Biomedical subjects

Michael Grimm

Publications and source records attributed to Michael Grimm.

At least 19 recordsLinked to original sources

PubMed2006

Heart transplantation provides long-term survival benefit in stable patients experiencing heart failure without reverse left ventricular remodeling.

BACKGROUND: Heart transplantation does not provide short-term survival benefit in stable patients experiencing chronic heart failure (CHF) with optimized medical therapy. This study compared the outcome of stable patients with CHF with patients after heart transplantation in the long-term. METHODS: Between January 1995 and September 1997, 318 potential transplant candidates (New York Heart Association class III or IV, left ventricular ejection fraction [LVEF] <35%) were evaluated. After three months of therapeutic optimization, 108 patients were stable outpatients with maximally uptitrated neurohormonal antagonists. Seventy of the 318 patients underwent transplantation between January 1995 and December 1997. RESULTS: After an observation period of 7 to 10 years, stable patients with CHF had a significantly lower survival compared with transplanted patients (hazard ratio, 0.90; 95% confidence interval, 0.83-0.98; P=0.01). One-year LVEF (> or =30%) was the best independent predictor of long-term survival. Patients with an LVEF > or =30% had a similar survival; patients with an LVEF <30% had a significantly lower survival (hazard ratio, 0.82; 95% confidence interval, 0.75-0.90; P<0.001) compared with transplanted patients. CONCLUSION: Not in the short term (1.5 years) but in the long term (7-10 years), heart transplantation seems to provide survival benefit in stable patients with CHF except in patients with improved LVEF (> or =30%) after medical optimization.

Female↗

PubMed2006

Ten-year follow-up of a prospective, randomized trial of BT563/bb10 versus anti-thymocyte globulin as induction therapy after heart transplantation.

BACKGROUND: Alloantigen-activated T cells express high-affinity interleukin-2 receptor (IL-2R). Specific blockade of this receptor has been associated with lower rejection episodes in clinical transplantation when compared with placebo. The first short-term results of the newer IL-2R antagonists are becoming available but little is known about the long-term effects of these drugs. The aim of the study was to compare the clinical efficacy of the IL-2R antagonist BT563 with polyclonal rabbit anti-thymocyte globulin (ATG) in heart transplant recipients. METHODS: Forty patients undergoing cardiac transplantation were randomly assigned to receive either BT563 or rabbit ATG as induction therapy, combined with triple immunosuppression thereafter. Ten-year surveillance for rejection, infection, allograft vasculopathy and tumorgenicity was performed. Allograft rejection and vasculopathy were assessed by endomyocardial biopsy and coronary angiography, respectively. Screening for infection included blood, urine or tracheobronchial cultures and serology. RESULTS: No difference was detected in terms of 10-year survival between the two groups (50% for the IL-2R group and 70% for the ATG group, p = 0.16). Actuarial incidence of severe rejection was significantly higher in the IL-2R group (55% vs 10% at 10 years post-operatively, p = 0.028; 55% vs 5% during the first month post-operatively, p = 0.0005). Patients receiving ATG had a higher incidence of viral infection. Freedom from allograft vasculopathy was significantly higher in the ATG group (80% vs 60%, p = 0.031). CONCLUSIONS: BT563/BB10 is less effective than ATG for prevention of both acute allograft rejection and allograft vasculopathy after cardiac transplantation. Clinically relevant infections or tumorgenicity were not increased with the use of ATG.

Adult↗

PubMed2006

Activation of the purine salvage pathway in mononuclear cells of cardiac recipients treated with mycophenolate mofetil.

