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 main reason for myocardial dysfunction is chronical myocardial ischemia. Recently we could show, that NCAM (CD56), a neural cell adhesion molecule and member of the immunoglobuline superfamily, and the transcription factor AML1 (RUNX1) are overexpressed in chronic ischemic human heart failure compaired to normal hearts. Here we demonstrate, that the overexpression of NCAM (CD56) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy, hypertrophic obstrutive cardiomyopathy, myocarditis and sarcoidosis. Concerning the transcriptional regulation of NCAM (CD56) by AML1 (RUNX1) we isolated 3 novel isoforms of AML 1 (RUNX1) with different transactivating function, that might be a regulatory element of the NCAM (CD56) overexpression in chronical myocardial ischemia.
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PMID:[The overexpression of NCAM (CD56) in human hearts is specific for ischemic damage]. 1689 59

We describe 2 patients who developed prolonged QTc interval on electrocardiogram while being treated with voriconazole. The first patient had undergone induction chemotherapy for acute myelogenous leukemia, and her course had been complicated by invasive aspergillosis and an acute cardiomyopathy. She developed torsades de pointes 3 weeks after starting voriconazole therapy. She was re-challenged with voriconazole without recurrent QTc prolongation or cardiac dysfunction. The second patient had a significantly prolonged QTc interval while on voriconazole therapy. We recommend careful monitoring for QTc prolongation and arrhythmia in patients who are receiving voriconazole, particularly those who have significant electrolyte disturbances, are on concomitant QT prolonging medications, have heart failure such as from a dilated cardiomyopathy, or have recently received anthracycline-based chemotherapy. The potential for synergistic cardiotoxicity must be carefully considered.
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PMID:Torsades de pointes associated with voriconazole use. 1731 69

Pleural effusion has various causes. In the setting of aortic stenosis, new onset pleural effusion is generally considered as a consequence of heart failure. Here, we describe a 50-year-old male patient who had been followed with aortic stenosis for 30 years. During his admission he presented with exertional dyspnea and pleuritic chest pain. He had no other symptoms or findings of cardiac failure. Complete blood count revealed neutrophilic leukocytosis, a normal hemoglobin level and normal platelet count. Left sided pleural effusion was noted on the posteroanterior chest X-ray. Examination of the pleural fluid revealed myeloid blasts. Bone marrow aspiration smear and flow cytometric analysis of the bone marrow and pleural fluid were consistent with acute myeloid leukemia.
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PMID:An unusual cause of unilateral pleural effusion in the setting of aortic stenosis: acute myeloid leukemia. 1738 3

Hepatic angiomyolipoma is an extremely rare mesenchymal tumor. To study the clinical feature, diagnosis, treatment and prognosis of the rare presentation, the medical records of 8 patients presenting to Cancer Institute and Hospital, CAMS with the diagnosis of hepatic AML from January 1989 to December 2000 were reviewed retrospectively. There were five female and three male, with age ranged from 25 to 59 years (mean 39.6 years). Five tumors located in the right lobe of the liver, and three in the left lobe. Ultrasonography and computed tomography were performed in all cases. Magnetic resonance imaging and angiography were done in some cases. The myoid cells in all tumors showed over-expression of HMB-45. All patients had hepatic resection. Except for one patient died of heart failure after surgery, others survived well to date without tumor. In conclusion, comprehensive imaging features can reveal the characteristic components of hepatic angiomyolipoma. Reaction for HMB-45 can be used to confirm the diagnosis. Surgical resection is an effective treatment of hepatic angiomyolipoma.
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PMID:Hepatic angiomyolipoma: report of 8 cases and review of literature. 1758 51

Essential thrombocythaemia (ET) is an acquired myeloproliferative disorder with a prolonged clinical course and a near-normal life expectancy. Therapy is stratified according to risk of thrombohaemorrhagic events. In high-risk patients, platelet reduction is generally recommended. In intermediate-risk patients, therapy should be considered depending on the severity of associated risk factors, especially cardiovascular. In low-risk patients, a watch-and-wait approach is appropriate. Hydroxycarbamide is generally first-line therapy. Concerns for possible leukemogenicity make anagrelide or interferon-alpha possible choices in younger patients and those who are resistant or intolerant to hydroxycarbamide. Each pharmacotherapy is associated with specific long-term risks and benefits. The potential risk of major bleeding is the main drawback of aspirin. Hydroxycarbamide is an established, effective drug for ET, but it may increase the risk of transformation to acute myeloid leukaemia and may give mucocutaneous ulcers. Anagrelide is a licensed treatment that also reduces platelet counts and is generally well tolerated, with evidence that some common side effects diminish over time. Anagrelide can have cardiac effects due to inhibition of phosphodiesterase III and therefore requires cautious use in patients with cardiac insufficiency. There is no evidence of leukaemogenicity with anagrelide or interferon-alpha therapy. Interferon-alpha is the only treatment suitable for use during pregnancy, although it is not licensed in ET. While it is effective for platelet reduction, the use of interferon-alpha is restricted by psychiatric side effects. Our knowledge of the optimum pharmacotherapy for each patient with ET continues to evolve through research and clinical trials, particularly into the molecular basis of the disease.
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PMID:Long-term management of thrombocytosis in essential thrombocythaemia. 1862 98

