[Hemodynamics and physical capacity in patients with left ventricular assist devices : An overview]. / Hämodynamik und körperliche Belastbarkeit bei Patienten mit Linksherzunterstützungssystem : Ein Überblick.

In the course of time implantation of left ventricular assist devices (LVAD) has become an alternative to heart transplantation due to the enormous technical developments and miniaturization of these systems. Following implantation most patients show a significant improvement in their clinical condition and exercise capacity as measured by the New York Heart Association (NYHA) classification; nevertheless, exercise tolerance remains clearly limited even after LVAD implantation. The complex physiological and hemodynamic changes in LVAD patients both at rest and during exercise are ultimately not completely understood. The aim of this article is to describe the current state of scientific knowledge with respect to the physical capacity of patients with terminal heart failure after LVAD implantation at rest and during exercise. The influence of increasing the pump speed and continuous physical exercise training on the physical capacity in the long-term course is reviewed. The significance of new diagnostic tools, such as the non-invasive inert gas rebreathing method for measurement of cardiac output and arteriovenous oxygen difference (AVDO2) in assessment of the performance of LVAD patients is discussed.

Physiological and psychological effects of imagery techniques on health anxiety.

Previous research has shown that intrusions are part of the psychopathology of mental disorders. Imagery techniques seem to be an effective treatment of negative intrusions. Since negative mental imagery is part of health anxiety, the present study investigated the impact of imagery techniques on health anxiety. A total of 159 students with elevated scores in a health anxiety questionnaire watched an aversive film concerning a cancer patient and were randomly allocated to one of three interventions (positive imagery, imagery reexperiencing, imagery rescripting) or the control group. The intervention lasted 9 min. Physiological data (heart rate and cortisol) as well as psychological measures, such as mood ratings, health anxiety scores, and intrusions, were assessed during the appointment, while psychological measures were assessed over a period of 1 week after the intervention. Cortisol levels changed over time depending on the intervention. Heart rate changed during the 9-min interventions as well, with the fastest decrease during imagery rescripting. Moreover, negative mood and distress decreased after the intervention, while intrusions were reduced 1 week after the intervention in all groups equally. The results suggest that imagery rescripting is a promising technique that seems to activate a process of deep elaboration. Therefore, it might be an adequate way to target health anxiety symptoms such as anxiety, intrusions, and avoidance or safety-seeking behavior. Further studies should focus on imagery rescripting in clinical samples with health anxiety and target individual intrusive images to increase effectiveness. Nevertheless, the development of a long-term explanatory model of rescripting is needed.

Results after orthotopic heart transplantation accepting donor hearts >50 years: experience at La Pitie Salpetriere, Paris.

INTRODUCTION: We sought to examine the results of orthotopic heart transplantation accepting hearts from donors >50 years of age with special regard to the usefulness of peripheral extracorporeal membrane oxygenation for posttransplant graft dysfunction. PATIENTS: Between January 2000 and December 2004, a total of 247 patients underwent orthotopic heart transplantation. In 143 patients (58%) the heart donor was <50 years (group I, mean age of donor hearts 36 +/- 11 years; range, 8-49 years). In 104 recipients (42%) the heart donor was >50 years (group II, mean age of donor hearts 56 +/- 15 years; range, 50-67 years). Pretransplant characteristics of the two groups showed no significant differences. RESULTS: The in-hospital mortality was slightly increased in group II (24% vs 20% in group I, NS) and the 5-year survival rate significantly increased in group I (75% vs 63% in group II). Freedom from transplant vasculopathy after 3 years was similar in both groups (86% in group I vs 87% in group II). A total of 25 patients (17%) in group I and 27 patients (26%) in group II developed graft dysfunction. Eleven patients in group I and 10 patients in group II were treated using peripheral extracorporeal membrane oxygenation, whereas 3 of the 11 patients in group I and 5 of the 10 patients in group II were discharged following a complete recovery. Two patients in group I and 4 patients in group II were survivors beyond year. CONCLUSION: In our experience it was possible to increase the cardiac donor pool by accepting allografts from donors >50 years of age in selected cases. The incidence of transplant vasculopathy was not increased, whereas in-hospital mortality was slightly higher. In our limited cohort, patients with older donor hearts was developed graft dysfunction profited from primary extracorporeal membrane oxygenation implantation, an indication that should be examined further without delay.

