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

We report a case of renal cell carcinoma with pulmonary metastases treated with recombinant alpha interferon and subsequently presenting as congestive heart failure due to a dilated cardiomyopathy. A 66-year-old man presented himself to the department of internal medicine at our hospital with a complaint of persistent cough with sputum on August 27, 1988. Ultrasonogram, computed tomography and angiography showed a right renal cell carcinoma and chest x-ray films disclosed bilateral multiple nodular shadows, probably representing metastases of the renal tumor. After being transferred to our department, the patient underwent the ligation of the right renal artery and vein and the postoperative treatment with recombinant alpha interferon, achieving a complete response for pulmonary metastases and a partial response for the primary region. On February 14, 1990 the patient was admitted to our hospital with a complaint of dyspnea to be diagnosed as congestive heart failure due to dilated cardiomyopathy. The interferon therapy was suspected to have caused the heart disease, and four months after discontinuation of interferon therapy the heart failure symptoms had improved, but hypokinesis of the cardiac wall still persisted. To our knowledge, this may be the first case of alpha interferon-related cardiomyopathy in Japan.
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PMID:[Dilated cardiomyopathy following alpha interferon therapy of renal tumor with pulmonary metastases: a case report]. 141 58

Although most cases of viral myocarditis are subclinical, some patients develop overt symptomatic disease. These patients may present with findings that range from benign myopericarditis to frank heart failure. Furthermore, a growing body of evidence links viral myocarditis with idiopathic dilated cardiomyopathy, sudden death, and chronic arrythmias. The pathogenesis of the disease is currently incompletely understood in humans but is being investigated in animal models. A multifactorial process involving direct viral damage, autoimmunity, and possibly vascular damage is emerging. Breakthroughs in rapid diagnosis, such as the use of DNA probes, are occurring and may soon provide the opportunity for early intervention. Although there is currently no widely accepted standard of treatment, promising new therapeutic modalities are under investigation. These include the use of general immunosuppressive agents, T cell monoclonal antibody, interferon, specific immunization, and synthetic antiviral agents.
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PMID:Viral myocarditis. 196 11

All major types of human interferons (IFNs) have been purified and clinically administered as antitumor agents. We summarize here experience to date with toxicity of IFNs in cancer patients. The acute syndrome consists of fever, chills, myalgias, arthralgias, and headache, with some variation according to type of IFN, route of administration, schedule, and dose. Fatigue, perhaps reflecting CNS toxicity, is the most prevalent nonacute symptom. At high doses, IFNs are neurotoxic; the abnormalities seen by EEG resemble those in diffuse encephalitis. Hematologic toxicity consists mainly of leukopenia, but anemia and thrombocytopenia occur in some patients. Nausea, vomiting, and diarrhea are the main gastrointestinal symptoms. Elevation of serum transaminases seems to reflect liver toxicity. Renal function is well preserved, except for rare instances of acute renal failure. Cardiac toxicity remains questionable, although heart failure and arrhythmias have been associated with the administration of IFNs. Most, if not all, of these effects are reversible or can be ameliorated. With IFN alpha, the type most widely used in clinical studies, doses of 1 million to 9 million units (MU) are generally well tolerated, but doses greater than or equal to 18 MU yield moderate to severe toxicity. Doses greater than or equal to 36 MU can induce severe toxicity and significantly alter the performance status of the patient.
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PMID:Clinical toxicity of interferons in cancer patients: a review. 241 69

