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

Endocarditis produced by Erysipelothrix rhusiopathiae is an uncommon disease in humans. This bacterial species is found worldwide as a commensal or a pathogen in many animals. Infection in humans is usually due to occupational exposure. The case is reported of a 43-year-old male parrot breeder with native aortic and mitral valve endocarditis and NYHA class II heart failure at six months after wound infection. The patient was discharged after six weeks' treatment with intravenous penicillin G and replacement of the mitral and aortic valves due to severe regurgitation. At one year after surgery the patient was asymptomatic and infection-free.
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PMID:Mitro-aortic infective endocarditis produced by Erysipelothrix rhusiopathiae: case report and review of the literature. 1597 25

Alternaria is a saprophytic fungus that naturally subsists on decaying plant materials, but may be an opportunistic pathogen in immunocompromised hosts. We describe a case of dermal cutaneous alternariosis in a 70-year-old patient, who was on systemic steroid administration for autoimmune hemolytic anemia. The patient also had chronic heart failure, liver dysfunction, and diabetes mellitus. Infection was confirmed by histological examination, and multiple positive culture results. Treatment with oral terbinafine and itraconazole was ineffective. We review the literature of dermal cutaneous alternariosis reported in Japan; including our case, 15 cases have been reported. Recognition of Alternaria as a potential opportunistic pathogen is important for the differential diagnosis of dermatologic lesion, such as granulomatous lesion or ulcer, in immunocompromised hosts.
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PMID:[A case of dermal cutaneous alternariosis]. 1609 93

Parvovirus B19 is a widespread infection that may affects 1-5% of pregnant women, mainly with normal pregnancy outcome. The prevalence of infection is higher during epidemics - between 3 and 20% with sero-conversion rate of 3-34%. Infection during pregnancy can cause a variety of other signs of fetal damage. The risk of adverse fetal outcome is increased if maternal infection occurs during the first two trimesters of pregnancy but may also happen during the third trimester. It is a significant cause of fetal loss throughout pregnancy, but has a higher impact in the second half of pregnancy when spontaneous fetal loss from other causes is relatively rare. Parvovirus infection can cause severe fetal anemia as a result of fetal erythroid progenitor cells infection with shortened half life of erythrocytes, causing high output cardiac failure and therefore nonimmune hydrops fetalis (NIHF). The P antigen expressed on fetal cardiac myocytes enables the Parvovirus B19 to infect myocardial cells and produce myocarditis that aggravates the cardiac failure. Although there are several reports of major congenital anomalies among offspring of mothers infected by Parvovirus, the virus does not seem to be a significant teratogen. Since Parvovirus B19 infection can cause severe morbidity and mortality, it should be part of the routine work up of complicated pregnancies. Risk assessment for maternal infection during pregnancy is especially important during epidemics when sero-conversion rates are high.
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PMID:Parvovirus B19 in pregnancy. 1658 Sep 42

Heart failure is a leading cause of death in developed nations despite medical management. Cardiac transplantation is a potentially lifesaving intervention for approximately 4000 advanced heart failure patients per year; however, the demand for donor hearts far exceeds the supply. Ventricular assist devices provide temporary support for patients with severe heart failure until myocardial recovery occurs or a donor heart becomes available. For those ineligible for transplantation, ventricular assist devices may be used permanently and have demonstrated reduced mortality and an improved quality of life compared with continued medical therapy. Nonetheless, these devices are under-used, in part due to the frequency of complications. Device-related infections are one of the most frequent sequelae of ventricular assist device placement and occur in 18-59% of cases. Infections can involve any part of the device and confer substantial morbidity and mortality. Here, we provide an introduction to ventricular assist devices, explore the nature and pathogenesis of ventricular assist device-related infections, discuss problems with diagnosis, and present treatment and prevention strategies.
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PMID:Ventricular assist device-related infections. 1679 Mar 83