Implantation of CardioWest total artificial heart for irreversible acute myocardial infarction shock.

Patients who develop cardiogenic shock after acute myocardial infarction have a very high mortality rate despite early reperfusion therapy. Hemodynamic stabilization can often only be achieved by implanting a mechanical circulatory support system. When, in cases representing expansive myocardial impairment without any chance of recovery, pharmacological therapy and the use of percutaneous assist devices have failed, the implantation of a total artificial heart is indicated. We report our first experiences with this extensive and innovative method of managing irreversible cardiogenic shock patients. The CardioWest total artificial heart was implanted in 5 patients (male; mean age, 50 years). All patients were in irreversible cardiogenic shock despite maximum dosages of catecholamines, an intra-aortic balloon pump and/or a femoro-femoral bypass. In all patients early reperfusion therapy was performed. After implantation of the Cardio West system, all dysfunctional organ systems rapidly recovered in all patients. Four of 5 patients underwent successful heart transplantation after a mean support time of 156 days. One patient died because of enterocolic necroses caused by an embolic event after termination of dicumarol therapy. In summary, our first experiences justify this extensive management in young patients who would otherwise have died within a few hours.

[Rehabilitation standards for follow-up treatment and rehabilitation of patients with ventricular assist device (VAD)]. / Rehabilitationsstandards für die Anschlussheilbehandlung und allgemeine Rehabilitation von Patienten mit einem Herzunterstützungssystem (VAD - ventricular assist device).

The increasing use of ventricular assist devices (VADs) in terminal heart failure patients provides new challenges to cardiac rehabilitation physicians. Structured cardiac rehabilitation strategies are still poorly implemented for this special patient group. Clear guidance and more evidence for optimal modalities are needed. Thereby, attention has to be paid to specific aspects, such as psychological and social support and education (e.g., device management, INR self-management, drive-line care, and medication).In Germany, the post-implant treatment and rehabilitation of VAD Patients working group was founded in 2012. This working group has developed clear recommendations for the rehabilitation of VAD patients according to the available literature. All facets of VAD patients' rehabilitation are covered. The present paper is unique in Europe and represents a milestone to overcome the heterogeneity of VAD patient rehabilitation.

Characterization of glucocorticoid inhibition of antigen-induced inositolphosphate formation by rat basophilic leukemia cells: possible involvement of phosphatases.

The suppressive effect of glucocorticoids (GC) upon antigen-induced phosphatidylinositol phospholipase C (PI-PLC) activity and inositol phosphate formation by rat basophilic leukemia cells (RBL-2H3) has been characterized. Addition of antigen for a period of 1-30 min enhanced production of [3H]inositol monophosphate (IP1), inositol 1,4-bisphosphate (IP2) and inositol 1,4,5-trisphosphate (IP3) by about 5-10-fold. Pretreatment with hydrocortisone (HC) reduced formation of the various inositol phosphates (IPs) and degradation of phosphatidylinositol 4,5-bisphosphate (PIP2) by an average of 50%. Maximal inhibition of hydrolysis of PIP2 and reduction in stimulation of IP3 formation was reached after 4 h of preincubation with 2.10(-6) M of HC. Cycloheximide and RU486, a GC receptor antagonist, completely prevented the inhibitory effect of HC on IP formation. Other GC, dexamethasone (DEX) and triamcinolone (each at 2.10(-7) M) markedly suppressed antigen induced IP3 production, while aldosterone and sex steroids such as estradiol and progesterone (each at 2.10(-6) M) were virtually inactive. Antigen-stimulated phosphorylation of a 18 kDa and other proteins was inhibited by about 60% following pretreatment with the GC. This inhibition was in turn prevented by cycloheximide. DEX also doubled the activity of cellular acid phosphatase activity. The results suggest that the inhibitory effect of GC is specific, receptor-mediated, dependent on protein synthesis and possibly mediated by protein phosphatase activity.

