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)

New effective therapies have been producing longer survival times for HIV-patients. Thus non-infectious complications of late stage of HIV infection (such as the development of left ventricular dysfunction) have emerged; in fact cardiac involvement has been identified frequently at autopsy and is described in 80% of patients with acquired immunodeficiency syndrome (AIDS) as an evidence of the virus cardiotrophism, while clinical findings of left ventricular dysfunction were only detected in about 15% of the patients. It is possible that the development of heart failure had been underestimated in those years; in fact signs and symptoms of cardiac involvement had been often misinterpreted as the results of non cardiac causes (pulmonary failure or infections) also determining a delay in the beginning of cardiac therapy. The aim of this study was to follow 16 human immunodeficiency-virus positive patients during a 3-year period to evaluate the usefulness of early detection of heart failure in order to start a specific therapy as soon as possible. The follow-up consisted of a clinical and electrocardiographic control every 4 months. Echocardiography was carried out when involvement of the cardiac muscle was suspected. During the follow-up we could reveal an early involvement in 5/16 patients (31.2%) and in 2 of them (40%) early therapy caused clinical and echocardiographic regression of left ventricular dysfunction. The present study demonstrates that periodical clinical and echocardiographic controls are useful in patients with HIV infection.
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PMID:[Early detection of heart involvement using serial cardiologic controls in the follow-up of patients with AIDS]. 961 56

We report on two sibs and two other unrelated patients with agenesis of corpus callosum, oculocutaneous albinism, repeated infections, and cardiomyopathy. All manifested postnatal growth retardation, microcephaly, and profound developmental delay. Additional central nervous system anomalies present in at least one patient included hypoplasia of the cerebellar vermis, white matter neuronal heterotopia, or bilateral schizencephaly. Repeated viral, bacterial, and fungal infections were consistent with a primary immunodeficiency. However, immunological studies showed variable, nonspecific findings. Cardiomyopathy with progressive heart failure or infection led to death before age 2 years in three of the patients. This syndrome was first described by Vici et al. [1988: Am. J. Med. Genet. 29:1-8]. The four patients reported herein confirm this unique disorder. Affected sibs of both sexes born to unaffected parents provide evidence for autosomal recessive inheritance.
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PMID:Albinism and agenesis of the corpus callosum with profound developmental delay: Vici syndrome, evidence for autosomal recessive inheritance. 1040 46

We present a four-month-old girl with severe hemolytic anemia and reticulocytopenia. This case is the youngest with hemolytic anemia encountered in our hospital. Findings of autoimmune hemolytic anemia were preceded by diphtheria-pertussis-tetanus (DPT) and oral polio vaccines which were given one month before. At admission, she had heart failure, her hemoglobin (Hb) was 27 gm/L, hematocrit (Hct) 8.5 percent, reticulocyte count 0.2 percent, and gamma and non-gamma Coombs tests were positive. Plasma Hb was 23 percent (N < 3%) and haptoglobin 0 mg/dl. Bone marrow aspiration smear revealed erythroid hyperplasia. No infection, immunodeficiency or malignancy could be established. She received multiple transfusions and did not respond to methyl prednisolone therapy of seven days' duration, but was successfully treated with a combination of immunosuppressive therapy (cyclophosphamide, 6-mercaptopurine, intravenous immunoglobulin and prednisolone, which was added later). This case is interesting in that the disease was preceded by DPT vaccination, was associated with reticulocytopenia and was resistant to steroids.
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PMID:A warm antibody mediated acute hemolytic anemia with reticulocytopenia in a four-month-old girl requiring immunosuppressive therapy. 1077 Jun 64

The amino acid, taurine, is an important nutrient found in very high concentration in excitable tissue. Cellular depletion of taurine has been linked to developmental defects, retinal damage, immunodeficiency, impaired cellular growth and the development of a cardiomyopathy. These findings have encouraged the use of taurine in infant formula, nutritional supplements and energy promoting drinks. Nonetheless, the use of taurine as a drug to treat specific diseases has been limited. One disease that responds favorably to taurine therapy is congestive heart failure. In this review, we discuss three mechanisms that might underlie the beneficial effect of taurine in heart failure. First, taurine promotes natriuresis and diuresis, presumably through its osmoregulatory activity in the kidney, its modulation of atrial natriuretic factor secretion and its putative regulation of vasopressin release. However, it remains to be determined whether taurine treatment promotes salt and water excretion in humans with heart failure. Second, taurine mediates a modest positive inotropic effect by regulating [Na+]i and Na+/Ca2+ exchanger flux. Although this effect of taurine has not been examined in human tissue, it is significant that it bypasses the major calcium transport defects found in the failing human heart. Third, taurine attenuates the actions of angiotensin II on Ca2+ transport, protein synthesis and angiotensin II signaling. Through this mechanism taurine would be expected to minimize many of the adverse actions of angiotensin II, including the induction of cardiac hypertrophy, volume overload and myocardial remodeling. Since the ACE inhibitors are the mainstay in the treatment of congestive heart failure, this action of taurine is probably very important.
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PMID:Interaction between the actions of taurine and angiotensin II. 1094 14

