1.36 +/- 0.26 mg/dl in the OKT3 group compared with 1.45 +/- 0.73 mg/dl in the triple-drug group. Finally, patient survival at 1 year for the monoclonal induction immunosuppression group was 100% compared with 91% for the triple-drug group.(ABSTRACT TRUNCATED AT 250 WORDS)