BACKGROUND: The objective of this study was to investigate purine nucleotide metabolism in peripheral blood mononuclear cells (PBMC) of cardiac transplant recipients switched from azathioprine to mycophenolate mofetil (MMF). METHODS: Concentrations of guanosine 5'triphosphate (GTP) and adenosine 5'triphosphate (ATP), the activities of inosine monophosphate dehydrogenase (IMPDH), guanine phosphoribosyltransferase (GPRT), and hypoxanthine phosphoribosyltransferase (HPRT) were determined in PBMC of 27 cardiac transplant recipients before switch to MMF and 3, 6, and 12 months thereafter. RESULTS: There was no difference in the activities of IMPDH and salvage pathway enzymes GPRT and HRPT as well as in intracellular GTP and ATP concentrations between the patients before switch to MMF and healthy controls. The GTP and ATP concentrations in PBMC of cardiac recipients did not change during the entire observation period. Although the MPA trough level remained similar, IMPDH activity declined from 897 to 316 pmol/10(6)PBMC/h 3 months after MMF onset, was almost completely inhibited after 6 months, and partially restored to 143 pmol/10(6)PBMC/h 12 months after switch to MMF. In contrast, GPRT activity increased after 3, 6, and 12 months of MMF therapy and HPRT activity 3 and 6 months after switch to MMF. CONCLUSIONS: We demonstrated for the first time an induction of salvage pathway enzyme activities in PBMC under MMF therapy. This probably accounts for the maintenance of intracellular purine nucleotide pools and prevents the GTP depletion.

Adenosine Triphosphate↗

PubMed2006

The MLCK-mediated alpha1-adrenergic inotropic effect in atrial myocardium is negatively modulated by PKCepsilon signaling.

The present study examined the role of myosin light chain kinase (MLCK), PKC isozymes, and inositol 1,4,5-trisphosphate (IP(3)) receptor in the positive inotropic effect of alpha(1)-adrenergic stimulation in atrial myocardium. We measured inotropic effects of phenylephrine (0.3-300 microM) in isolated left atrial preparations (1 Hz, 37 degrees C, 1.8 mM Ca(2+), 0.3 microM nadolol) from male 8-week FVB mice (n=200). Phenylephrine concentration-dependently increased force of contraction from 1.5+/-0.1 to 2.8+/-0.1 mN (mean+/-s.e.m., n=42), which was associated with increased MLC-2a phosphorylation at serine 21 and 22 by 67% and translocation of PKCepsilon but not PKCalpha to membrane (+30%) and myofilament (+50%) fractions.MLCK inhibition using ML-7 or wortmannin right-shifted the concentration-response curve of phenylephrine, reducing its inotropic effect at 10 microM by 73% and 81%, respectively. The compound KIE1-1 (500 nM), an intracellularly acting PKCepsilon translocation inhibitor peptide, prevented PKCepsilon translocation and augmented the maximal inotropic effect of phenylephrine by 40%. In contrast, inhibition of Ca(2+)-dependent PKC translocation (KIC1-1, 500 nM) had no effect. Chelerythrine, a PKC inhibitor, decreased basal force without changing the inotropic effect of phenylephrine. The IP(3) receptor blocker 2-APB (2 and 20 microM) concentration-dependently decreased basal force, but did not affect the concentration-response curve of phenylephrine. These results indicate that activation of MLCK is required for the positive inotropic effect of alpha(1)-adrenergic stimulation, that the Ca(2+)-independent PKCepsilon negatively modulates this effect, and that PKCalpha and IP(3) receptor activation is not involved.

Adrenergic beta-Agonists↗

PubMed2006

Transposition of the supraaortic branches for extended endovascular arch repair.

BACKGROUND: Supraaortic branches limit extended application of endovascular aortic repair. For this purpose, we applied extensive reconstructions. METHODS: Between October 2002 and March 2005, 11 patients (mean age 72.3 years) presented with acute or chronic aortic diseases originating from the aortic arch (arch aneurysms n=8, type B dissections n=3). Treatment was by autologous sequential transposition of the left carotid artery into the brachiocephalic trunk and of the left subclavian artery into the already transposed left common carotid artery in nine patients and by additional reconstruction of the brachiocephalic trunk in two patients. Endovascular stent-graft placement was successfully performed thereafter. RESULTS: Procedure-related mortality was 0%. At completion angiography, all reconstructions were fully patent. One patient had a small type Ia endoleak that resolved spontaneously within one week. Mean follow-up was 18 months (1-29 months). One patient underwent redo stent-graft placement after 25 months due to a type III endoleak. The remaining patients had normal follow-up CT scans with regular perfusion of the supraaortic branches without any signs of endoleaks. CONCLUSIONS: Extended application of this technique will enable safe and effective treatment of a highly selected group of patients by avoiding conventional repair.