Heart failure is a disease characterized by chronically high levels of plasma norepinephrine and anergy in the cytotoxicity of circulating natural killer (NK) lymphocytes. This study shows that NK anergy extends to a significantly reduced cytotoxicity in response to the powerful NK stimulants, interleukin (IL)-2 and interferon (IFN)-alpha. Fifteen patients with heart failure, New York Heart Association stage III or IV, were studied for NK-cell-mediated cytotoxicity. The patients were divided into two groups based upon their NK cytotoxicity function: (1) those who had minimal baseline cytotoxicity and failed to respond following stimulation by IL-2 and IFN-alpha (n = 6), and (2) those who were about at the level of normal controls, and were responsive to IL-2 and IFN-alpha (n = 9). There was no relationship between the anergy and the etiology of the heart failure, laboratory indicators of heart failure, serum albumin or sodium, state anxiety, age or sex of the subjects. There was a statistically significant negative correlation between the response of NK cells to the stimulators IL-2 and IFN-alpha and the level of plasma norepinephrine in the heart failure patients. This was corroborated by in vitro testing of direct effects of norepinephrine on normal NK cells, which indicated that baseline cytotoxicity and the ability of these cells to respond to IL-2 were inhibited in a dose-dependent manner. The findings indicate that the NK cell anergy seen in heart failure patients extends to the response to the stimulators IL-2 and IFN-alpha in a subgroup of patients.
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PMID:Natural killer cell anergy to cytokine stimulants in a subgroup of patients with heart failure: relationship to norepinephrine. 761 55

Hemangiomas are the most common benign neoplasm in the neonatal period. While most small hemangiomas involute spontaneously, up to 20% may grow to a massive size and never completely involute. Massive hemangiomas are also frequently associated with life-threatening complications, such as airway obstruction, platelet trapping (Kasabach-Merritt syndrome), and high-output heart failure. The use of interferon alfa-2a for the treatment of massive hemangiomas not responsive to traditional therapy has recently been reported. We present the successful use of interferon alfa-2a in a series of five patients with massive hemangiomas complicated by airway compromise, congestive heart failure, need for tracheotomy, Kasabach-Merritt syndrome, and failure to thrive, despite traditional therapy.
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PMID:The use of interferon alfa-2a for life-threatening hemangiomas. 777 25

Among the various anticancer drugs, used alone or in combination during courses of chemotherapy, anthracyclines (leader: doxorubicin) are responsible for direct myocardial toxicity, which can exceptionally be acute, but more often chronic with a delayed onset. This cardiotoxicity is directly proportional to the cumulative dose administered and the recommended total dose for doxorubicin is 550 mg/m2. The risk factors able to potentiate cardiotoxicity must be analysed before starting chemotherapy and follow-up by ultrasonography and/or isotope ejection fraction must be repeated before each course. The treatment of anthracycline-induced heart failure consists of digitalis alkaloids combined with angiotensin converting enzyme inhibitors. The cardiac toxicity of 5FU is currently explained by the theory of coronary spasm, based on clinical findings such as chest pain associated with ischaemic electrical modifications. The incidence of this toxicity is low, but it can be fatal. Exceptional examples include the cardiotoxicity induced by high-dose cyclophosphamide responsible for acute haemorrhagic myocarditis, potentiation of the cardiotoxic effect of anthracyclines by dacarbazine and plicamycin, and serious ventricular and supraventricular arrhythmias induced by amsacrine. Among the various cytokines used in oncology, interferon is responsible for heart failure, reversible after stopping treatment, but also for ventricular arrhythmias, or even sudden death, the pathophysiology of which still remains unclear.
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PMID:[Chemotherapy and cardiotoxicity]. 866 96

We report our management of a newborn presenting in utero with congestive heart failure secondary to a giant hepatic haemangioendothelioma. Control of heart failure was achieved by transcatheter hepatic artery embolization, and rapid regression of the tumor was observed after a course of alpha 1 interferon. The combination of hepatic artery embolization and interferon may be a useful approach in the management of this rare, potentially fatal condition.
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PMID:Hepatic haemangioendothelioma presenting with early heart failure in a newborn: treatment with hepatic artery embolization and interferon. 895 71

This report describes a female baby having a hemangioma over the right thigh that had appeared as an irregular bruise since two days old. Severe thrombocytopenia, consumptive coagulopathy, anemia, and heart failure developed at three months old. With a diagnosis of Kasabach-Merritt syndrome, systemic corticosteroid, vincristine, subcutaneous alpha-interferon, and massive plate transfusion were given. However, the platelet count remained low and the skin lesion enlarged gradually. Trans-feeding-arterial embolotherapy with a 5 ml pure ethanol (1 ml/kg) injection was performed at four months of age. Thirty days later, her platelet count recovered and the hemangioma shrunk in size. This case illustrates that absolute ethanol embolotherapy is an effective treatment for hemangioma with Kasabach-Merritt syndrome and may be life-saving for those with lesions refractory to medical therapy.
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PMID:Absolute ethanol embolotherapy for hemangioma with Kasabach-Merritt syndrome. 955 94

