Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The management and clinical course of patients with myasthenia gravis admitted to a neurological intensive therapy unit (ITU) over a 66 month period were reviewed. Twenty-seven patients were admitted in myasthenic crisis, eight of whom had multiple admissions. One patient had a cholinergic crisis and a further patient an acute myocardial infarction. A specific aetiological factor precipitating myasthenic crisis was identified in 19 instances: infection (8), reduction in medication (5), menstruation (4), and steroid administration (2). Thirteen patients with crisis had had a previous thymectomy, six with thymoma. Twenty-three out of 35 (66%) patients admitted in crisis required intubation; nine subsequently needed a tracheostomy. Twenty-nine patients received plasma exchange and seven intravenous immunoglobulin. Four patients in myasthenic crisis died in ITU [adult respiratory distress syndrome (1), disseminated intravascular coagulation and cytomegalovirus (CMV) pneumonitis (1), cardiac failure (1) and multiple organ failure (1)]. Appropriate management of myasthenia gravis requires the easy availability of specialised neuro-intensive care facilities. Copyright Rapid Science Ltd
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PMID:The management and outcome of patients with myasthenia gravis treated acutely in a neurological intensive care unit. 1021 Aug 24

The incidence of aspergillosis in kidney transplant recipients is low and most commonly occurs in the early posttransplantation period. We report an unusual case of a 52-year-old female patient with Aspergillus endocarditis as a late complication after kidney transplantation, presumably spread from a necrosis in the gut, associated with previous cytomegalovirus colitis. As complications, the patient experienced septic embolization into the coronary and pulmonary arteries, and an infarction of the right parietal cortex and insula. The patient died as a result of global heart failure after a 10-day course of antimycotic therapy with amphotericin B plus 5-flucytosine during surgical valve replacement.
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PMID:An unusual case of Aspergillus endocarditis in a kidney transplant recipient. 1060 62

The hereditary form comprises approximately 1/5 of patients with dilated cardiomyopathy (DCM) and is a major cause of advanced heart failure. Medical and socioeconomic settings require novel treatments other than cardiac transplantation. TO-2 strain hamsters with congenital DCM show similar clinical and genetic backgrounds to human cases that have defects in the delta-sarcoglycan (delta-SG) gene. To examine the long-term in vivo supplement of normal delta-SG gene driven by cytomegalovirus promoter, we analyzed the pathophysiologic effects of the transgene expression in TO-2 hearts by using recombinant adeno-associated virus vector. The transgene preserved sarcolemmal permeability detected in situ by mutual exclusivity between cardiomyocytes taking up intravenously administered Evans blue dye and expressing the delta-SG transgene throughout life. The persistent amelioration of sarcolemmal integrity improved wall thickness and the calcification score postmortem. Furthermore, in vivo myocardial contractility and hemodynamics, measured by echocardiography and cardiac catheterization, respectively, were normalized, especially in the diastolic performance. Most importantly, the survival period of the TO-2 hamsters was prolonged after the delta-SG gene transduction, and the animals remained active, exceeding the life expectancy of animals without transduction of the responsible gene. These results provide the first evidence that somatic gene therapy is promising for human DCM treatment, if the rAAV vector can be justified for clinical use.
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PMID:Rescue of hereditary form of dilated cardiomyopathy by rAAV-mediated somatic gene therapy: amelioration of morphological findings, sarcolemmal permeability, cardiac performances, and the prognosis of TO-2 hamsters. 1180 34