The authors discuss the importance that molecular medicine has assumed in recent years. Molecular methodologies have clearly demonstrated that immunological diversity is based fundamentally on the rearrangement of the genes encoding antigen B and T cell receptors. The importance of oncogenes, and their translocation in tumoral pathologies is emphasized, a case in point being the alterations observed in chronic myeloid leukemia and acute promyelocytic leukemia and their implication for innovative therapy. The importance of prothrombin and factor V genetic-molecular alterations in thromboembolic pathology and of the activation of calcineurin phosphatase or other intracellular signal regulator molecules during cardiac insufficiency genesis is also discussed. Particular attention is paid to progress regarding the socially important Alzheimer's syndrome, and the diagnosis of endocrine tumors. Moreover, the authors believe that the identification of new endocrine nuclear receptors, "orphans" of hormonal ligands, will open up interesting prospects--even therapeutic--in endocrinology. The authors conclude by reviewing the therapeutic prospects for immunodeficiency syndromes and malignant tumors, offered by new gene therapy methodologies. They also discuss recent results of studies on the aging process which, until not many years ago, appeared adventuristic. Today they are opening prospects of great interest.
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PMID:[Molecular medicine: new tools for better understanding and treatment of diseases in humans]. 1105 61

A 35-year old man presented with fever, weight loss, drenching night sweats and symptoms of cardiac failure for three months. Examination revealed wasting, peripheral oedema, bilateral pleural effusion and constrictive pericarditis. A diagnosis of constrictive pericarditis with bilateral pleural effusion probably due to tuberculosis was made. Human immunodeficiency virus antibodies and six sputum for acidfast bacilli were negative. Electrocardiograph revealed low voltages globally and echocardiography showed global myocardial hypokinesia. He had pericardiectomy, pericardial and pleural histology was non-specific inflammatory reaction but myocardial histology showed granulomatous changes of tuberculous myocarditis. We suggest that in experienced hands myocardial biopsy could be useful in making the diagnosis.
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PMID:Tuberculosis myocarditis: a case report. 1192 29

Cardiovascular infections due to Salmonella enterica are infrequently reported, so their clinical features, prognosis, and optimal treatment are not completely known. Mortality associated with aortitis and endocarditis caused by nontyphoidal Salmonella remains exceedingly high. In this review of cases of cardiovascular infections due to Salmonella enterica studied in 2 hospitals in Madrid, we tried to assess the clinical manifestations and the procedures leading to diagnosis in addition to treatment and outcome. To complete the spectrum of infections related to cardiovascular surgery, cases of postoperative mediastinitis, pericarditis, and infections associated with cardiac devices were also included.Twenty-three patients were reviewed: 11 had mycotic aneurysms; 7 had endocarditis; 2 had device-related infections; and 3 had pericarditis, mediastinitis, and infection of an arteriovenous fistula, respectively. The risk of endovascular infection in patients older than 60 years with bacteremia due to nontyphoidal Salmonella was 23%. Most patients with aortitis had risk factors for atherosclerosis, and 6 had preexisting atherosclerotic aortic aneurysms. All except 1 patient with endocarditis had underlying cardiac disorders. Acquired immunodeficiency disease (AIDS) was a major risk factor for salmonella bacteremia in 1 patient with aortitis and 1 with endocarditis. Fever, unremitting sepsis, "breakthrough" and relapsing bacteremia were the most common clinical findings. In addition, abdominal or thoracic pain and cardiac failure and pericarditis were common features in patients with aortitis and endocarditis respectively. Computed tomography (CT) scan, arteriography, and echocardiography were the main diagnostic tools. Mortality associated with mycotic aneurysms and endocarditis due to S. enterica was 45% and 28%, respectively. Thoracic aneurysms, rupture, and shock at the time of diagnosis were associated with increased mortality in patients with aortitis. In situ bypass grafting was successfully performed in most cases. After surgery, antimicrobial therapy was continued for 4-9 weeks. No relapses were observed after a mean follow-up of 64 months. Antimicrobial therapy alone or combined with valve replacement or excision of a ventricular aneurysm was successful treatment for most patients with salmonella endocarditis. Combined medical and surgical treatment was required for patients with mediastinitis and pericarditis, and patients with device-related infections needed removal of the complete device. Diagnosis of aortitis due to nontyphoidal Salmonella should be established as early as possible to reduce mortality. Patients older than 60 years who have positive blood cultures for Salmonella along with fever and back, abdominal, or chest pain should have an extensive workup for infective aortitis. Immediate bactericidal antimicrobial therapy should be started and a CT scan should be performed on an emergency basis. If a mycotic aneurysm is found, surgical resection should follow as soon as possible. Resection of the aneurysm with in situ bypass grafting is the procedure of choice. Postoperative antimicrobial therapy for 6-8 weeks seems enough to avoid relapses. Optimal treatment of patients with endocarditis occurring on ventricular aneurysms must include resection of the aneurysmal sac. Salmonella endocarditis can be successfully treated with antimicrobials alone. Valve replacement should be reserved for patients with cardiac failure or persisting sepsis, and for those who relapse after discontinuation of antimicrobial therapy.
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PMID:The spectrum of cardiovascular infections due to Salmonella enterica: a review of clinical features and factors determining outcome. 1502 66