Arachidonic acid release by basophilic leukemia cells and macrophages stimulated by Ca2+ ionophores, antigen and diacylglycerol: essential role for protein kinase C and prevention by glucocorticosteroids.

The role of protein kinase C in phospholipase A2 (PLA2) activation in rat basophilic leukemia cells (RBL-2H3) and macrophages was investigated. 12-O-Tetradecanoyl phorbol 13-acetate (TPA) doubled ionomycin-induced PLA2 activity, assessed by [3H]arachidonate release. Protein kinase C inhibitors, staurosporine and K252a (100 nM) or H-7 (15 micrograms/ml) inhibited ionomycin-stimulation of PLA2 activity by 62, 75 and 80%, respectively. Down-regulation of protein kinase C by prolonged treatment with TPA inhibited Ca2(+)-ionophore A23187 or antigen-stimulation of [3H]arachidonate release by 80%. We examined whether the inhibitory effect of dexamethasone (DEX) on PLA2 activity is related to modulation of protein kinase C activity. The 50% inhibition by DEX of ionomycin elevation of [3H]arachidonate release was almost overcome by addition of TPA. The Ca2+ ionophore and antigen-induced increase in [3H]TPA binding to intact RBL cells was not impaired by DEX. However, DEX markedly reduced phosphorylation of several proteins. 1-Oleoyl-2-acetyl-glycerol (OAG) had a sustained stimulatory effect on PLA2 activity in isolated plasma membranes derived from treated bone-marrow intact mouse macrophages, while both DEX and staurosporine reduced elevated PLA2 activity by 68 and 84%, respectively. The results support an essential role for protein kinase C in regulation of PLA2 activity.

Stimulation of Jun N-terminal kinase (JNK) by gonadotropin-releasing hormone in pituitary alpha T3-1 cell line is mediated by protein kinase C, c-Src, and CDC42.

The signaling of ligands operating via heterotrimeric G proteins is mediated by a complex network that involves sequential phosphorylation events. Signaling by the G protein-coupled receptor GnRH was shown to include elevation of Ca2+ and activation of phospholipases, protein kinase C (PKC) and extra-cellular signal-regulated kinase (ERK). In this study, GnRH was shown to activate Jun N-Terminal Kinase (JNK)/SAPK in alpha T3-1 cells in a PKC- and tyrosine kinase-dependent manner. GnRH as well as tumor-promoting agent (TPA) also increased c-Src activity, which peaked at 2 min after GnRH stimulation and was sensitive both to PKC and to tyrosine kinase inhibitors. Coexpression of Csk, which serves as a Src-dominant interfering kinase, and constitutively active forms of Src, together with JNK, confirmed the involvement of c-Src downstream of PKC in the GnRH-JNK pathway. Coexpression of dominant negative and constitutively active forms of CDC42, Rac1, Ras, MEKK1, and MEK1 with JNK indicated that JNK activation by GnRH and TPA is mediated by CDC42 and MEKK1. Ras and MEK1, which are involved in a related mitogen-activated protein kinase (MAPK) pathway, did not affect JNK activation in alpha T3-1 cells. Taken together, our results suggest that GnRH stimulation of JNK activity is mediated by a unique pathway that includes sequential activation of PKC, c-Src, CDC42, and probably also MEKK1.

Mechanical valve replacement in congenital heart defects in the era of international normalized ratio self-management.

