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)

In 18 patients who presented in less than 2 years with heart disease characterized by arrhythmias (including atrial fibrillation, ventricular arrhythmias and heart block), atypical chest pain, pericarditis and cardiac failure, extensive investigation revealed no cause for the disease except for evidence of toxoplasmic infection. One patient had acute toxoplasmosis; the other 17 patients had chronically increased titers, higher than the expected level in the community and also higher than in a control series of patients with well defined heart disease. Toxoplasmosis is probably a fairly common cause of heart disease in this community. The source of infection appeared to be cats, uncooked meat and congenital infection. Patients received chemotherapy with either pyrimethamine and sulfadiazine or tetracycline. Serious relapse occurrred in three patients and embolic complications in two. Experimental myocarditis occurs when toxoplasmic cysts rupture within the heart; therefore clinical symptoms may occur sporadically during a chronic infection.
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PMID:Toxoplasmic infection in cardiac disease. 42 23

Three recent cases from one institution using the total artificial heart (TAH) before transplantation are reviewed. The first patient was implanted for 12 hours with the pneumatic Phoenix total artificial heart after failure of a donor heart 1 day after transplant. Following retransplantation the patient died from severe pulmonary edema, pulmonary hypertension, right ventricular failure, and Pseudomonas septicemia. The second patient was implanted with the Jarvik-7 total artificial heart for rapidly deteriorating idiopathic cardiomyopathy. Major complications during the 9 1/2-day implant consisted of severe pulmonary edema for the first 4 days and a multifocal cerebral embolic event on the seventh day after implantation from which he fully recovered. Major problems after transplant included disseminated toxoplasmosis and two mild episodes of rejection. The patient was discharged 68 days after surgery and remains well. The third patient was a 40-year-old woman with rapidly progressing acute influenza A viral myocarditis. Despite immunosuppressive and antiviral therapy, cardiogenic shock with multiple organ failure developed. The 70 ml Jarvik-7 was implanted for 4 1/2 days. Acute humoral rejection from autoantibodies and alloantibodies led to a cardiac arrest on the second day after transplantation. A second 70 ml Jarvik-7 implant was followed by severe multisystem and infectious complications. After prolonged intensive care support, the patient recovered and is now awaiting transplantation. Nearly 100% cytotoxic antibody reactivity caused by multiple antigenic stimuli is preventing ready access to donor hearts for this patient. We view the current role of the total artificial heart as a tool to preserve life until a suitable donor heart can be found, reverse the end-organ effects of progressive heart failure and low output, and restore transplant candidacy in selected patients with temporary reversible contraindications to transplantation.
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PMID:Three recent cases of the total artificial heart before transplantation. 330 69

The diagnosis of acute myocarditis in children is based on histological criteria. Often viral in origin, it results in acute left ventricular dysfunction, the clinical manifestations of which are very variable. The potential severity of the disease is maximal in its initial phase, justifying rapid and intensive treatment. Long-term outcome is relatively good although there is a risk of chronic left ventricular dysfunction. This retrospective study is based on 11 cases of acute myocarditis admitted to the paediatric unit of Clermont-Ferrand University Hospital between February 1989 and March 1999. The initial symptoms were non-specific. Echocardiography was the key diagnostic procedure. Half of the patients had severe cardiac failure requiring admission to the intensive care unit. Four cases presented with a severe complication: two embolic events, one syncopal atrioventricular block and one cardiac arrest. The cardiac treatment was classical (digitalis, diuretics, angiotensin converting enzyme inhibitors, anticoagulants). The aetiology was established in 3 cases (toxoplasmosis, haemolytic and uraemic syndrome, Kawasaki) and a viral cause was suspected in 6 other cases (adenovirus in 3 cases, herpes virus, RSV and enterovirus in 1 case). There were no deaths in the acute phase. The long-term outcome was globally good: complete regression in 8 cases, 1 chronic left ventricular dysfunction and 2 late deaths due to intractable cardiac failure. This short series illustrates the often misleading presentation of acute myocarditis in childhood, the value of systematic investigation in the hope of a specific treatment becoming available in the near future for the often viral aetiology.
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PMID:[Acute myocarditis in children. Study of 11 clinical cases]. 1085 55