Acute Disease↗

PubMed2006

Entire rerouting of the supraaortic branches for endovascular stent-graft placement of an aortic arch aneurysm.

Conventional surgical repair of the aortic arch using cardiopulmonary bypass and deep hypothermic circulatory arrest still carries a substantial rate of mortality and morbidity. Endovascular stent-graft placement has developed as a safe and effective treatment modality in various diseases of the aorta. We report on the case of a 64-year-old male presenting with an aortic arch aneurysm involving the origin of the brachiocephalic trunk. A second thoracic aortic aneurysm was detected in the distal third of the descending aorta. The patient was treated by entire prosthetic rerouting of the supraaortic branches. Metachronously, the patient underwent endovascular stent-graft placement from the distal ascending aorta up the thoracoabdominal transition.

Aorta, Thoracic↗

PubMed2006

Long-term neurocognitive function after mechanical aortic valve replacement.

BACKGROUND: Mechanical aortic valves are a possible source of microemboli potentially causing cerebral injury. Therefore, the long-term impact of mechanical aortic valve replacement on neurocognitive function is uncertain. METHODS: In this prospective, contemporary study, we followed 32 consecutive patients (aged 51 +/- 8 years; range, 38 to 70; EuroSCORE [European System for Cardiac Operative Risk Evaluation] 4.4 +/- 1.7) undergoing isolated aortic valve replacement with a mechanical prosthesis. A cohort of age- and sex-matched patients (n = 28, aged 50 +/- 7 years) served as nonsurgical controls. After aortic valve replacement, neurocognitive function was serially reevaluated at 7-day (n = 32), 4-month (n = 31), and 3-year (n = 29) follow-up. Neurocognitive function was measured by means of P300 auditory evoked potentials. RESULTS: Before the operation, P300 peak latencies were comparable between surgical patients (361 +/- 32 ms) and nonsurgical controls (365 +/- 33 ms, p = 0.783). In patients undergoing aortic valve replacement, P300 peak latencies were prolonged 7 days after surgery (380 +/- 32 ms) as compared with before the operation (361 +/- 32 ms, p < 0.0001) and as compared with nonsurgical controls (364 +/- 34 ms, p = 0.002). At 4-month (369 +/- 30 ms, p = 0.752) and 3-year (370 +/- 31 ms, p = 0.825) follow-up, P300 peak latencies normalized as compared with before operation and as compared with nonsurgical controls (4-month follow-up 363 +/- 31 ms, p = 0.832; 3-year follow-up 366 +/- 32 ms, p = 0.432). We found no difference in patients with different valve types. CONCLUSIONS: Despite previous assumptions based on the potential occurrence of microemboli in patients with mechanical valves, mechanical aortic valve replacement has no adverse long-term impact on neurocognitive function. This finding is only valid for patients with a comparable age range undergoing isolated aortic valve replacement.

Adult↗

PubMed2006

Late vascular complications after extracorporeal membrane oxygenation support.

BACKGROUND: Extracorporeal membrane oxygenation support through the groin vessels is an established treatment option for patients with life-threatening conditions, resistant to medical treatment. However, because of critical status and type of vascular access, late vascular complications are a potential risk. METHODS: From January 1998 through December 2004, 174 adults (mean age, 45 +/- 19 years) undergoing either cardiac surgery (n = 54, 31.4%) or lung transplantation (n = 120, 68.6%) were supported with extracorporeal membrane oxygenation. Data were prospectively collected and retrospectively analyzed. Follow-up extended up to 60 months (mean, 30 +/- 10 months). Multivariable regression analysis was used to identify predictors of late vascular complications. RESULTS: Hospital survival was 57.3%. A total of 12 hospital survivors (12.2%) experienced late vascular complications. All late vascular complications were local stenosis at the former arterial cannulation site. Treatment was done by means of femorofemoral crossover bypass (n = 3), iliofemoral bypass (n = 1), thromboendarterectomy (n = 3), and percutaneous transluminal angioplasty (n = 5). We experienced no limb loss during follow-up. Predictors for long-term vascular complications were technical problems during extracorporeal membrane oxygenation explantation (p = 0.002; odds ratio, 23.2) and history of peripheral vascular disease (p = 0.015; odds ratio, 3.1). CONCLUSIONS: Extracorporal membrane oxygenation support is associated with the development of late vascular complications at the femoral access site. In selected patients alternative cannulation sites should be considered.