As the number of patients with congenital heart defects requiring heart valve replacement increases, the need for durable valve substitutes with good hemodynamic performance and a low incidence of complications becomes more apparent. The use of porcine xenografts is burdened with early fibrocalcific degeneration, whereas the use of mechanical heart valves led to an increased number of thromboembolic events, especially when implanted in the right side of the heart. We report on our experiences implanting bileaflet heart valves in congenital heart defects since the introduction of international normalized ratio (INR) self-management. The data of 68 long-term survivors (33 males, 35 females) who underwent mechanical heart valve replacement in congenital heart defect were reviewed. Patient age at the time of valve replacement ranged from 5 months to 61 years (mean 21 years). Underlying diagnoses were tetralogy of Fallot (n=33), morbus Ebstein (n=4), atrioventricular canal (n=13), truncus arteriosus communis (n=5), transposition of the great arteries (n=10), and congenitally corrected transposition of the great arteries (n=3). In all patients, bileaflet valves were implanted (St. Jude Medical n=40, Carbomedics n=28). Anticoagulation was performed using dicumarol (Marcumar) and INR self-management in all cases. The mean follow-up was 72 months (range 6-132 months; 409 patient-years). Valve thrombosis developed in 3 of 68 patients (4.4%, all three had tetralogy of Fallot, mean age 9.8 years) after a mean follow-up of 3.5 years. In two of these three patients, re-pulmonary valve replacement was necessary, whereas the third patient was treated by thrombolysis. From our experience, we conclude that mechanical heart valve replacement is a good therapy option with a low complication rate for patients with congenital heart defects requiring valve replacement, especially when INR self-management is performed.

Mechanism of mitogen-activated protein kinase activation by gonadotropin-releasing hormone in the pituitary of alphaT3-1 cell line: differential roles of calcium and protein kinase C.

The mechanism of mitogen-activated protein kinase (MAPK, ERK) stimulation by the GnRH analog [D-Trp6]GnRH (GnRH-a) was investigated in the gonadotroph-derived alphaT3-1 cell line. GnRH-a as well as the protein kinase C (PKC) activator 12-O-tetradecanoyl phorbol-13-acetate (TPA) stimulated a sustained response of MAPK activity, whereas epidermal growth factor (EGF) stimulated a transient response. MAPK kinase (MEK) is also activated by GnRH-a, but in a transient manner. GnRH-a and TPA apparently activated mainly the MAPK isoform ERK1, as revealed by Mono-Q fast protein liquid chromatography followed by Western blotting as well as by gel kinase assay. GnRH-a and TPA stimulated the tyrosine phosphorylation of several proteins, and this effect as well as the stimulation of MAPK activity were inhibited by the PKC inhibitor GF 109203X. Similarly, down-regulation of TPA-sensitive PKC subspecies nearly abolished the effect of GnRH-a and TPA on MAPK activity. Furthermore, the protein tyrosine kinase (PTK) inhibitor genistein inhibited protein tyrosine phosphorylation and reduced GnRH-a-stimulated MAPK activity by 50%, suggesting the participation of genistein-sensitive and insensitive pathways in GnRH-a action. Although Ca2+ ionophores have only a marginal stimulatory effect, the removal of Ca2+ markedly reduced MAPK activation by GnRH-a and TPA, but had no effect on GnRH-a and TPA stimulation of protein tyrosine phosphorylation. Interestingly, the removal of Ca2+ also partly inhibited the activation of MAPK by EGF and vanadate/H2O2. Thus, a calcium-dependent component(s) downstream of PKC and PTK might also participate in MAPK activation. Elevation of cAMP by forskolin exerted partial inhibition on EGF, but not on TPA or GnRH-a action, suggesting that MEK activators other than Raf-1 might be involved in GnRH action. We conclude that Ca2+, PTK, and PKC participate in the activation of MAPK by GnRH-a, with Ca2+ being necessary downstream to PKC and PTK.

Clinical, biochemical, and genetic findings in a large pedigree of male and female patients with 5 alpha-reductase 2 deficiency.