The clinical picture of myocarditis/myopericarditis is of importance in differential diagnosis, especially in younger patients with suspected myocardial infarction. Myocarditis/myopericarditis commonly presents with chest pain, and the diagnosis is usually established on clinical grounds. However, endomyocardial biopsy is necessary to confirm the diagnosis. We evaluated the characteristics of acute myocarditis over the years 1980-1998 in 54 patients of the Department of Medicine of the University Hospital, Zurich. Two to 6 patients per year were hospitalised with this diagnosis. In most cases the diagnosis was established by a combination of criteria, such as a preceding infection of the upper respiratory tract, thoracic pain, ST segment elevations in different precordial leads followed by T wave inversions, arrhythmias, elevation of cardiac enzymes, reversible hypokinesia by echocardiography and normal coronary arteries. At least 3 of 5 criteria were requested. In a first step we analysed retrospectively all patients with acute myocarditis/myopericarditis in the years 1980-1993. Among 30 cases of acute myocarditis/myopericarditis the following causes could be identified: one influenza B, one Toxoplasma gondii infection, 2 Epstein-Barr infections and one bacterial myocarditis with gram-negative rods. The aetiology of the other 25 cases remained unknown. The majority of myocarditis/myopericarditis healed without complications. One patient with Epstein-Barr myocarditis and one with Toxoplasma gondii infection died. Two patients developed dilated cardiomyopathy. In a second phase we analysed prospectively all cases with acute myocarditis/myopericarditis over the period 1994-1998: 24 patients with acute myocarditis/myopericarditis were hospitalised. At that time coronary angiography and endomyocardial biopsies were performed more frequently. We found 2 patients with giant cell myocarditis and 2 with Toxoplasma gondii infection and HIV, all of whom died. In addition, there were 2 patients with eosinophilic myocarditis, one with Lyme carditis, one with Epstein-Barr myocarditis, one with myopericarditis after Campylobacter enteritis and one histologically proven myocarditis after pneumonia with Haemophilus influenzae. The aetiology of the remaining 13 cases with myocarditis/myopericarditis could not be established. Three patients with probable viral myocarditis developed cardiogenic shock requiring intraaortic balloon pump, and fully recovered. The patient with Lyme carditis manifested with total atrioventricular block and was treated with a temporary pacemaker. One patient with lymphocytic myocarditis required heart transplantation because of terminal heart failure and one female patient with histologically proven diffuse lympho-monocytic myocarditis died of cardiogenic shock. All the other cases healed without complications. Serologies are of little diagnostic value and should be restricted to serologies with therapeutic implications. We believe that the apparent increase in myocarditis/myopericarditis in recent years is a result of better diagnostic tools, such as more specific cardiac enzyme tests, coronary angiography and endomyocardial biopsies. In most cases the therapy remains symptomatic. In elected, severe cases steroids and other immunosuppressive drugs are sometimes used.
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PMID:[Diagnosis and course of myocarditis: a survey in the medical clinics of Zurich University Hospital 1980 to 1998]. 1102 70

Clinical toxoplasmosis is commonly reported in the cat, with the most consistent findings being ocular, pulmonic, hepatic, neurological, gastrointestinal and muscular abnormalities. Myocarditis, whilst frequently identified at post-mortem examination, has not been identified ante-mortem. In immunocompromised humans, myocarditis associated with toxoplasmosis is not an uncommon complication. In such cases, lymphocytic myocardial infiltration can lead to depressed myocardial function, which can be associated with congestive heart failure, rhythm disturbances and pericardial effusions. In addition, myocardial failure has been reported in immunocompetent humans associated with active toxoplasmosis [Chandenier J, Jarry G, Nassif D, Douadi Y, Paris L, Thulliez P, Bourges-Petit E, Raccurt C (2000) Congestive heart failure and myocarditis after seroconversion for toxoplasmosis in two immunocompetent patients. European Journal of Clinical Microbiological Infectious Disease 19, 375-379]. Here we describe a cat with echocardiographic changes consistent with infiltrative or inflammatory disease, and elevated IgG and IgM titres to Toxoplasma gondii. There was resolution of these myocardial changes once the toxoplasmosis was treated.
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PMID:Suspected toxoplasma-associated myocarditis in a cat. 1592 27