Adult↗

PubMed2006

Treatment of acute type a dissection by percutaneous endovascular stent-graft placement.

Acute type A dissections are a life threatening condition requiring immediate surgical intervention to avoid aortic rupture or pericardial tamponade. Success of surgical intervention is markedly limited in those patients with advanced age, neurological deficits, and multiple co-morbidities at the time of treatment. We report the successful endovascular stent-graft treatment in a patient suffering from an acute type A dissection. Due to the presence of multiple comorbidities the patient was considered too high risk for surgical treatment.

Acute Disease↗

PubMed2005

Prediction of cyclosporine blood levels in heart transplantation patients using a pharmacokinetic model identified by evolutionary algorithms.

BACKGROUND: Artificial intelligence (AI)-based computation methods have been recently shown to be applicable in several clinical diagnostic fields. The purpose of this study was to introduce a novel AI method called evolutionary algorithms (EAs) to clinical predictions. The technique was used to create a pharmacokinetic model for the prediction of whole blood levels of cyclosporine (CyA). METHODS: One hundred one adult cardiac transplant recipients were randomly selected and included in this study. All patients had been receiving oral cyclosporine twice daily, and the trough levels in whole blood were measured by monoclonal-specific radioimmunoassay. An evolutionary algorithm (EA)-based software tool was trained with pre- and post-operative variables from 64 patients. The results of this process were then tested on data sets from 37 patients. RESULTS: The mean value of the predicted CyA level throughout the measurement period for the test data was 175 +/- 27 ng/ml, which compared well with the mean observed CyA level of 180 +/- 31 ng/ml. The system bias expressed as the mean percent error (MPE) for the training and test data sets were 7.1 +/- 5.4% (0.1% to 26.7%) and 8.0 +/- 6.7% (0.8% to 28.8%), respectively. The prediction accuracy ranged from 80% to 90%. The correlation coefficient between predicted and observed CyA concentration for the training data were 0.93 (p < 0.001) and for the test data were 0.85 (p < 0.001), respectively. CONCLUSIONS: The results of this study suggest that the use of evolutionary algorithms to identify pharmacokinetic models yields accurate prediction of cyclosporine whole blood levels in heart transplant recipients. This and other similar technologies should be considered as future clinical tools to reduce costs in our health systems.

Adult↗

PubMed2005

Key role of myosin light chain (MLC) kinase-mediated MLC2a phosphorylation in the alpha 1-adrenergic positive inotropic effect in human atrium.

OBJECTIVE: Mechanisms of the positive inotropic response to alpha(1)-adrenergic stimulation in the heart remain poorly understood, but recent evidence in rat papillary muscle suggests an important role of regulatory myosin light chain (MLC2) phosphorylation. This study investigated alpha(1)-adrenergic contractile effects and the role of MLC kinase (MLCK)-dependent phosphorylation of MLC2 in human atrial muscle strips. METHODS: Force measurement was performed on electrically stimulated atrial muscle strips (n=140; 20 hearts) in the presence of the beta-blocker nadolol. MLC2a phosphorylation was determined by 2D-polyacrylamide gel electrophoresis and Western blotting of muscle strips that were immediately freeze-clamped following force measurements. RESULTS: The alpha(1)-agonist phenylephrine (PE; 0.3-100 microM) exerted a concentration-dependent, monophasic, sustained positive inotropic effect (86% above basal) that was accompanied by an 80% increase in MLC2a phosphorylation. Desinhibition of MLC phosphatase by the Rho kinase inhibitor Y-27632 (10 microM) reduced the effect of PE by 16%. The MLCK inhibitor wortmannin (10 microM) completely abolished both the PE-induced increase in force and MLC2a phosphorylation. The structurally unrelated MLCK inhibitor ML-7 (10 microM) had similar effects. Neither Y-27632 nor wortmannin or ML-7 affected beta-adrenergic force stimulation. In contrast to our findings in atrial muscle strips, we observed no increase in MLC2v phosphorylation after PE in human ventricular muscle strips and wortmannin failed to inhibit PE-induced force of contraction. CONCLUSION: alpha(1)-Adrenergic receptors mediate a prominent increase in contractile force in human atria that depends on MLCK activity and is accompanied by an increase in MLC2 phosphorylation.

