Biomedical subjects

E Loh

Publications and source records attributed to E Loh.

At least 19 recordsLinked to original sources

PubMed2001

Controlled trial of intravenous immune globulin in recent-onset dilated cardiomyopathy.

BACKGROUND: This prospective placebo-controlled trial was designed to determine whether intravenous immune globulin (IVIG) improves left ventricular ejection fraction (LVEF) in adults with recent onset of idiopathic dilated cardiomyopathy or myocarditis. METHODS AND RESULTS: Sixty-two patients (37 men, 25 women; mean age +/-SD 43.0+/-12.3 years) with recent onset (</=6 months of symptoms) of dilated cardiomyopathy and LVEF </=0.40 were randomized to 2 g/kg IVIG or placebo. All underwent an endomyocardial biopsy before randomization, which revealed cellular inflammation in 16%. The primary outcome was change in LVEF at 6 and 12 months after randomiz. Overall, LVEF improved from 0.25+/-0.08 to 0.41+/-0.17 at 6 months (P<0.001) and 0.42+/-0.14 (P<0.001 versus baseline) at 12 months. The increase was virtually identical in patients receiving IVIG and those given placebo (6 months: IVIG 0.14+/-0.12, placebo 0.14+/-0.14; 12 months: IVIG 0.16+/-0.12, placebo 0.15+/-0.16). Overall, 31 (56%) of 55 patients at 1 year had an increase in LVEF >/=0.10 from study entry, and 20 (36%) of 56 normalized their ejection fraction (>/=0.50). The transplant-free survival rate was 92% at 1 year and 88% at 2 years. CONCLUSIONS: These results suggest that for patients with recent-onset dilated cardiomyopathy, IVIG does not augment the improvement in LVEF. However, in this overall cohort, LVEF improved significantly during follow-up, and the short-term prognosis remains favorable.

Acute Disease↗

PubMed2001

Hemodynamic effects of inhaled nitric oxide in women with mitral stenosis and pulmonary hypertension.

Mitral stenosis (MS) is associated with elevated left atrial pressure, increased pulmonary vascular resistance (PVR), and pulmonary hypertension (PH). The hemodynamic effects of inhaled nitric oxide (NO) in adults with MS are unknown. We sought to determine the acute hemodynamic effects of inhaled NO in adults with MS and PH. Eighteen consecutive women (mean age 58 +/- 15 years) with MS and PH underwent heart catheterization. Hemodynamic measurements were recorded at baseline, after NO inhalation at 80 ppm, and after percutaneous balloon valvuloplasty (n = 10). NO reduced pulmonary artery systolic pressure (62 +/- 14 mm Hg [baseline] vs 54 +/- 15 mm Hg [NO]; p <0.001) and PVR (3.7 +/- 2.5 Wood U [baseline] vs 2.2 +/- 1.4 Wood U [NO]; p <0.001). NO had no effect on mean aortic pressure, left ventricular end-diastolic pressure, left atrial pressure, cardiac output, or systemic vascular resistance. Mitral valve area increased after valvuloplasty (0.9 +/- 0.2 cm2 [baseline] vs 1.6 +/- 0.3 cm2 [postvalvuloplasty]; p <0.001). A decrease in left atrial pressure (25 +/- 4 mm Hg [baseline] vs 17 +/- 4 mm Hg [after valvuloplasty]; p <0.001) and pulmonary artery systolic pressure (58 +/- 12 mm Hg [baseline] vs 45 +/- 8 mm Hg [after valvuloplasty]; p <0.001) was observed after valvuloplasty. No change in cardiac output or PVR was observed. Thus inhaled NO, but not balloon valvuloplasty, acutely reduced PVR in women with MS and PH. This suggests that a reversible, endothelium-dependent regulatory abnormality of vascular tone is an important mechanism of elevated PVR in MS.

Administration, Inhalation↗

PubMed2001

A randomized multicenter study comparing the efficacy and safety of intravenous milrinone and intravenous nitroglycerin in patients with advanced heart failure.