The spectrum of acute renal failure (ARF) in the elderly population and the factors predicting poor outcome in these patients are not well defined in literature. Identification of risk factors and poor prognostic markers in these patients can help in planning strategies to prevent ARF and to prioritise the utilization of sparse and expensive therapeutic modalities, especially in a developing country like ours. We retrospectively analyzed data of 454 elderly patients (age >or=60 years), detected having ARF in a tertiary care super-speciality hospital in North India, from April 2000 to March 2004. The mean age of this population was 66.4 years with 70.5% being male. 64% patients had more than one precipitating factors for ARF, with volume depletion being the most common precipitating factor (33% cases). Infection/sepsis (21.6%) and drugs (11.5%) were other important precipitating factors. 31.8% were recorded as having oliguric ARF (urine output <400 ml/day) and 33.5% required renal replacement therapy (RRT). Acute peritoneal dialysis was the most frequent form of RRT given (62.5%). Mortality was 41.2% (187 cases), of whom 56 (29.8%) died inspite of recovery from ARF. Among the survivors, 103 patients (22.7%) had complete renal recovery, 141 (31.1%) had partial renal recovery, while 23 (8.6%), remained dialysis dependent. The factors which were found to be associated with increased mortality were; age >or=70 years, presence of previous chronic illness, ARF precipitated by cardiac failure and infection, need for RRT, oliguria and increasing numbers of failed organs. To conclude, ARF among elderly is a common problem in nephrology practice at our institute and is responsible for 48.9% of nephrology admissions/consultations among elderly patients. Majority of these patients are prone to multiple renal insults. Underlying chronic illness, presence of cardiac failure and sepsis, oliguria, need for RRT and increasing number of organ failure is associated with poor outcome.
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PMID:Factors affecting the outcome of acute renal failure among the elderly population in India: a hospital based study. 1686 17

Intravascular devices such as pacemakers, implantable cardioverter-defibrillators (ICDs), left ventricular assist devices (LVADs), and prosthetic vascular grafts are life-saving therapies for patients with malignant arrhythmias, heart failure, and various vascular diseases. As indications for their use have increased, so has the prevalence of infectious complications associated with these devices. We present a review of the clinical literature on the epidemiology, diagnosis, and management of infectious complications of these intravascular devices. Most intravascular device infections are thought to result from skin flora contamination during implantation. Infection of the subcutaneous portion of the device can subsequently track to deeper intravascular tissues. Infection that involves the intravascular or intracardiac portion of these devices carries a high morbidity and mortality. Despite appropriate antibiotic therapy, cure of infection is frequently possible only with device removal. Well-designed placebo-controlled, randomized studies evaluating antimicrobial therapy for treatment of intravascular device infections are lacking. In the absence of better information, authorities recommend antibiotics targeted toward cultured organisms for approximately 4 to 6 weeks and device removal.
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PMID:Intravascular device infections: epidemiology, diagnosis, and management. 1717 79

Junctin is a transmembrane protein located at the cardiac junctional sarcoplasmic reticulum (SR) and forms a quaternary complex with the Ca(2+) release channel, triadin and calsequestrin. Impaired protein interactions within this complex may alter the Ca(2+) sensitivity of the Ca(2+) release channel and may lead to cardiac dysfunction, including hypertrophy, depressed contractility, and abnormal Ca(2+) transients. To study the expression of junctin and, for comparison, triadin, in heart failure, we measured the levels of these proteins in SR from normal and failing human hearts. Junctin was below our level of detection in SR membranes from failing human hearts, and triadin was downregulated by 22%. To better understand the role of junctin in the regulation of Ca(2+) homeostasis and contraction of cardiac myocytes, we used an adenoviral approach to overexpress junctin in isolated rat cardiac myocytes. A recombinant adenovirus encoding the green fluorescent protein served as a control. Infection of myocytes with the junctin-expressing virus resulted in an increased RNA and protein expression of junctin. Ca(2+) transients showed a decreased maximum Ca(2+) amplitude, and contractility of myocytes was depressed. Our results demonstrate that an increased expression of junctin is associated with an impaired Ca(2+) homeostasis. Downregulation of junctin in human heart failure may thus be a compensatory mechanism.
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PMID:On the role of junctin in cardiac Ca2+ handling, contractility, and heart failure. 1740 Jul 17