The present report describes a cluster of eight patients with male pseudohermaphroditism from a large pedigree with steroid 5 alpha-reductase 2 deficiency (5 alpha RD), who reside in Southern Lebanon. They were born with unambiguous female external genitalia and reared as girls until puberty, when masculinization occurred, followed by a change of gender role. Semen analysis and testicular histology revealed maturation arrest of spermatogenesis, with low sperm count and motility. Determination of urinary 5 alpha- and 5 beta-reduced adrenal steroids enabled us to diagnose the disease in a male patient with the full-blown clinical syndrome, in another male patient who had undergone bilateral orchidectomy, and in three female individuals with the biochemical derangement. The female patients were unique in this family with respect to their low degree of virilization, but had normal menstrual cycles. Molecular genetic studies were performed on DNA extracted from peripheral leukocytes and from cultured genital skin fibroblasts. The coding sequence of the 5 alpha R2 gene (SRD5A2) was studied by exon-specific PCR, single strand conformation polymorphism, and direct sequencing. A homozygous point mutation was identified in exon 1, leading to a thymidine for adenine substitution, predicting amino acid substitution of leucine for glutamine at position 55.

Phospholipid-dependent Ca2+-activated protein kinase (C-kinase) in the pituitary: further characterization and endogenous redistribution.

Phospholipid-dependent, Ca2+-activated protein kinase (C-kinase) was recently shown to be expressed in rat pituitary. The enzyme is activated by Ca2+ and phosphatidylserine (PS). Diacylglycerol (DG), which is liberated during phosphoinositide turnover, and the potent tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) activate pituitary C-kinase in the presence of PS, even at resting levels of intracellular Ca2+ (10(-7) M), and increase the apparent affinity of the enzyme for Ca2+. While micromolar concentration of Ca2+ had no effect on the apparent affinity of the enzyme for PS (Km approximately 15 micrograms/ml), elevation of Ca2+ to the millimolar range produced a sharp increase in the apparent affinity for PS (Km approximately 5 micrograms/ml). Elevation of PS (up to 500 micrograms/ml) could not replace Ca2+ in supporting maximal enzyme activity even in the presence of DG. Cytosolic pituitary C-kinase (70% of total enzyme activity) is recovered in an inactive state and can be activated without further purification. The particulate enzyme (30%) is recovered in a cofactors-insensitive form but can be activated after detergent-solubilization and anion exchange chromatography. Endogenous redistribution of soluble pituitary C-kinase to the membrane does not convert it to its proteolytic product which is insensitive to Ca2+, PS and DG. Pituitary C-kinase characterized here most likely plays a key role in signal transduction mechanisms involved in pituitary functions.

Involvement of protein phosphatases in gonadotropin releasing hormone regulated gonadotropin secretion.

The role of persistent protein phosphorylation upon gonadotropin releasing hormone (GnRH) stimulated luteinizing hormone (LH) release was investigated by the use of the selective inhibitors of protein phosphatase type 1 (PP1) and 2A (PP2A), okadaic acid (OA) and calyculin A. Pre-incubation of cultured rat pituitary cells with OA (24 h) or calyculin A (30 min) resulted in inhibition of GnRH-stimulated LH release with significant inhibition being detected at 10 nM and 30 nM for OA and calyculin A, respectively. The inactive OA analog norokadone and the protein tyrosine phosphatase inhibitor vanadyl hydroperoxide had no significant effect on GnRH-induced LH release. The stimulatory effects of the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol 13-acetate (TPA, 50 ng/ml) or the Ca2+ ionophore, ionomycin (1 micron), upon LH release were also abolished by pretreatment with OA (10-20 nM) or calyculin A (30 nM). Stimulation of LH release by high K+ (28 mM) or residual LH release stimulated by GnRH in Ca(2+)-free medium were also blocked by OA. These observations indicate that protein dephosphorylation is involved positively in GnRH-stimulated LH release. The site of action of the protein phosphatases PP1 and PP2A is most likely downstream to Ca2+ elevation and PKC activation by GnRH.

Nafoxidine-responsive uterine protein: further characterization and distinction from the "estrogen-induced" protein (IP).