Spontaneous hepatobiliary tumors in non-human primates are uncommon. Here we report a case of hepatic carcinoma and a case of hepatic focal nodular hyperplasia (FNH) and myelolipoma in two captive chimpanzees. A 16-year-old male chimpanzee (4X0392) died after an 8-month history of hepatic amyloidosis and low-grade anemia. Necropsy findings included a hepatic neoplasm with highly pleomorphic hepatocytes arranged into irregular thickened trabeculae. The diagnosis was high-grade hepatocellular carcinoma. A second male chimpanzee (4X0080), 23 years of age, died suddenly of heart failure secondary to cardiomyopathy. An incidental finding at necropsy was a liver mass characterized by multinodularity, prominent fibrous septa, and biliary hyperplasia. These features were consistent with FNH. While 4X0392 had no history of experimental viral exposure, 4X0080 was vaccinated with inactivated hepatitis B virus, an attenuated hepatitis A virus, and was experimentally infected with hepatitis C virus and human immunodeficiency virus. A survey of the literature revealed 68 reported cases of hepatobiliary tumors in non-human primates, including 12 hepatocellular adenomas, eight cholangiocellular adenomas/cystadenomas, 22 hepatocellular carcinomas, seven cholangiocarcinomas, and seven gallbladder adenocarcinomas. The majority of reported cases have been in prosimians and Old World monkeys. Hepatic neoplasia is rare in chimpanzees. Only four hepatic neoplasms have been reported in chimpanzees, three of which were associated with viral hepatitis. FNH has not been previously described in any non-human primate.
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PMID:A case report of hepatocellular carcinoma and focal nodular hyperplasia with a myelolipoma in two chimpanzees and a review of spontaneous hepatobiliary tumors in non-human primates. 1506 32

Highly active antiretroviral therapy is effective in the management of AIDS. It has improved the prognosis of human immunodeficiency virus (HIV) infection. However, with increased survival, adverse effects from medications used in HIV treatment have become more apparent. Cardiac complications from HIV infection include arrhythmias, heart failure, and coronary artery disease. Heart failure in HIV disease may be related to the virus itself or to noninfectious reasons. The association of HIV medications with heart failure is controversial as patients with HIV disease often have multiple risk factors for developing heart failure. We present a case of acute onset heart failure in a patient with HIV, coronary artery disease, and hypertension who was recently started on antiretroviral therapy. There was complete resolution of heart failure after cessation of HIV medications. This case highlights the need to consider HIV medications as a cause of deterioration in cardiac function, even in the presence of other well-established risk factors for heart failure.
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PMID:Acute reversible heart failure with highly active antiretroviral therapy. 1526 27

Over the past decade, the course of human immunodeficiency virus (HIV) infection has been markedly altered by highly active antiretroviral therapy (HAART). As advances in early diagnosis and aggressive therapy, as well as better supportive care, become available to more HIV-infected patients, survival is being prolonged and more patients are experiencing cardiac abnormalities. Cardiovascular manifestations of pediatric HIV infection have especially proven to be an ongoing challenge to practicing physicians, who face cardiac abnormalities ranging from asymptomatic cardiomyopathy to severe heart failure. Antiretroviral therapy has substantially decreased vertical transmission of HIV; however, studies of adults receiving HAART have found increased peripheral and coronary artery disease. Children exposed to this therapy in utero are thus at an increased risk for toxicity and cardiac abnormalities, regardless of their HIV status. Preliminary studies have reported complications including lactic acidosis and mitochondrial toxicity, as well as cardiomyopathy. Further studies are needed to explore the long-term effects and possible toxicities of prophylactic antiretroviral therapy on infants born to HIV-infected mothers.
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PMID:Cardiovascular effects of HAART in infants and children of HIV-infected mothers. 1547 Feb 74


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