Repeated bouts of ischemia in the heart lead to fibrosis and eventually to heart failure. Although certain genes, such as SOD or hemoxygenase and antisense to AT(1)R, ACE, and (beta(1)-AR can provide short-term protection of the heart from ischemia, there is no known mechanism for constantly responding to repeated incidences of ischemia. We hypothesized that a "vigilant vector," designed to be expressed specifically in the heart and switch on therapeutic genes only during hypoxia, would provide cardioprotection. To attain cardiac specificity, we inserted an MLC2v promoter into an adeno-associated virus (AAV) designed to deliver AS to AT(1)R and gfp. In in vitro experiments in cardiomyocytes (H9C2 cells), the MLC2v-AAV-gfp drove gene expression in all cells at levels comparable to a cytomegalovirus (CMV) promoter. In in vivo experiments, the rAAV-MLC2v-gfp was injected intravenously into mice or rats. Green fluorescence protein (GFP) DNA was located in kidney, heart (right and left ventricle), lung, adrenal and spleen. GFP mRNA, however, was expressed only in the heart and absent in other tissues. To switch on the rAAV transgene during ischemia, we inserted a hypoxia response element (HRE). This upregulates transcription when O(2) levels are low. Thus, there are 4 components to the vigilant vector; a gene switch (HRE), a heart-specific promoter (MLC2v), a therapeutic gene (AS-AT(1)R) and a reporter gene (gfp). To silence or lower basal level of expression while retaining specificity, we have reduced the length of the MLC2v promoter from 3 kb to 1775 bp or 281 bp. The truncated promoter is equally effective in heart specific expression. Preliminary studies with the rAAV-HRE-gfp in vitro show an increased expression in 1% O(2) in 4 to 6 hours. By adding additional hypoxia-inducible factor (HIFalpha) (5 microg), the MLC2v-gfp expression is increased by 4-fold in 1% O(2). Further amplification of the gene to 400-fold in 1% O(2) can be achieved with a double plasmid. The construct may serve as a prototype "vigilant vector" to switch on therapeutic genes in specific tissue with physiological signals.
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PMID:Vigilant vector: heart-specific promoter in an adeno-associated virus vector for cardioprotection. 1188 25

In heart transplant recipients, infection is one of the leading causes of morbidity and mortality. In adult heart transplant patients, cytomegalovirus is the most frequently encountered viral pathogen. Conversely, disseminated adenoviral infection is observed mainly in children, where it is predictive of allograft rejection and coronary vasculopathy. The literature contains only a few reports of adenoviral infections in adult heart transplant recipients. Limited information is available concerning the diagnosis and epidemiology of such infections and their relationship to organ rejection, heart failure and overall outcomes in these patients. To promote an awareness of this potentially lethal complication, we present a case of fatal disseminated adenoviral infection in an adult heart transplant recipient.
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PMID:Fatal disseminated adenoviral infection in an adult heart transplant patient. 1547 17

Nonimmune hydrops fetalis (NIHF) or generalized soft tissue edema and cavity effusions may be due to cardiovascular diseases, congenital infections, genitourinary malformations, thoracic masses, placental conditions, chromosomal abnormalities, and idiopathic. We report 32 cases of NIHF from among 429 neonates who underwent autopsies (incidence 7.45%). Sixteen cases (50%) had cardiovascular disease; all were due to low output cardiac failure; 7 had structural congenital heart disease. Three of the children with congenital heart disease also had chromosomal abnormalities: 2 had trisomy 18 and 1 had Noonan syndrome. Among myocardial conditions were five subjects with cardiomyopathies (1 of each of the following types): oncocytic, dilated, endocardial fibroelastosis, cardiac glycogenosis, and carnitine deficiency; 3 had myocarditis, and 1 had cardiac rhabdomyomas. Congenital infections were due to cytomegalovirus in 3 cases, bacteria in 2, and parvovirus in 1. The mechanism of NIHF in these cases might be a combination of decreased myocardial contractility due to myocarditis and fetal anemia. Genitourinary diseases were present in 5 newborns: Two had congenital nephrotic syndrome, 1 had VACTER association, 1 had prune-belly syndrome, and 1 had urogenital sinus malformation. Intrathoracic lesions were found in 2 babies (pulmonary sequestration and diaphragmatic hernia). One twin died of volume overload due to twin transfusion syndrome. Only 2 newborns were classified as idiopathic. Our study shows that cardiovascular diseases that lead to heart failure or impaired venous return are more common in the liveborn (50%), whereas congenital infections are more common in the stillborn with NIHF.
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PMID:Nonimmune hydrops fetalis in the liveborn: series of 32 autopsies. 1601 Apr 81