In a previous paper, we reported that nafoxidine (UA) stimulated the synthesis of a uterine protein showing the same electrophoretic mobility as the "estrogen-induced protein" (E2-IP) first described by Notides and Gorski. In the present work, we analyzed the IP-containing electrophoretic zone by SDS polyacrylamide-gel electrophoresis, and found that estradiol-17 beta (E2) and nafoxidine stimulated the synthesis of different proteins. As expected, estradiol-17 beta stimulated the synthesis of the E2-IP of 46 000 Mr. On the other hand, UA stimulated the synthesis of 27 000 and 30 000 Mr proteins (UA-IP). These UA-IP were not precipitated by an antiserum raised against E2-IP. Therefore, UA-IP appear to be independent entities and not degradation or precursor products of E2-IP. Both UA-IP are constitutively present in the uterus and even in higher relative amounts in rat brain. The present finding, that an "anti-estrogen", such as nafoxidine, stimulates the synthesis of different proteins than estrogen, provides a new approach to the study of the molecular mechanism of estrogen action.

Developmental expression of protein kinase C subspecies in rat brain-pituitary axis.

We have examined the neonatal developmental expression of protein kinase C subspecies (PKCs) in rat brain, pituitary glands and cells by enzymatic activity assays, immunohistochemistry and Western blot analysis with type-specific antibodies. A very large increase (455%) was noticed in brain PKC activity during the first week of life with the particulate fraction (22% of total enzyme activity on day 1) increasing dramatically (900%) during the first week to 50% of enzyme activity. In contrast, the pituitary gland showed high activity on day 1 that decreased progressively to reach the lowest levels at 1 year of age. Paradoxically, the number of pituitary cells immunolabeled for PKC increases as a function of age. Western blot analysis showed only small changes in PKC alpha, PKC beta and PKC epsilon when brains from 6-day-old and 3-month-old female rats were compared, whereas PKC tau and PKC delta increased markedly during this period. On the other hand, brain PKC zeta decreased between 6 days and 3 months of age. Western blot analysis showed no major changes in pituitary PKC alpha, PKC beta and PKC zeta when 6-day-old and 3-month-old female rats were compared, while PKC tau was not detected. The major band of pituitary PKC delta (76 kDa) decreased markedly between 6 days and 3 months of age whereas the minor band (68 kDa) did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Thoracic and cardiovascular interventions after orthotopic heart transplantation.

BACKGROUND: The long-term outcome of orthotopic heart transplantation is limited by the development of cardiac allograft vasculopathy, rejection, infection, and malignancy. METHODS: After heart transplantation, we treated patients with thoracic and cardiovascular diseases: preexisting coronary artery sclerosis in 2 patients, cardiac allograft vasculopathy in 19, valvular disease in 3, mycotic ascending aortic aneurysm in 2, superior vena cava stenosis in 2, and lung neoplasm in 10 patients. RESULTS: We successfully performed coronary artery bypass grafting for preexisting coronary artery sclerosis, valve replacement for valvular disease, and patch enlargement for superior vena cava stenosis. Percutaneous transluminal coronary angioplasty for cardiac allograft vasculopathy achieved excellent initial results, but the incidence of restenosis was high (67%). One patient who underwent coronary artery bypass grafting for cardiac allograft vasculopathy died immediately after operation. Graft replacement was performed for mycotic aortic aneurysm, but 1 patient required reoperation because of recurrent aneurysm. The long-term survival rate in patients undergoing surgical resection for lung neoplasm was poor (50%). CONCLUSIONS: The need for thoracic and cardiovascular interventions in patients after heart transplantation was low (4.7%). Use of the appropriate procedures can improve the long-term survival after heart transplantation.

Ontogeny and estrogen responsiveness of creatine kinase and glycolytic enzymes in brain and uterus of rat.