Adolescent↗

PubMed2005

Microsatellite polymorphism in the heme oxygenase-1 gene promoter and cardiac allograft vasculopathy.

BACKGROUND: The heme oxygenase-1 (HO-1) isoenzyme has recently been suggested to protect transplants from ischemia-reperfusion and immunologic injury. Inducibility of this enzyme is modulated by a (GT)n dinucleotide length polymorphism in the HO-1 gene promoter. Short (class S) repeats are associated with greater up-regulation of HO-1 than are long repeats. In the present study, we investigated the impact of the promoter polymorphism on the development of cardiac allograft vasculopathy (CAV) in human heart transplants. METHODS: We enrolled 152 recipients of a heart allograft with at least 1 year survival post-transplantation in this retrospective study. The HO-1 genotype was assessed using genomic DNA isolated from paraffin-embedded allograft biopsy specimens. Patients were followed angiographically for CAV. Angiographic vessel-wall abnormalities were defined as CAV, and a stenosis of more than 50% in at least 1 vessel area was defined as severe CAV. RESULTS: Eighty-seven patients (57%) had received a heart from a donor with at least 1 class S allele. Within the mean follow-up period of 9 years, 95 patients (63%) showed signs of CAV, among which 60 patients (40%) developed severe CAV. The frequency of CAV and severe CAV was not significantly different between class S allele recipients and non-recipients (CAV, 57/87 vs 38/65, p = 0.12; severe CAV, 35/87 vs 25/65, p = 0.30). CONCLUSION: In contrast to recent findings in renal allografts and vascular injury, the HO-1 gene promoter polymorphism does not show an association with the development of CAV in heart transplants.

Adult↗

PubMed2005

An alternative approach in treating an aortic arch aneurysm with an anatomic variant by supraaortic reconstruction and stent-graft placement.

We report the case of a 78-year-old man who presented with an aortic arch aneurysm that involved the origin of the left carotid artery and extended up to the origin of the brachiocephalic trunk. The left vertebral artery originated separately from the arch. The patient was treated by a reversed bifurcated prosthesis from the ascending aorta to the brachiocephalic trunk as well as to the left common carotid artery, and a simultaneous left-sided vertebral-to-carotid artery transposition was also performed. Metachronously, the patient later underwent successful endovascular stent-graft placement into the entire aortic arch.

Aged↗

PubMed2005

Is the transpulmonary pressure gradient a predictor for mortality after orthotopic cardiac transplantation?