A randomized, open-label, parallel-group design was used to determine the percentage of patients achieving improvements in predetermined baseline hemodynamic end points (>20% to 30% increase in cardiac index depending on baseline values and >25% decrease in pulmonary capillary wedge pressure), assessed at hour 0 (end of initial dose titration) and 1, 2, 4, 8, and 24 hours after the infusion of milrinone or nitroglycerin. In total, 125 patients (60 milrinone, 65 nitroglycerin) enrolled in this study, and 119 (58 milrinone, 61 nitroglycerin) were evaluable for the efficacy analysis. A significantly greater proportion of milrinone-treated patients reached (45% v 14%, P =.005) and maintained (24% v 6%, P =.026) hemodynamic goals than did nitroglycerin-treated patients; the time to achieve hemodynamic goals was significantly less in milrinone-treated patients (33 +/- 2 v 54 +/- 10 minutes, P <.001). Milrinone was also significantly more effective in decreasing systemic vascular resistance (P =.004), increasing stroke volume (P =.008), and improving global clinical status. Inodilator therapy with milrinone seems more efficacious in attaining sustained hemodynamic improvement than does pure intravenous vasodilator therapy with nitroglycerin in treating patients with decompensated heart failure.

Cardiac Output↗

PubMed2001

Overview: old and new controversies in the treatment of advanced congestive heart failure.

In 2001, patients with decompensated congestive heart failure can be treated with various intravenous inotropic agents, vasodilator agents, invasive hemodynamic monitoring, ventricular assist devices, and cardiac transplantation. The use of many of these agents is limited by toxicities and potentially incremental costs associated with intensive care unit stays. As new pharmacologic therapies become available, such as beta-blockers and natriuretic peptides, the combinatorial use of agents for the treatment of patients with decompensated heart failure presents new opportunities with potentially reduced toxicities. Finally, given the natural history of patients with advanced heart failure, it behooves all caregivers to understand the wishes and preferences of the patients who face life-threatening decompensation. This is particularly true with long-term intravenous inotropic therapy. This review article addresses some of the issues that can affect the balance between efficacy, toxicity, and patient preferences for end-of-life care.

Adrenergic beta-Antagonists↗

PubMed2001

Pharmacodynamic effects of milrinone with and without a bolus loading infusion.

BACKGROUND: Milrinone is a positive inotropic agent with vasodilatory and lusitropic activity. Milrinone dosed as a 50 microg/kg bolus followed by a continuous infusion provides an immediate and sustained hemodynamic response. The comparative pharmacodynamics of a placebo bolus and a milrinone bolus followed by a continuous milrinone infusion in patients with decompensated heart failure are unknown. METHODS: Nineteen patients with decompensated heart failure underwent right heart catheterization and were randomized to receive an intravenous infusion of milrinone at a rate of 0.50 microg/kg/min with (n = 9) or without (n = 10) a preceding 50 microg/kg bolus. Pulmonary capillary wedge pressure, cardiac index, and plasma milrinone levels were measured serially over 24 hours. RESULTS: In the milrinone bolus group, maximal effects on plasma concentration (352.3 ng/mL), cardiac index (+0.97 L/min/m(2), P =.02), and pulmonary capillary wedge pressure (-11.25 mm Hg, P <.001) were seen after the loading dose. In the placebo loading dose group, significant hemodynamic effects were observed starting at 30 minutes after the start of the continuous infusion. Changes in pulmonary capillary wedge pressure (placebo -8.6 vs milrinone -8.78 mm Hg, P not significant [NS]) were similar in both groups at 2 hours, whereas changes in cardiac index (placebo loading +0.81 vs milrinone loading +0.78 L/min/m(2), P NS) and milrinone levels (placebo loading 168.0 vs milrinone loading 165.6 ng/mL, P NS) were similar at 3 hours. One patient randomized to a milrinone bolus demonstrated a marked decrease in blood pressure and was discontinued from therapy. CONCLUSIONS: A milrinone infusion without a bolus appears to be a rapidly effective inotropic strategy that may have an improved safety profile during the initiation of therapy compared with a continuous infusion strategy initiated with a bolus.