Secondary acute myeloid leukaemia (AML) occurring after breast cancer is a rare long-term complication of the chemo- and/or radiation therapy required to treat breast cancer. The usually recognized curative option of these secondary AML includes courses of anthracycline-based chemotherapy followed by haematopoietic stem cell transplantation (HSCT). Cardiac dysfunction during AML treatment of these patients previously treated with anthracyclines for breast cancer has not been reported to date. We evaluated the evolution of cardiac function in seven patients treated with anthracyclines and/or autologous or allogeneic bone marrow transplantation for secondary AML occurring after breast cancer. All of the patients who received a cumulative anthracycline dose above the cardiac toxicity threshold developed cardiac symptoms during AML chemotherapy courses. Moreover, four of the five transplanted patients developed severe heart failure among which two were fatal. Thus, the risk of severe cardiac dysfunction after treatment of secondary AML following breast cancer must be taken in account as part of the therapeutic strategy of those patients. As discussed here, an accurate evaluation of risk factors, the use of sensitive detection tests and of cardioprotective drugs as well as that of non-cardiotoxic chemotherapy might decrease the occurrence and severity of this life-threatening complication.
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PMID:[High risk of cardiac dysfunction after treatment of secondary acute myeloid leukemia following chemotherapy and radiotherapy for breast cancer]. 1981 76

According to principles of clinical trial design, the demonstration of efficacy of a new treatment is based on comparing the response in the treated group with that of a control group receiving placebo or another active treatment. The need for a control group is also recommended by the major international institutions that govern the ethics and the practice of clinical research. Despite these principles and recommendations, inspection of a purposive sample of ongoing clinical trials listed in the NIH registry ( http://ClinicalTrials.gov ) reveals that as many as one-third of trials are uncontrolled. Since these trials were approved through a formal evaluation by ethics committees, the lack of adequate control was not perceived as a major deficiency in the study design. Most uncontrolled trials belong to the oncology/hematology area. If two extreme disease conditions for nature and progression are analyzed, such as acute myeloid leukemia (AML) and chronic heart failure (CHF), the difference in the prevalence of uncontrolled trials is very striking. The number of uncontrolled trials is only 13% in CHF, whereas it reaches 66% in the AML group. I believe that the underlying disease condition plays a primary role in orienting the design of the study: oncology and hematology may be fields in which uncontrolled studies are common, whereas in other fields, e.g., cardiology, this phenomenon can be reduced. Within the limitations of the selection process of the examined trials, the current analysis indicates that the clinical trial reality does not strictly follow experimental design theory and official recommendations.
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PMID:The uncontrolled clinical trial: scientific, ethical, and practical reasons for being. 2016 22

Although cardiac complications are some of the most serious complications of HSCT for leukemia, it is difficult to predict them. QTD has been reported as a predictor of heart failure and fatal arrhythmia in adults. The purpose of this study is to examine whether QTD predicts cardiac complications in pediatric HSCT. Eighteen patients (mean age, 6.9 yr; 11 ALL and seven AML) underwent high-dose cyclophosphamide treatment and total body irradiation as preparative conditioning for HSCT. QTD, QTcD, echocardiographic functional parameters, and cumulative anthracycline dose were evaluated. We compared these values between patients with and without cardiac complications. Among 18 patients, seven patients experienced cardiac complications (heart failure in four, arrhythmia in three). There were significant differences in QTD (43.7 ms in patients with cardiac complications vs. 30.2 ms in patients without the complications, p = 0.019) and QTcD (55.3 vs. 36.9 ms, p = 0.003) between the two groups. On the other hand, the cumulative dose of anthracycline and echocardiographic parameters were not significantly different between the two groups. Increases in QTD and QTcD during the pretreatment period may be risk factors for the development of cardiac complications during and after conditioning for pediatric HSCT.
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PMID:Increased pretransplant QT dispersion as a risk factor for the development of cardiac complications during and after preparative conditioning for pediatric allogeneic hematopoietic stem cell transplantation. 2110 6

Hodgkin lymphoma (HL) is a malignancy of the lymphatic system with an incidence of 2-3/100.000/year in developed countries. With modern multi-agent chemotherapy protocols optionally combined with radiotherapy (RT), 80% to 90% of HL patients achieve long-term remission and can be considered cured. However, current standard approaches bear a considerable risk for the development of treatment-related late effects. Thus, one major focus of current clinical research in HL is reducing the incidence of these late effects that include heart failure, infertility, chronic fatigue and therapy-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/t-AML). In previous analyses, t-MDS/t-AML after treatment for HL was associated with a poor prognosis. Nearly all patients died rapidly after diagnosis. However, more recent analyses indicated an improved outcome among patients with t-MDS/t-AML who are eligible for modern anti-leukemic treatment and allogeneic stem cell transplantation (aSCT). This article gives an overview of recent reports on the incidence and the treatment of t-MDS/t-AML after HL therapy and describes the efforts currently made to reduce the risk to develop this severe late effect.
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PMID:Therapy-related myeloid neoplasms in patients treated for hodgkin lymphoma. 2211 Aug 96

In this report, we present a successful reuse of a transplanted heart under complex clinical conditions. Our patient was the second recipient, a 63-year-old man with end-stage heart failure due to amyloid-induced cardiomyopathy. After an uneventful postoperative course, he was diagnosed with acute myelogenous leukemia 6 months after transplantation and died 10 months after transplantation. This outcome was determined by a malignancy in an immunosuppressed patient. Reuse of a transplanted heart in carefully selected patients is a possible alternative in an era of donor organ shortage.
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PMID:One heart in 3 patients. 2317 56


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