Elevated pulmonary vascular resistance (PVR) is a well-known risk factor for right ventricular failure after orthotopic cardiac transplantation. The influence of preoperative transpulmonary pressure gradient (TPG) and PVR on post-transplant 30 days mortality was evaluated. To analyze the response of PVR and TPG to cardiac transplantation, we analyzed 718 adult patients undergoing primary cardiac transplantation. Indications for operation were: 35.2% ischemic cardiomyopathy (ICM), 61.2% idiopathic dilated cardiomyopathy (DCM), and 3.3% other diagnosis (e.g. hypertrophic cardiomyopathy). The mean age (51.9) and the mean ischemic time (169.7 min) were comparable between 30 days survivors and nonsurvivors. Student's t-tests and chi-square analysis were used to compare data from 30-day survivors and nonsurvivors. Statistical significance was defined as P < 0.05. Fisher's exact test and multiple logistic regression analysis was performed to evaluate the relationship between hemodynamic parameters and outcome after transplantation. Primary end-point was 30 days mortality and secondary end-point long-term survival of patient groups with different TPG and PVR values. In survivors the mean TPG was 10.3 +/- 5.1 (mean +/- SD) vs. 13 +/- 6.6 in patients who died after transplantation (P = 0.0012). The PVR was 2.6 +/- 1.4 vs. 3.5 +/- 2.2 (P = 0.0012). In multivariate logistic regression, the parameters TPG and PVR exhibit a significant influence between survivors and nonsurvivors after cardiac transplantation within 30 days (TPG: P = 0.0012; PVR: P = 0.0012). The mortality rates in patients with TPG > 11 mmHg and PVR < 2.8 Wood units or TPG < 11 mmHg and PVR > 2.8 Wood units were comparable to those with TPG < 11 mmHg and PVR < 2.8 mmHg. The TPG is an important predictor in nonrejection-related early mortality after orthotopic cardiac transplantation. The determination of TPG in combination with PVR is a more reliable predictor of early post-transplant survival than PVR alone.

Adult↗

PubMed2005

Differential role of TGF-beta1/bFGF and ET-1 in graft fibrosis in heart failure patients.

Collagen overproduction characteristic for dilated cardiomyopathy (DCM) is coregulated by endothelin (ET)-1, transforming growth factor (TGF)-beta1, basic fibroblast growth factor (bFGF) and matrix metalloproteases (MMPs). Whether these molecules affect grafts transplanted to heart failure patients is unknown. In 67 idiopathic DCM patients, 31 patients with ischemic cardiomyopathy (ICM) and 16 controls, the myocardial bFGF, TGF-beta1, pro-collagen (PrCol) type 1 (PrCol1-alpha1, -alpha2) and MMP expressions were examined using real-time RT-PCR or Western blotting. mRNA expression was measured in grafts for 1 year. TGF-beta1/bFGF stimulation or gene silencing was used to examine their effect on collagen synthesis in cardiac tissue cultures. TGF-beta1 and PrCol1 were upregulated in DCM only, while bFGF was upregulated in both groups versus controls. TGF-beta1 downregulated MMP-1 and upregulated collagen 1, whereas bFGF upregulated MMP-13 in DCM tissue. Post-transplant PrCol1-alpha1, -alpha2 and ET-1 mRNA increased over time in grafts of DCM patients only, while other factors returned to control baseline levels in DCM and ICM. These data indicate that cardiac transplantation corrects the dysregulated TGF/bFGF/MMP-1/MMP-13, but not the excess collagen and ET-1 synthesis in cardiac grafts transplanted to DCM patients. ET-1 might be a major pathologic trigger for graft fibrosis in DCM.

Adult↗

PubMed2004

Comparison of combined prophylaxis of cytomegalovirus hyperimmune globulin plus ganciclovir versus cytomegalovirus hyperimmune globulin alone in high-risk heart transplant recipients.

BACKGROUND: Seronegative heart transplant recipients who receive an allograft from seropositive donors have a higher risk of developing cytomegalovirus (CMV) disease and cardiac allograft vasculopathy (CAV) and dysfunction. Neither CMV-specific hyperimmune globulin nor ganciclovir as sole CMV prophylaxis is sufficient to prevent CMV disease in high-risk patients. We retrospectively evaluated the efficacy of CMV-hyperimmune globulin with and without ganciclovir in 207 D+/R- heart transplant recipients. METHODS: The study population was divided into two groups: Group A was composed of 96 patients who received CMV hyperimmune globulin as sole CMV prophylaxis, and group B was composed of 111 patients who received combined CMV prophylaxis. All recipients were subjected to quadruple cytolytic immunosuppression. Primary and secondary end points included prevention of CMV-associated death, CMV disease and productive infection, CAV, and overall infection. RESULTS: There was no difference in overall survival between the two groups. Four patients in the group A died of CMV sepsis, whereas no CMV-associated death was observed in group B (P =0.0326). The actuarial incidence of CMV disease was significantly lower in patients who received double CMV prophylaxis (32.29 vs. 11.71, P =0.0003). Although no difference was observed with regard to productive CMV infection (53.12 vs. 65.77, P =not significant), CAV and overall infection rates were significantly higher in the first group (7.29 vs. 0.9, P =0.0157 and 70.83 vs. 62.16, P =0.03, respectively). CONCLUSIONS: Double CMV prophylaxis consisting of CMV hyperimmune globulin and ganciclovir is able to abolish CMV death and prevent CMV disease in high-risk heart transplant recipients. Therefore, the use of a combination regimen is recommended for seronegative recipients with seropositive donors.