Blood Pressure↗

PubMed2000

Frequency, risk factors, and clinical outcomes of left ventricular assist device-associated ventricular thrombus.

A retrospective, transesophageal study of 51 consecutive patients receiving a left ventricular (LV) assist device (AD) over a 2-year period showed that LVAD-associated LV thrombosis (16%) was predicted by acute myocardial infarction, atrial cannulation, and postimplantation bleeding, and was associated with a fourfold increased risk of stroke compared with patients without thrombosis. LV cannulation, when using short-term LVADs, may decrease the incidence of LV thrombosis, and early transition to Heartmate-LVAD support may improve outcome.

Aged↗

PubMed2000

Acute hemodynamic and clinical effects of levosimendan in patients with severe heart failure. Study Investigators.

BACKGROUND: We determined the short-term hemodynamic and clinical effects of levosimendan, a novel calcium-sensitizing agent, in patients with decompensated heart failure. METHODS AND RESULTS: One hundred forty-six patients with New York Heart Association functional class III or IV heart failure (mean left ventricular ejection fraction 21+/-1%) who had a pulmonary capillary wedge pressure >/=15 mm Hg and a cardiac index </=2.5 L x min(-1) x m(-2) were enrolled in a multicenter, double-blind, placebo-controlled study and randomized 2:1 to intravenous infusion of levosimendan or placebo. Drug infusions were uptitrated over 4 hours from an initial infusion rate of 0.1 microg x kg(-1) x min(-1) to a maximum rate of 0.4 microg x kg(-1) x min(-1) and maintained at the maximal tolerated infusion rate for an additional 2 hours. Levosimendan caused dose-dependent increases in stroke volume and cardiac index beginning with the lowest infusion rate and achieving maximal increases in stroke volume and cardiac index of 28% and 39%, respectively. Heart rate increased modestly (8%) at the maximal infusion rate and was not increased at the 2 lowest infusion rates. Levosimendan caused dose-dependent decreases in pulmonary capillary wedge, right atrial, pulmonary arterial, and mean arterial pressures. Levosimendan appeared to improve dyspnea and fatigue, as assessed by the patient and physician, and was not associated with a significant increase in adverse events. CONCLUSIONS: Levosimendan caused rapid dose-dependent improvement in hemodynamic function in patients with decompensated heart failure. These hemodynamic effects appeared to be accompanied by symptom improvement and were not associated with a significant increase in the number of adverse events. Levosimendan may be of value in the short-term management of patients with decompensated heart failure.

Cardiotonic Agents↗

PubMed2000

Acute endothelin A receptor blockade causes selective pulmonary vasodilation in patients with chronic heart failure.

BACKGROUND: Elevated plasma endothelin-1 (ET-1) levels in patients with chronic heart failure correlate with pulmonary artery pressures and pulmonary vascular resistance. ET(A) receptors on vascular smooth muscle cells mediate pulmonary vascular contraction and hypertrophy. We determined the acute hemodynamic effects of sitaxsentan, a selective ET(A) receptor antagonist, in patients with chronic stable heart failure receiving conventional therapy. METHODS AND RESULTS: This multicenter, double-blind, placebo-controlled trial enrolled 48 patients with chronic New York Heart Association functional class III or IV heart failure (mean left ventricular ejection fraction 21+/-1%) treated with ACE inhibitors and diuretics. Patients with a baseline pulmonary capillary wedge pressure >/=15 mm Hg and a cardiac index </=2.5 L. min(-1). m(-2) were randomized to 1 of 3 doses (1.5, 3.0, or 6.0 mg/kg) of sitaxsentan or placebo as an intravenous infusion over 15 minutes. Hemodynamic responses were assessed by catheterization of the right side of the heart for 6 hours. Sitaxsentan decreased pulmonary artery systolic pressure, pulmonary vascular resistance, mean pulmonary artery pressure, and right atrial pressure (P</=0.001, 0.003, 0.017, and 0.031, respectively) but had no effect on heart rate, mean arterial pressure, pulmonary capillary wedge pressure, cardiac index, or systemic vascular resistance. Plasma ET-1 levels were elevated at baseline and decreased with sitaxsentan. CONCLUSIONS: In patients with moderate to severe heart failure receiving conventional therapy, acute ET(A) receptor blockade caused selective pulmonary vasodilation associated with a reduction in plasma ET-1. Sitaxsentan may be of value in the treatment of patients with pulmonary hypertension secondary to chronic heart failure.

