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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Paediatric cardiac transplantation (pHTX) has gained widespread acceptance as a therapy in end-stage myocardial failure and some forms of congenital heart disease, particularly hypoplastic left heart syndrome (HLHS). The major problems to the anaesthesiologist in these patients are induction of anaesthesia in infants with HLHS and treatment of pulmonary hypertension in the early post-bypass period. PATIENTS AND METHODS. Anaesthesia for pHTX was performed in 15 children < 1 year of age (4-237 days); 12 suffered from HLHS, 2 from endocardial fibroelastosis, and 1 from dilatative cardiomyopathy. Induction of anaesthesia in patients with HLHS IS a challenge to the anaesthesiologist, as he has to maintain the delicate balance between pulmonary and systemic blood flow. Anaesthesia was induced with fentanyl (10-15 micrograms/kg) and pancuronium (0.2-0.4 mg/kg) and maintained with fentanyl (total dosage 70-100 micrograms/kg). Modification of ventilatory parameters such as FiO2, PaCO2, and airway pressure (PEEP, I:E ratio) was used to influence systemic and pulmonary blood distribution in the pre-bypass period according to changes in haemodynamics (target: O2 saturation approximately 75%-80%, PaCO2 45-50 mmHg). Treatment of pulmonary hypertension in the weaning and early post-bypass period consisted of respiratory (PaCO2 < 30 mmHg) and metabolic alkalinisation (pH 7.45-7.55, BE > +3 mmol/l), the use of prostaglandin E1 (3-6-12 micrograms/kg.h), and the phosphodiesterase inhibitor enoximone (10-15 micrograms/kg.min). Additional positive inotropic support was achieved with dobutamine (5-10 micrograms/kg.min), adrenaline (0.1-0.5 micrograms/kg.min), and/or orciprenaline (0.1-0.2 micrograms/kg.min) and calcium chloride (25-100 mg/kg). RESULTS. Two children died intraoperatively and 1 on the 1st postoperative day from overwhelming pulmonary vascular resistance and right ventricular failure. Three children died between 3 and 4 weeks postoperatively, 1 from cytomegalovirus infection, 1 from sepsis, and 1 from acute rejection. Nine patients survived and are well up to 5.5 years after transplantation. CONCLUSION. Pulmonary hypertension in the weaning and early post-bypass period is the main anaesthesiological problem of pHTX, particularly in children with HLHS. A polypragmatic approach to this problem consisting of alkalinisation, pulmonary vasodilatation, and inotropic support is presented and seems to be effective. Further improvements in concepts of pHTX are limited by the lack of donor organs. Though the experience with pHTX in neonates and infants is growing slowly, it might be a routine procedure from the anaesthesiological point of view within a few years in some selected centres.
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PMID:[Anesthesia for heart transplantation in newborn and suckling infants. Special aspects of the hypoplastic left heart syndrome]. 778 53

Fatal cytomegalovirus (CMV) myocarditis occurred in a 2 year old boy with acute lymphoblastic leukemia (ALL) in remission. The patient showed mild hepatic dysfunction and a rapid progress of pancytopenia after complete remission had been achieved. At the fifth week of complete remission, he presented signs of heart failure such as tachycardia, S4 gallop on auscultation and decreased ejection fraction on echocardiography. However, no significant electrocardiographic changes were recognized. In addition to the cardiac dysfunction, the patient presented a marked tachypnea and dyspnea associated with hypoxemia. These were dramatically improved by methylprednisolone pulse therapy (30 mg/kg per day, for 3 days) and CMV high titer immunoglobulin (400 mg/kg per day, for 3 days). On the sixth day after signs of respiratory failure were improved, the patient suddenly presented a paroxysmal atrial tachycardia followed by a fatal ventricular fibrillation. Although we could detect neither a specific IgM antibody, a significant increase of IgG antibody, nor CMV genome by DNA hybridization techniques during the course of the illness, microscopic examination of necropsy specimens of the heart showed a marked disruption and disintegration of muscle bands associated with cytomegalic inclusion bodies. Polymerase chain reaction (PCR) yielded a 305 bp amplification product in the heart and lung tissues, supporting the view that myocarditis was caused by CMV.
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PMID:Fatal cytomegalovirus myocarditis in a seronegative ALL patient. 779 59