Adolescent↗

PubMed2004

Neurocognitive deficit following coronary artery bypass grafting: a prospective study of surgical patients and nonsurgical controls.

BACKGROUND: To objectively measure long-term neurocognitive deficit in patients undergoing coronary artery bypass grafting and compare the findings with nonsurgical controls. METHODS: We prospectively measured neurocognitive function in patients undergoing coronary artery bypass grafting (CABG) with cardiopulmonary bypass (n = 104; mean age 64.1 years old; EuroSCORE 2.7 [means]). A cohort of age- and sex-matched patients (n = 80; mean age 63.4 years old) served as nonsurgical controls. After CABG, neurocognitive function was serially reevaluated at 7-day (n = 104), 4-month (n = 100), and 3-year follow-up (n = 88). Neurocognitive function was objectively measured by means of cognitive P300 evoked potentials. Additionally, standard psychometric tests were performed (Trailmaking Test A, Mini Mental State Examination). RESULTS: As compared to preoperative measures (364 +/- 36 ms), cognitive P300 evoked potentials were prolonged (=impaired) at 7-day (381 +/- 36 ms; p = 0.001), 4-month (378 +/- 31 ms; p = 0.08), and 3-year follow-up (379 +/- 35 ms; p = 0.002), respectively. Trailmaking Test A was abnormal, as compared to preoperative, at 3-year follow-up (p < 0.001). Before the operation, surgical patients were fully comparable in P300 measures to nonsurgical controls (363 +/- 32 ms; p = 0.362). Most importantly, throughout the entire postoperative follow-up cognitive measures in surgical patients were prolonged (=impaired) as compared with controls (7-day p = 0.001; 4-month p = 0.002 and 3-year p = 0.003, respectively). In stepwise multivariate regression analysis, neurocognitive deficit at 4-month follow-up (p < 0.001), age (p = 0.012), and persistent atrial fibrillation (p = 0.024) were predictive for long-term neurocognitive deficit at 3-year follow-up. CONCLUSIONS: As shown by means of objective measures, and in comparison to nonsurgical controls, coronary artery bypass grafting with cardiopulmonary bypass grafting causes long-term neurocognitive deficit.

Aged↗

PubMed2004

Extracorporeal membrane oxygenation is superior to right ventricular assist device for acute right ventricular failure after heart transplantation.

BACKGROUND: Acute right ventricular failure after heart transplantation is a life-threatening condition, and sometimes the use of mechanical circulatory support is inevitable. The aim of this retrospective study was to investigate the effectiveness of two different mechanical circulatory support systems for this indication. METHODS: From 1984 to 2003, 28 heart transplant recipients exhibited right ventricular failure resistant to drug therapy. Right ventricular assist device (n = 15) or extracorporeal membrane oxygenation (n = 13) was implanted to support the failing heart. RESULTS: Overall in-hospital survival was 43%. In the right ventricular assist device group, only 2 patients (13%) could be weaned from mechanical circulatory support compared with 10 patients (77%) in the extracorporeal membrane oxygenation group (p = 0.001). Retransplantation was necessary in 6 patients in the right ventricular assist device group and in 1 patient in the extracorporeal membrane oxygenation group (p = 0.049). There was no difference in patient survival between groups, but graft survival was significantly better in the extracorporeal membrane oxygenation group (p = 0.005). CONCLUSIONS: In view of these results, extracorporeal membrane oxygenation seems to be the better option as mechanical circulatory support for right ventricular failure in heart transplantation.

Aged↗