Parvovirus B19 infection during pregnancy is at risk of adverse fetal outcome. The risk is increased if maternal infection occurs during the first two trimesters, but may also happen during the third trimester. Adverse first and third trimester fetal outcome were recently highlighted by polymerase chain reaction (PCR) viral DNA detection. Parvovirus does not seem to be a significant teratogen. Infection during pregnancy can cause severe fetal anaemia and nonimmune hydrops fetalis. Cardiac tropism of the virus can cause myocarditis and aggravate the cardiac failure. Follow up of in utero anaemia is based upon the middle cerebral artery peak systolic flow velocity evaluation and treatment is based upon cordocentesis transfusion.
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PMID:[Parvovirus B19 in pregnancy: literature review]. 1800 56

The aim of this study was to investigate the efficacy and feasibility of anti-CD25 monoclonal antibody (basiliximab) in treating steroid-refractory acute graft-versus-host disease (aGVHD) following haploidentical bone marrow transplantation (hiBMT). 15 cases who developed II-IV grade steroid-resistant aGVHD after haploidentical BMT were treated by intravenous injection of basiliximab at a dose of 20 mg on days 1 and 4. In those patients not achieving CR after 1 week, basiliximab injection was repeated. The results showed that 8 cases (53.33%) got complete response (CR). Out of them 4 cases have been still in disease-free survival, 2 cases have been in survival with limited cGVHD, 2 cases died from pulmonary infection; 3 cases (65%) got partial response (PR), out of whom 1 case has been still in disease-free survival, one died from GVHD and infection, and another one died from pulmonary infection; 4 cases without response died from GVHD, pulmonary infection and cardiac failure. Overall response rate was 73.3% and long-term survival rate was 46. 7%. There were no infusion-associated side-effects after treatment with basiliximab. It is concluded that the anti-CD25 monoclonal antibody is efficacious and feasible for steroid-refractory grade II-IV aGVHD after hiBMT, but the overall survival rate is low. Infection is the main cause of death. Thereby, it is especially important to strengthen environmental protection and prevent infection.
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PMID:[Efficacy of anti-CD25 monoclonal antibody used in treating steroid-resistant acute graft-versus-host disease following haploidentical bone marrow transplantation]. 1923 70

Heart failure development goes along with a transition from hypertrophic growth to apoptosis induction. In adult cardiomyocytes SMAD proteins are only activated under apoptotic, but not under hypertrophic conditions and are increased at the transition to heart failure. Therefore, SMADs could be candidates that turn the balance from hypertrophic growth to apoptosis resulting in heart failure development. To test this hypothesis we infected isolated rat ventricular cardiomyocytes with adenovirus encoding SMAD4 (AdSMAD4) and investigated the impact of SMAD4 overexpression on the development of apoptosis and hypertrophy under stimulation with phenylephrine (PE). Infection of cardiomyocytes with AdSMAD4 significantly enhanced SMAD-binding activity while apoptosis after 24 and 36 h infection did not rise. But when SMAD4 overexpressing cardiomyocytes were incubated with PE (10 microM), the number of apoptotic cells increased (Ctrl: 94.97 +/- 6.91%; PE: 102.48 +/- 4.78% vs. AdSMAD4 + PE: 118.64 +/- 3.28%). Furthermore expression of caspase 3 as well as bax/bcl2 ratio increased in SMAD4 overexpressing, PE-stimulated cardiomyocytes. In addition, the effects of SMAD4 overexpression on PE-induced hypertrophic growth were analyzed. Protein synthesis 36 h after AdSMAD4 infection was comparable to control cells, whereas the increase in protein synthesis stimulated by phyenylephrine was significantly reduced in SMAD4 overexpressing cells (134.28 +/- 10.02% vs. 100.57 +/- 8.86%). SMAD4 triggers the transition from hypertrophy to apoptosis in ventricular cardiomyocytes. Since SMADs are increased under several pathophysiological conditions in the heart, it can be assumed that it triggers apoptosis induction and therefore contributes to negative remodeling and heart failure progression.
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PMID:SMAD-proteins as a molecular switch from hypertrophy to apoptosis induction in adult ventricular cardiomyocytes. 1941 95


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