Cardiac Output, Low↗

PubMed2000

Detection of anti-HLA antibody by flow cytometry in patients with a left ventricular assist device is associated with early rejection following heart transplantation.

BACKGROUND: Patients with a left ventricular assist device (LVAD) as a bridge to heart transplantation (HT) often have elevated levels of panel reactive antibodies (PRA). The clinical significance of anti-human histocompatibility leukocyte antigen (HLA) antibodies detected by flow cytometry in PRA negative patients remains unclear. METHODS: Eighteen patients who underwent LVAD placement as a successful bridge to HT had standard anti-human globulin complement-dependent cytotoxicity and retrospective flow cytometry assays performed to detect class I anti-HLA antibodies. A positive flow result was defined as a fluorescent ratio of 23:1 versus a negative control. RESULTS: Six patients had anti-HLA antibodies detected by flow cytometry. Univariate analysis demonstrated more moderate-severe rejection episodes (ISHLT > or = IIIA) at 2 months (0.83+/-0.75 vs. 0; P=0.04) and a trend toward decreased time to first rejection (61+/-17 vs. 225+/-62 days; P=0.06) in these patients. No differences were observed in donor-recipient HLA mismatch or 1 year Kaplan-Meier survival between patients with or without anti-HLA antibodies. CONCLUSION: Despite a negative PRA, LVAD patients with class I anti-HLA antibodies detected by flow cytometry have a greater incidence of moderate-severe rejection in the first 2 months after HT. Flow cytometry may be a useful clinical tool in screening PRA negative LVAD patients before transplantation. Patients with positive anti-HLA antibody screening by flow cytometry may require more intensive immunosuppression in the early post-HT period.

Adult↗

PubMed2000

CD4(+), HLA class I-restricted, cytolytic T-lymphocyte clone against primary malignant melanoma cells.

The involvement of HLA-class I in target cell lysis by CD4(+) cytolytic T cells (CTL) has been a controversial issue. A CTL clone of CD4 phenotype was derived from the peripheral blood lymphocytes of a patient with primary melanoma. The CTL clone stably lysed the autologous primary melanoma cells for approximately 9 months in culture. Both the Valpha2/Vbeta8 T-cell receptor and CD4 were involved in CTL cytotoxicity. Of a large panel of allogeneic primary and metastatic melanoma or colorectal carcinoma cells, autologous and allogeneic Epstein-Barr virus-transformed B cells and autologous fibroblasts, only allogeneic metastatic melanoma cells matched with the autologous tumor cells for HLA-class I (B57[17]) were lysed and induced IFN-gamma secretion by the CTL clone. Lysis of the autologous tumor cells was significantly blocked by monoclonal antibody to HLA-B17. Importantly, allogeneic, HLA-class I- and class II-unmatched melanoma cells were lysed by the CTL only following transfection of the cells with B57[17] cDNA. Our results provide direct evidence for the involvement of both CD4 and HLA-class I in tumor cell lysis by CD4(+) CTL.

Adult↗

PubMed2000

Maximizing management of patients with decompensated heart failure.