We report the case of a 28-year old asthmatic female patient, who developed an acute heart failure beginning with diarrhea, fever, and dyspnea 5 weeks after delivery. After improvement of all vital functions and dismissal from hospital care unit a marked blood hypereosinophilia, left ventricular congestive heart failure, pericardium effusion and fever up to 40 degrees C followed. Endomycardial, bone marrow and skeletal muscle biopsies and the pericardial fluid showed a marked eosinophilic infiltration or polymyositis, respectively, which could be treated successfully with steroids and azathioprin. During steroid medication cytomegalovirus-associated myocarditis developed and was diagnosed by in situ hybridization. CMV hyperimmunoglobulin treatment (Cytotect, Biotest) was started (2 ml/kg bw on day 1 and 3, and 1 ml/kg on days 5, 7 and 9), which led to the eradication of the residual infiltrate and CMV-DNA in the myocardium. After discontinuation of all medication, eosinophilia and asthma recurred so that immunosuppressive treatment was continued.
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PMID:[Eosinophilic endomyocarditis post partum or pregnancy-related cardiomyopathy]. 792 30

Cytomegalovirus (CMV) infections are commonly found in patients on immunosuppressive therapy following liver transplantation. However, acute myocarditis is an extremely rare manifestation of CMV infection in this setting. We report the case of a patient who developed acute myocarditis with severe biventricular failure with a cardiac ejection fraction of less than 10%, 6 weeks following orthotopic liver transplantation. Systemic CMV infection was diagnosed on the basis of a clinical viraemia, the presence of CMV antigen in urine, blood, and throat swab, and an associated four-fold rise in serum antibody titres to CMV. A full recovery ensued following treatment with standard anti-cardiac failure therapy and a 10 day course of intravenous ganciclovir.
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PMID:Cytomegalovirus myocarditis following liver transplantation. 797 35

A 23-year-old white woman was admitted because of cardiac failure (functional class II), palpable purpura and hypereosinophilia. A month before, she had been operated due to right femoral embolus. In this occasion, enhanced cardiac size on X-ray film of the chest and 12,300 eosinophils/mm3 were observed. She was asthmatic from her childhood. The laboratory data did not detect an etiology of hypereosinophilia. Serologic test for collagenous diseases, Chagas, hydatidosis, toxocariasis, Coxsackie B 1-6 and cytomegalovirus were not considered reactive. Three parasitologic stool examinations were negative. Duodenal sounding was negative. Myocardial dilatation was confirmed by mode M and B echocardiogram (60 mm left ventricular diastolic diameter), and by 99Tc radiocardiogram (left ventricular ejection fraction -LVEF-: 29% and right VEF: 15%). On the 25th day of treatment with 16-beta-methyl-prednisone (1 mg/K/d), eosinophil count was reduced to 300/mm3. On the 45th day, clinical improvement, dilatation reduction on echocardiogram and a 32% LVEF were observed. On the 10th month, the patient has no signs or symptoms of cardiac failure under treatment. Although endomyocardial biopsy was not performed but considering the low prevalence of myocardial dilatation at such an age, it is possible to postulate that the patient has undergone the initial necrotic stage (dilated cardiomyopathy) and the intermedial thrombotic stage (femoral embolus) of the eosinophilic endomyocardial disease.
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PMID:[Dilated cardiomyopathy and hypereosinophilia in a young female patient]. 824 31

Lung function of patients with heart failure is characterized by a variety of changes proposed as being due to passive congestion, secondary pulmonary fibrosis, and/or recurrent pulmonary emboli. A diffusion impairment thought to be due to cyclosporine has also been noted in patients following heart transplantation. Similar changes of unclear origin have been observed in renal transplant recipients. The objective of this study was to determine the extent to which lung function changes are reversible by cardiac transplantation and relate changes to the status of the recipients lung in the presence of possible vascular, iatrogenic, immune, or infectious injury. We analyzed the data of 22 patients who underwent lung function testing before and after heart transplantation and correlated changes to hemodynamic change, episodes of rejection, concentration of cyclosporine, and cytomegalovirus infection. Despite excellent graft function, the carbon monoxide transfer factor deteriorated to a mean of 57 percent of predicted postoperatively. The fall in diffusion factor did not correlate with episodes of cardiac rejection, cyclosporine levels, or hemodynamic status. In those patients who had serologic evidence of cytomegalovirus infection, the reduction in transfer factor was greater compared to those without infection despite a normal chest radiograph. The effects of cardiopulmonary bypass were unlikely to have been responsible for the abnormalities as lung function was assessed at a mean of 14 months after surgery. In heart transplant recipients, a change in diffusion capacity may represent an additional marker for cytomegalovirus infection and reflect infectious/immune injury late following surgery.
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PMID:Pulmonary diffusion abnormalities in heart transplant recipients. Relationship to cytomegalovirus infection. 840 71