Acquired toxoplasmosis is a widespread parasitic disease caused by an obligate intracellular protozoan, Toxoplasma gondii. Humans are infected by consuming undercooked or raw meat containing tissue cysts or by ingesting oocysts in food or water contaminated with feline faeces. Most cases of Toxoplasma gondii infections in immunocompetent individuals are asymptomatic. Although acquired toxoplasmosis is usually a mild infection, it may be life-threatening in immunocompromised patients. In this report we present a 67-year-old HIV-negative woman with acute toxoplasmic perimyocarditis, heart failure and with a history of ischemic heart disease, hypertension and dyslipidemia. The diagnosis was based on clinical characteristics, echocardiographic examinations, elevated inflammatory markers and the presence of IgM and IgG antibodies against Toxoplasma gondii. We conclude that Toxoplasma gondii infection should be considered in each case of perimyocarditis with concomitant, significant diagnostic and therapeutic problems, especially in immunocompromised patients. This paper also reviews differential diagnosis of elevated CA 125 serum levels in postmenopausal women.
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PMID:[Acute toxoplasmic perimyocarditis in a 67-year-old HIV-negative woman--a case report]. 1696 18

A 44-year-old man with myelodysplastic syndrome (RAEB-2) underwent allogeneic bone marrow transplantation from an unrelated donor after being conditioned with myeloablative regimen. Tacrolimus and short-term methotrexate were given for prophylaxis against graft-versus-host disease (GVHD). Engraftment was achieved on Day 17. He developed Grade II acute GVHD involving the skin and gastrointestinal tract and methylprednisolone (2 mg/kg) was initiated. On Day 60, he developed fever and liver dysfunction followed by diffuse interstitial infiltration of the lungs. Respiratory and cardiac failure rapidly progressed and the patient died on Day 66 despite treatment with antimicrobial agents and intravenous immunoglobulin. Autopsy findings revealed disseminated toxoplasmosis involving the lungs, heart, liver, gastrointestinal tract, and kidneys. Toxoplasmosis after allogeneic hematopoietic stem cell transplantation (HSCT) generally manifests as encephalopathy or brain abscess; however, disseminated disease has been sporadically reported. It should be recognized as a possible cause of rapidly progressing interstitial pneumonitis and cardiac dysfunction after allogeneic HSCT.
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PMID:[Fatal disseminated toxoplasmosis after unrelated bone marrow transplantation for myelodysplastic syndrome]. 2297 19

Neglected parasitic infections, including Chagas disease, toxocariasis, cysticercosis, and toxoplasmosis, affect millions of persons in the United States. Relatively few resources have been devoted to surveillance, prevention, and treatment of these diseases. Chagas disease primarily affects Latin American immigrants and can cause heart failure and death if not treated. Immediate antiparasitic treatment is indicated for most patients with acute Chagas disease. Treatment is recommended for patients younger than 18 years who have chronic Chagas disease and is generally recommended for adults younger than 50 years who do not have advanced cardiomyopathy; treatment decisions for other patients should be made on an individual basis. Toxocariasis primarily affects children and can cause gastrointestinal, respiratory, and ophthalmologic disease. Treatment options include albendazole and mebendazole. Patients with ocular infection require referral to an ophthalmologist. Neurocysticercosis, a form of cysticercosis, is the most common infectious cause of seizures in some parts of the United States. Initial treatment should focus on symptom control. Humans generally acquire toxoplasmosis by eating undercooked contaminated meat or ingesting things that have been contaminated with cat feces. Congenital infection can result in miscarriage or adverse fetal effects. Treatment is recommended for immunosuppressed persons, pregnant women, and immunocompetent persons with severe symptoms.
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PMID:Neglected parasitic infections: what every family physician needs to know. 2486 16

In August 2015, Turing Pharmaceuticals acquired the marketing rights to Daraprim (pyrimethamine), a drug used to treat parasitic infections like malaria and toxoplasmosis. Soon after, Turing caused an uproar when it announced that it would raise the price per tablet of Daraprim from [Formula: see text], a 5500% price hike for a drug that has been on the market for over 60 years and off patent since the 1970s. Old, off-patent drugs are becoming increasingly expensive; Daraprim is the archetypal example. Turing had the power to set a high price for Daraprim because the drug's limited patient population, the absence of competing manufacturers, and a lack of therapeutic alternatives all created an effective monopoly. Similar forces have driven up the prices of other off-patent drugs that treat diseases as diverse as heart failure and multi-drug-resistant tuberculosis. Thus, policymakers will have to consider how the high cost of off-patent drugs impacts public health as well as public spending. In this Note I outline the extent of the high-cost off-patent drug problem, drawing special attention to the problem's negative effects on both health outcomes and government budgets. After discussing some of the problem's underlying causes, I present several solutions to the problem that policymakers could consider, with a focus on proposals like reference pricing and expanded compounding that have received relatively little media attention.
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PMID:Off-patent drugs at brand-name prices: a puzzle for policymakers. 2777 47