Patients with decompensated congestive heart failure can be categorized into those with either acute or chronic presentations. Patients with acute decompensated heart failure most often have an acute injury that affects either myocardial performance (i.e., myocardial infarction) or valvular/chamber integrity (mitral regurgitation, ventricular septal rupture), which leads to an acute rise in left ventricular (LV) filling pressures resulting in pulmonary edema and dyspnea. Therapy for these patients is aimed at treating the underlying cause of the myocardial injury as well as pharmacologic strategies to reduce LV filling pressures and to improve cardiac performance. In contrast, the therapy of patients presenting with decompensated heart failure in the setting of chronic LV systolic dysfunction, treated with angiotensin-converting enzyme inhibitors, digoxin, diuretics, and may be beta blockers, represent a poorly defined clinical entity that lacks clear guidelines for treatment. These patients can present with symptoms of volume overload and/or low cardiac output without evidence for a volume overloaded state. Potential diagnostic and therapeutic approaches include (1) a pulmonary artery catheter for invasive hemodynamic monitoring, (2) intravenous inotropic therapy, (3) LV mechanical assist device therapy, and (4) cardiac transplantation. This review presents some of the advantages and disadvantages of each of these interventions for patients with chronic systolic dysfunction who present with decompensated symptoms and require specialized management in the hospital setting.

Acute Disease↗

PubMed2000

Cardiomyopathy and embolization: risks and benefits of anticoagulation in sinus rhythm.

Systemic embolic complications in patients with cardiomyopathy are associated with significant morbidity and mortality. Despite the lack of prospective, randomized control data, the literature supports the use of left ventricular ejection fraction as an important determinant of the need for systemic anticoagulation therapy in patients with systolic dysfunction. This review discusses the risks and benefits of systemic anticoagulation for patients with cardiomyopathy and proposes a treatment algorithm for its initiation.

Algorithms↗

PubMed2000

Changes in lipoprotein(a) concentration after orthotopic heart transplantation.

BACKGROUND: Elevated concentrations of lipoprotein(a) have been considered an important risk factor in the development of premature cardiovascular disease and have been proposed as a risk factor in the development of accelerated cardiac allograft vasculopathy after orthotopic heart transplantation. METHODS: We prospectively measured lipoprotein(a), fasting cholesterol, and triglyceride concentrations before (n = 38), 6 months (n = 38), and 1 year (n = 21) after orthotopic heart transplantation. The mean age of the patients was 52 +/- 2 years. Eighty-seven percent of the patients were men, 82% were white, and 61% had ischemic cardiomyopathy. RESULTS: Mean lipoprotein(a) concentration was lower 6 months after transplantation than it was before the operation (23 +/- 3 mg/dL vs 17 +/- 3 mg/dL; P =.014) and remained low 1 year after transplantation (23 +/- 3 mg/dL vs 18 +/- 4 mg/dL; P = not significant). In contrast, mean cholesterol concentration was higher 6 months after transplantation (171 +/- 8 mg/dL vs 221 +/- 8 mg/dL; P <.001) and 1 year (171 +/- 8 mg/dL vs 205 +/- 10 mg/dL; P <.01) than it was before transplantation. Triglyceride concentration was higher 1 year after transplantation than it was before the operation (146 +/- 13 mg/dL vs 184 +/- 20 mg/dL; P =.017). CONCLUSIONS: Lipoprotein(a) concentrations decrease during the 6 months after transplantation and stay low for at least 1 year after the operation. Additional studies are needed to ascertain the effect these changes in lipoprotein(a) concentration on the development of cardiac allograft vasculopathy.

Adolescent↗

PubMed2000

Hepatitis C transmission and infection by orthotopic heart transplantation.