We evaluated patients presenting with large and recurrent sterile serosal effusions following bone marrow transplants. From a review of the Minnesota BMT Database from 1974 to 1993, seven patients with unexplained multiple effusions involving two or more of the pleural, pericardial or peritoneal cavities were identified. Patients with veno-occlusive disease (VOD), infections, cardiac insufficiency, tumor relapse and GM-CSF toxicity were excluded. All had onset following engraftment and six occurred before day 100. Unexplained multiple effusions were observed in recipients of allogeneic transplants but not autologous transplants and were found only in patients with acute and/or chronic GVHD. Five of seven patients also had cytomegalovirus (CMV) disease. Multiple effusions appear to be part of the presentation of severe acute or chronic GVHD, often in association with CMV disease in patients who receive allogeneic donor marrow.
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PMID:Unexplained effusions: association with allogeneic bone marrow transplantation and acute or chronic graft-versus-host disease. 1456

Cytomegalovirus (CMV) infection has been reported to cause serious event in nonimmunocompromised patients after major surgery. Particularly in active case, the indication of surgical intervention is a difficult issue. A 7-months-old boy with ventricular septaldefect (VSD) has been diagnosed with CMV hepatitis. As his heart failure was not controlled with medication, he underwent closure of VSD at 9 months of age while CMV was still detected in the urine and serum by polymerase chain reaction method. During post operative course, he was treated with ganciclovir and intravenous CMV hyperimmune grobiln, and CMV in the serum became negative and he develops no aggravation of the CMV infection postoperatively.
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PMID:[A case of ventricular septal defect closure in patient with cytomegalo virus hepatitis]. 899 Aug 99

After heart transplantation a number of factors such as pre- and postoperative hypoxia of the myocardium, myocardial failure of the early postoperative period, acute rejection episodes, cytomegalovirus infection, and finally the progressive atherosclerosis of the coronary arteries lead to the development of transplanted heart failure. Severe alterations of the myocardial function at this end stage of the process correspond to incurable cardiomyopathy. The target of plasmapheresis in this case is to decrease the extent of the disturbances in the lipoprotein contents and blood rheology for the improvement of the coronary perfusion of the transplanted heart. Nine patients with 3-7 year survival periods after heart transplantations underwent plasmapheresis twice a year using the Haemonetics PCS-plus machine. 2,100-2,700 ml of plasma was removed. Biochemical data, rheology and coagulation, and the concentration of Sandimmune (Sandoz Pharma Ltd., Basel, Switzerland) were controlled, and radionuclide scintigraphy of the myocardium, coronarographia, and transesophageal ultrasound investigations were completed for these patients. The result was the significant improvement of the coronary perfusion of the myocardium. The level of immunosuppression after the plasmapheresis procedures did not change and therefore did not demand any correction. Thus, we think that plasmapheresis can be an effective method of treatment of posttransplantation cardiomyopathy; the improvement of coronary perfusion decreases the extent of chronic ischemia. Further studies are necessary to answer the question as to whether it is possible to prolong the time before retransplantation with the help of plasmapheresis.
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PMID:Plasmapheresis in the treatment of posttransplant cardiomyopathy. 952 79

Diagnosis of inflammatory dilated cardiomyopathy relies on the histological and immunohistological examination of endomyocardial biopsies. Only with the demonstration of the etiological agents in the myocardium specific therapy can be attempted. Whereas the spontaneous course of endemic myocarditis with little hemodynamic impairment is fair, the prognosis of symptomatic myocarditis and dilated cardiomyopathy is poor, with complete restitution in 35% and a 10-year survival rate of 30%. Restriction of physical activity is a validated form of therapy with normalization of the heart size in 40 to 60%. Symptomatic medical therapy consists of digitalis, diuretics, ACE-inhibitors and vasodilators and betablocker therapy, where a reduction of mortality was demonstrated in clinical (sub)studies up to 60%. Specific forms of therapy in inflammatory cardiomyopathy rely on the demonstration or lack of viral persistence or signs of autoreactivity in the myocardial tissue. Immunosuppressive therapy in autoimmune forms improved cardiac function in up to 60% of the patients in controlled trials, when compared to controls (40%). The double-blind randomized myocarditis treatment trial, which unfortunately did not distinguish viral from autoimmune myocarditis could not demonstrate such a benefit, however. Depending on the etiology of the disease, immunomodulation with immunoglobulins or interferon or antiviral therapy with hyperimmunoglobulins are presently tested in clinical treatment trials (ESETCID) in patients with enterovirus-positive or cytomegalovirus-positive and adenovirus-positive chronic myocarditis. Specific therapies are aimed to avoid the progression of the disease which may ultimately lead to heart failure with a cardiac assist device or heart transplantation as ultimate therapeutic option.
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PMID:[Therapy of dilated cardiomyopathies with and without inflammation]. 959 34


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