Inflammatory processes induced by viral or bacterial infections are believed to be one of the major pathogenetic mechanisms in myocardial diseases. Although the reason for progression to myocardial failure is not fully understood, postulated mechanisms include persistent viral infection alone or in combination with autoimmune processes. A variety of cardiotropic viruses have been identified to elicit myocarditis, with enteroviruses and adenoviruses as the most frequent causative agents in children and adolescents. However, parvovirus B19 (PVB19) has recently emerged as another potential pathogen in adult patients associated with inflammatory heart disease. Many dimensions of inflammatory heart disease coexist while different phases of the disease progress simultaneously: phase 1 is dominated by viral infection, phase 2 by the onset of (probably) multiple autoimmune reactions, and phase 3 by the progression to cardiac dilatation without the role of an infectious agent and cardiac inflammation. Taking these mechanisms into account, screening for viral and bacterial genome by polymerase chain reaction (PCR) and detection of inflammatory infiltrates by immunohistochemistry are considered crucial for establishing an aetiological diagnosis, thereby allowing initiation of specific therapeutic strategies. In a large cohort of 3345 consecutive patients with left ventricular dysfunction evaluated over a period of 10 years, prevalence of PVB19, coxsackievirus (CVB), human cytomegalovirus (HCMV), influenza A virus and adenovirus (ADV) genome was assessed by PCR. Inflammatory infiltrates within the myocardium were detected by immunohistochemistry according to the WHF criteria and by histopathology according to the Dallas criteria of myocarditis. For control, endomyocardial samples of patients with arterial hypertension were studied. Parvovirus B19 was the most often detected virus in all patient subgroups, with positivity ranging from 17% to 33%. Except for PVB19, CVB RNA (3%), ADV (2%) and CMV (3.9%) were the most frequently detected viral genomes. Interestingly, detection of PVB19 genome was significantly correlated with inflammatory heart disease and reduced ejection fraction. Importantly, an aetiological diagnosis requires the immunohistochemical and molecular biological investigation of endomyocardial biopsies. Such an approach may change the management of these diseases in the future. One of the aims of the study was to reveal the underlying dominant pathophysiological mechanisms in a for deciding on the most approriate therapy.
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PMID:Pathophysiology and aetiological diagnosis of inflammatory myocardial diseases with a special focus on parvovirus B19. 1631 98

A 42-year-old woman developed a rapidly progressing fatal heart failure. At the autopsy extensive necrosis of the myocardium was seen, with an almost complete absence of inflammatory cells and the presence of bacterial structures identified as Staphylococcus lugdunensis by PCR. In addition, the cytomegalovirus genome was found to be located inside the cardiomyocytes.
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PMID:Fatal myocardial necrosis caused by Staphylococcus lugdunensis and cytomegalovirus in a patient with scleroderma. 1675 44

The true incidence of influenza myocarditis in the general population is unknown, because of the variable clinical presentation and the absence of a established noninvasive diagnostic test that can confirm the diagnosis. Influenza is, however, one of the frequently implicated viruses caused myocarditis as well as Coxsackie B, adenovirus, echovirus and cytomegalovirus. The clinical manifestations of viral myocarditis vary greatly from asymptomatic electrocardiographic changes to fulminant heart failure with fatal arrhythmias. We should recognize that subtle cardiac symptoms and signs in many subclinical cases may be overshadowed by systemic manifestations of the underlying influenza infection. Although specific therapy consisted of anti-viral agents, intravenous gamma-globulin treatment or mechanical ventricular supports may be available for influenza myocarditis, it has not been established that the myocarditic process itself will be favorably affected.
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PMID:[Influenza myocarditis and pericarditis]. 1703 67

The results of recent studies favor the immunological theory of the pathogenesis of chronic heart failure (CHF). In this connection, of particular interest is a search for possible causes of cytokine hyperactivation in patients with CHF of ischemic etiology, one of which may be viral infection. The aim of the study was to evaluate the impact of herpesvirus simplex (HVS), cytomegalovirus (CMV), Chlamydia pneumoniae on the activation of cytokines in patients with CHF of ischemic etiology. Ninety patients with CHF of ischemic etiology were examined. After comprehensive study, the patients were divided into 2 groups: 1) Functional Class (FC) I-II CHF and 2) FC III-IV CHF Increases in the levels of proinflammatory cytokines (tumor necrosis factor-alpha, interferon-gamma and in the content of IgG and IgM to CMV and IgM to HVS were ascertained in patients with CHF of ischemic etiology. There were statistically significant correlations of the level of proinflammatory cytokines, CMV, and HVS with the FC of CHF and the echocardiographic indicators reflecting left ventricular systolic function.
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PMID:[Effect of infectious factors on the activation of proinflammatory cytokines in chronic heart failure]. 2000 Jan 13


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