BACKGROUND: The transmission and clinical consequences of hepatitis C viral (HCV) infection acquired by orthotopic heart transplantation (OHT) from an HCV-infected donor to an HCV-naive recipient have not been well described. We report our experience in 5 HCV-naive patients who were transplanted with hearts from HCV-positive donors. All transplants occurred within a 1-year period. METHODS: After cardiac transplantation we retrospectively examined the recipients' clinical course, liver-associated enzymes, HCV-antibody serology, quantitative HCV RNA level, and HCV genotype. RESULTS: Five subjects with rapidly deteriorating heart failure and negative serum antibodies to HCV received an emergent OHT from a donor known to be infected with HCV. Liver-associated enzymes peaked at 2 to 6 weeks post-transplant: mean peak alanine aminotransferase was 180 U/L (normal, 9 to 52) and aspartate aminotransferase was 111 U/L (normal, 14 to 36). Liver enzymes had returned to normal limits by 6 and 12 months post-OHT. At a mean 15 months after transplantation, only 1 of 5 patients has developed antibodies to HCV, but 4 of 5 have evidence of infection, as shown by serum HCV RNA. No patient has developed evidence of liver failure. CONCLUSIONS: (1) Transmission of HCV from an HCV-positive donor to an HCV-naive recipient at the time of OHT is likely. (2) Antibodies to HCV post-OHT may remain negative for more than 1 year in these patients. (3) Hepatitis C viral RNA using polymerase chain reaction should be the test of choice for diagnosis of HCV infection post-OHT. (4) Hepatitis C viral donor hearts should be limited to critically ill patients in extremis until the long-term consequences of acquisition of HCV by an OHT recipient are known.

Aged↗

PubMed2000

Early post-transplant lymphoproliferative disease following heart transplantation in the absence of lymphocytolytic induction therapy.

We report a case of post-transplant lymphoproliferative disease presenting as a disseminated polymorphous B-cell lymphoma involving the cardiac allograft 3 months following transplantation in a recipient who did not receive anti-lymphocyte induction immunosuppression. In situ hybridization for the lytic Epstein-Barr virus marker NOT I was positive within a lymphocytic infiltrate on endomyocardial biopsy. Our case is the third of early post-transplant lymphoproliferative disease (within 6 months of transplantation) involving the heart allograft in the absence of anti-lymphocyte induction immunosuppression. Post-transplant lymphoproliferative disease of the heart allograft should be considered in the presence of an atypical cardiac lymphocytic infiltrate, with possible differentiation from allograft rejection using in situ hybridization for Epstein-Barr virus.

Drug Therapy, Combination↗

PubMed2000

Mycophenolic acid concentrations are associated with cardiac allograft rejection.

BACKGROUND: Mycophenolate mofetil (MMF) therapy decreases the incidence of allograft rejection following solid-organ transplantation. Current dosing strategies of MMF are not routinely adjusted based on mycophenolic acid (MPA) area under the concentration-time curve (AUC), MPA trough, or free MPA (fMPA) AUC values. METHODS: To determine the clinical significance of MPA concentrations following orthotopic heart transplantation (OHT), we measured pre-dose MPA trough, MPA free fraction, an estimated MPA AUC using an abbreviated sampling schedule, and fMPA AUC in 38 consecutive patients. We measured MPA concentrations using a validated high-performance liquid chromatography method and graded endomyocardial biopsies based on the International Society for Heart and Lung Transplantation (ISHLT) grading system. RESULTS: The MPA values for the study group were as follows: MPA trough of 1.2 +/- 0.6 microg/ml; MPA free fraction of 1.9 +/- 0.4%; MPA AUC of 44.5 +/- 16. 1 microg/hour/ml; and fMPA AUC of 0.83 +/- 0.30 microg/hour/ml. We compared patients with Grade 0 (n = 22), Grade 1 (n = 13), or Grade 2/3 (n = 3). The MPA AUC values were lower in patients with Grade 2/3 than in patients with Grade 0 (26.1 +/- 6.6 vs 42.8 +/- 14.0 microg/hour/ml, p < 0.08) or Grade 1 rejection (26.1 +/- 6.6 vs 51.7 +/- 17.5 microg/hour/ml, p < 0.05). The fMPA AUC values were lower in patients with Grade 2/3 than with patients with Grade 0 (0.49 +/- 0.11 vs 0.81 +/- 0.25 microg/hour/ml, p < 0.05) or Grade 1 (0.49 +/- 0.25 vs 0.95 +/- 0.34 microg/hour/ml, p < 0.05) rejection. We noted a trend in MPA trough concentrations between patients with Grade 2/3 vs 0 (0.65 +/- 0.15 vs 1.20 +/- 0.58 microg/ml, p = 0.15) and Grade 1 (0.65 +/- 0.15 vs 1.24 +/- 0.72 microg/ml, p = 0.14) rejection. CONCLUSION: These preliminary results suggest that lower MPA AUC and fMPA AUC values are associated with cardiac allograft rejection in heart transplant recipients. Individualizing MMF dosing based on MPA determinations may minimize the risk of rejection following OHT.