We have studied the postnatal ontogeny of creatine kinase (CK) and the glycolytic enzymes phosphoglycerate kinase (PGK), phosphoglycerate mutase (PGM), enolase (En), and pyruvate kinase (PK) in rat brain and uterus. In 30-day-old rat, brain and uterus express the fetal isoforms CK-B, PGK-A, PGM-B, En-alpha and PK-M2, and the differentiated isoforms En-gamma and PK-M1. The activity of glycolytic enzymes in uterus of two-day-old rat is as in brain, while CK activity is 3 times higher in brain. The activity of the glycolytic enzymes in brain began to increase (3-4-fold) 10 days after birth, in a coordinated manner. CK activity began to increase 5 days after birth in both brain (4.2-fold) and uterus (4.5-fold), suggesting the dissociation of glycolytic enzyme ontogeny from CK. In contrast to brain, the levels of glycolytic enzymes in uterus were highest at birth, suggesting the action of a tissue-specific mechanism for regulation of the constitutive levels of glycolytic isozymes. Except for PGM, all enzymes showed an increase in total activity, in response to estrogen, in uterus but not in whole brain.

Intermittent obstruction of the Omnicarbon-valve prosthesis in the mitral position due to interference by papillary muscle. Diagnostic and surgical considerations.

The frequency of prosthetic heart valve malfunction caused by intrinsic factors has been markedly decreased by refinements of prosthetic design and by improved quality of the prosthetic material. Nevertheless, a variety of extrinsic factors, i.e. thrombus formation, bacterial endocarditis, inadequate suture technique and papillary muscle entrapment, are known to be responsible for mechanical malfunctions of prosthetic heart valves, occasionally leading to sudden cardiac death. In this report, a case of intermittent entrapment of papillary muscle in the Omnicarbon valve is presented; diagnostic and surgical aspects are discussed.

Implantation of the Biomedicus centrifugal pump in post-transplant right heart failure.

BACKGROUND: Right heart failure after heart transplantation represents a life-threatening complication. When conventional therapy including NO-inhalation fails the only choice to reach sufficient haemodynamic conditions may be the implantation of a right ventricular support system. METHODS: In all cases the Biomedicus centrifugal pump was implanted by cannulation of the right atrium and pulmonary artery. RESULTS: Since March 1989 950 heart transplant procedures were performed at our center. In nine cases (7 male, 2 female, mean age 52 years) implantation of a right ventricular support system was necessary because of deterioration of right ventricular function. The implantation was carried out in 7 cases immediately after transplantation, in 2 cases after 2 days. The support time ranged from 4-348 hours. Six patients could be weaned, 2 patients underwent retransplantation and died and 1 patient died on the support system. Three of the six weaned patients died in the further course because of multiorgan failure. CONCLUSIONS: Mechanical right ventricular support is often the only therapeutical tool to reach adequate haemodynamic conditions in post-transplant right heart failure. The Biomedicus centrifugal pump provides good conditions in these cases. Weaning is often possible after short-term support. The mortality rate is determined by multiorgan failure in immuno-suppressed patients. Retransplantation seems not to be successful despite maximal treatment.

Development and initial in vivo testing of a new hydraulic drive system (Paedipump) for circulatory support in infants.

The main limitation in the use of circulatory support in children is the lack of an adequate system with regard to size and pumping capacity. Recently, two pneumatically driven ventricular support systems with low volume chambers for use in a pediatric population became available. We have developed a hydraulic drive system with an advantageous exact control of the stroke volume. The system enables two different modes of operation: the full-empty and the filled-empty modes. In both cases the ventricle is empty at the end of systole. This new system was tested in experimental animals (6 pigs, body weight 9.5-14.0 kg) with normal and reduced left ventricular function (MAP<45 mmHg). A 25 ml ventricle (HIA-Medos) was implanted. The full-empty and the filled-empty mode used led to a significant load reduction, both in animals with normal and impaired cardiac function. Plasma lactate levels, pH-values and total body O2-consumption were in the normal range during circulatory support indicating adequate organ perfusion. Results showed that sufficient ventricular support was achieved during all pumping modes due to the possibility of controlling and modifying the stroke volume of the hydraulically driven support system employed according to necessity. This is a promising feature for its future application in infants with congenital or acquired heart diseases.