The main feature of idiopathic dilated cardiomyopathy is the dilation and impaired contractility of the left ventricle or both ventricles. The clinical picture with forward and backward failure is based on the pump impairment of the left ventricle. However, the clinical presentation of patients with dilated cardiomyopathy is indistinguishable from any other secondary form of heart failure. The symptoms of myocarditis are also often determined by the degree of left ventricular dysfunction and--apart from perimyocarditis-associated precordial discomfort--therefore also often indistinguishable from dilated cardiomyopathy. The differentiation of dilated cardiomyopathy from other myocardial diseases by noninvasive methods is insufficient. Without invasive tests about 1/3 of the patients will be diagnosed incorrectly. Therefore, invasive diagnostics including coronary angiography are necessary to differentiate dilated cardiomyopathy from other diseases, especially coronary artery disease. Standard laboratory findings and cytokine serum concentrations (e.g. TNF-alpha) are not suitable to differentiate dilated cardiomyopathy and myocarditis and endomyocardial biopsy is indicated. Endomyocardial biopsies have to undergo evaluation by standard histology and immunohistology, and should be tested for the persistence of infectious agents. According to cardiac catheterization and evaluation of the endomyocardial biopsy idiopathic left ventricular dysfunction can be further stratified using the criterion of a myocardial virus persistence and the presence/absence of inflammatory infiltrates. Idiopathic dilated cardiomyopathy (approximately 70 to 75%), virus-associated dilated cardiomyopathy (approximately 20 to 25%), myocarditis (approximately 7%) and autoimmune myocarditis (approximately 3%) are the 4 possible resulting forms of idiopathic left ventricular dysfunction. Beside conventional medical therapy there are new therapeutic concepts e.g. using interferon for enterovirus-positive patients and immunosuppression for autoimmune, virus-negative patients with a cellular infiltrate.
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PMID:[Clinical picture and differential diagnosis of cardiomyopathy and myocarditis]. 959 33

Diagnosis of inflammatory dilated cardiomyopathy relies on the histological and immunohistological examination of endomyocardial biopsies. Only with the demonstration of the etiological agents in the myocardium specific therapy can be attempted. Whereas the spontaneous course of endemic myocarditis with little hemodynamic impairment is fair, the prognosis of symptomatic myocarditis and dilated cardiomyopathy is poor, with complete restitution in 35% and a 10-year survival rate of 30%. Restriction of physical activity is a validated form of therapy with normalization of the heart size in 40 to 60%. Symptomatic medical therapy consists of digitalis, diuretics, ACE-inhibitors and vasodilators and betablocker therapy, where a reduction of mortality was demonstrated in clinical (sub)studies up to 60%. Specific forms of therapy in inflammatory cardiomyopathy rely on the demonstration or lack of viral persistence or signs of autoreactivity in the myocardial tissue. Immunosuppressive therapy in autoimmune forms improved cardiac function in up to 60% of the patients in controlled trials, when compared to controls (40%). The double-blind randomized myocarditis treatment trial, which unfortunately did not distinguish viral from autoimmune myocarditis could not demonstrate such a benefit, however. Depending on the etiology of the disease, immunomodulation with immunoglobulins or interferon or antiviral therapy with hyperimmunoglobulins are presently tested in clinical treatment trials (ESETCID) in patients with enterovirus-positive or cytomegalovirus-positive and adenovirus-positive chronic myocarditis. Specific therapies are aimed to avoid the progression of the disease which may ultimately lead to heart failure with a cardiac assist device or heart transplantation as ultimate therapeutic option.
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PMID:[Therapy of dilated cardiomyopathies with and without inflammation]. 959 34


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