Adult↗

PubMed2000

Preferences for treatment outcomes in patients with heart failure: symptoms versus survival.

BACKGROUND: Patient preferences for congestive heart failure therapy outcomes may vary depending on the goals of improving symptoms versus survival, but this has not been extensively investigated. Our objective was to analyze patient preferences for congestive heart failure therapy outcomes based on the goals of symptom versus survival improvement. METHODS AND RESULTS: This was a prospective, full-profile conjoint analysis study of individual preferences for congestive heart failure treatment outcomes. Conjoint analysis was based on ratings of 16 treatment-outcome profiles, each consisting of 4 attributes (tiredness, shortness of breath, depression, and survival) varied across 4 severity levels. Part-worths (utilities) and importance weights were calculated for each attribute to determine their relative contribution to the full-profile rating decision using standard full-profile conjoint analysis techniques. Fifty-one patients with congestive heart failure from our medical center (University of Pennsylvania Medical Center, Philadelphia, PA) and 47 age-, gender-, and race-matched control subjects were studied. Part-worths and importance weights were significantly different for shortness of breath and depression between patients and control subjects. Symptom-sensitive (n = 33) and survival-sensitive (n = 17) treatment outcome preference segments were identified within the patient group. Importance weights for symptom-sensitive versus survival-sensitive patients were as follows: tiredness 0.30+/-0.10 versus 0.16+/-0.09 (P < .01); shortness of breath 0.26+/-0.08 versus 0.21+/-0.08 (P = .07); depression 0.26+/-0.09 versus 0.19+/-0.09 (P = .01); and survival 0.18+/-0.07 versus 0.43+/-0.11 (P < .01). There were no significant predictors of which treatment outcome preference segment a patient belonged. Control subjects did not display similar preference segmentation. CONCLUSIONS: Symptomatic congestive heart-failure patients were clustered into symptom-sensitive and survival-sensitive segments in a manner suggesting that treatment outcomes of improved symptoms were of greater importance to the majority than longer survival. A full understanding of these individual preferences may have important implications for the design of therapy for heart-failure patients.

Adult↗

PubMed2000

Heart transplant center practice patterns affect access to donors and survival of patients classified as status 1 by the United Network of Organ Sharing.

OBJECTIVE: To determine the effect of adult cardiac transplant center practice patterns within a single organ procurement organization on access to donors and survival for patients listed as United Network of Organ Sharing (UNOS) status 1. METHODS: A total of 662 patients listed (January 1, 1992, through December 31, 1995) as UNOS status 1 for heart transplantation by the 4 adult cardiac transplant centers in an organ procurement organization were analyzed in a retrospective cohort study to determine differences in clinical outcomes. RESULTS: The specific center at which an individual was listed as UNOS status 1 was a significant independent predictor of receiving a transplant (odds ratios for 3 centers vs center with highest likelihood = 0.73, 0.64, 0.35, respectively; P <. 01). Only 1 center had a significantly increased mortality rate compared with the other centers (odds ratio 2.03, P <.01). CONCLUSION: Within a single regional organ procurement organization, cardiac transplant centers demonstrate significant variability in the likelihood of transplantation and survival for patients listed as UNOS status 1.

Adult↗