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

A study of 55 patients with heart disease suspected of being viral in origin was carried out a Medical College Hospital, Nagpur, over a period of 2 years. Virus studies as well as other routine tests were carried out on all patients. In 19 patients a virus aetiology of the heart disease was proved by isolation of one of the subtypes of Coxsackie B virus and/or on the basis of fourfold rise in neutralizing antibody titre in paired sera. Of these patients, 5 had acute myocarditis and 5 had acute myopericarditis; 3 had acute pericarditis; 3 had congestive cardiac failure of obscure aetiology; 2 had pleuropericarditis, and the remaining 1 developed post-partum heart failure with cardiogenic shock. All had electrocardiographic abnormalities. Thirteen had cardiomegaly; 1 had a right-sided pleural effusion and 2 had pericardial effusion. Virus could not be isolated from pericardial fluid or pleural fluid in these 3 patients. Follow-up studies up to 10 weeks from discharge revealed that 8 patients were clinically normal but 4 of these 8 had persisting ST-T wave changes, and in 4 the electrocardiogram had returned to normal. Of the remaining 11 patients, 3 had persistent chronic heart failure, 3 had vague symptoms of praecordial pain but no abnormal signs, and 5 patients were lost to follow-up.
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PMID:Heart disease caused by Coxsackie virus B infection. 12 98

A follow-up study was made of 29 patients aged 21 to 45 years, some 15-158 months after acute myopericarditis. The mean follow-up period was 72.9 months. The follow-up investigation included recording of history, physical examination, laboratory tests, radiologic examination of the heart and lungs and electrocardiography. All but one of the patients were fit for fulltime work. Nine had residual cardiac symptoms, but the physical examination was negative in all but 2 of them. One patient had chronic cardiac insufficiency and hepatic enlargement. Another had sinus tachycardia and cardiac enlargement of moderate degree and impaired working capacity in relation to heart size. Cardiac murmurs without clinical significance were audible in three cases. The resting ECG was pathologic in only 6 cases. Orthostatic ECG evoked ECG abnormalities in 6 more cases. Exercise tolerance tests showed reduced working capacity in relation to heart volume in 5 of the 29 cases (17%). Four of these 5 patients had cardiac enlargement. There was thus good correlation between increase in heart volume and reduction of physical capacity. The prognosis in regard to cardiac function was good, as was also found in other comparable series in which the observation time was somewhat shorter.
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PMID:Acute myopericarditis. A long-term follow-up study. 101 66

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

The clinical outcome of 18 patients, who presented with a Coxsackie virus myopericarditis in 1965, was evaluated 23 years later. Five patients had died, two of them had had heart failure. Thirteen patients and 23 healthy control subjects underwent exercise testing with gas exchange analysis. Left ventricular (LV) peak filling rate (PFR) was estimated by digitized M-mode echocardiography. Left ventricular ejection fraction was measured at rest and during exercise by radionuclide angiography. All patients were free of cardiac symptoms. Their clinical examination and the chest X-ray were normal. Peak oxygen consumption was not decreased in the patient group compared with the control group. PFR was significantly lower in the patient group than in the control group, 10.2 +/- 0.4 vs 13.2 +/- 0.4 cm s-1, P less than 0.001 (mean +/- SEM). LV ejection fraction was normal at rest in all patients (58 +/- 1%). An abnormal LV ejection fraction response to exercise was observed in two patients. Our data indicate that long-term prognosis after acute Coxsackie virus myopericarditis is good in a majority of patients.
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PMID:Clinical outcome and left ventricular function 23 years after acute coxsackie virus myopericarditis. 231 17

Over a period of 6 years, only twelve cases of dilated cardiomyopathy were clinically diagnosed in Nigerians between the ages of 11-30 years at the University College Hospital, Ibadan, Nigeria. Eleven presented with heart failure, while the twelfth patient presented with a cerebrovascular accident. Two other patients also had a cerebrovascular accident. A history of febrile illness was obtained in seven, but in only three was fever unresponsive to antimalarials, documented on admission. Antistreptolysin-O titre was normal and erythrocyte sedimentation rates elevated in each of the patients. Leucocytosis was present in six, three had a four-fold rise or fall in antibody titres against Coxsackie-B viruses and one, a four-fold rise or fall against Toxoplasma gondii. Histological evidences of myopericarditis were found in three of the six patients who died. It is concluded that dilated cardiomyopathy is rare in young adult Nigerians, and that constitutional upset is common, as in children, but prognosis is poorer. Infections by Coxsackie-B viruses, T. gondii and possibly other viruses appear to be of major aetiological factors
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PMID:Dilated cardiomyopathy in young adult Africans: a sequel to infections? 629 52

The cardiac effects of chemotherapeutic regimens using high doses of cyclophosphamide (180 mg/kg over four days) were assessed in 32 patients with hematologic malignant neoplasms. Left ventricular systolic function, determined by the fractional shortening on echocardiogram, declined substantially five to 16 days after the initiation of cyclophosphamide therapy. Although pericardial effusion on echocardiogram occurred in 33% of the patients studied, ECG voltage decreased five to 14 days after beginning cyclophosphamide therapy even in those patients without pericardial effusion. Congestive heart failure was noted in nine patients (28%) within three weeks of cyclophosphamide administration. Six of these patients (19%) died of myocardial failure. Pericardial tamponade occurred in six patients (19%), including five who died of myocardial failure. Histopathologic and electron microscopic findings showed endothelial injury and a hemorrhagic myopericarditis. Cyclophosphamide in this high dose is associated with a toxic, often fatal, pericardiomyopathy. Depression of ECG voltage and systolic left ventricular function, though common, do not necessarily predict clinical cardiac deterioration.
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PMID:Cardiotoxicity associated with high-dose cyclophosphamide therapy. 723 84

Mixed connective tissue disease (MCTD) was first reported 25 years ago. This report provides an assessment of the course of juvenile (J) MCTD in 224 patients available in the literature until 1996, including our own 33 patients. Most patients improved and remissions were observed in 3-5% (up to 27%). Among the long-term problems, a loss in joint function was seen in up to 29% of the cases, renal involvement in up to 47%, restrictive lung disease in up to 54% and gastrointestinal manifestations consisting of oesophageal dysmotility in up to 29%. Cerebral involvement was rare but severe. Cardiovascular problems observed include cardiomyopathy, myopericarditis and pulmonary hypertension. Among other long-term problems were Raynaud's phenomenon and scleroderma-like skin changes in up to 86% of the patients. Seventeen of the 224 patients had died (7.6%) because of sepsis or infection (7), cerebral complications (3), heart failure (2), pulmonary hypertension (2), renal failure (2) or gastrointestinal bleeding (1). The mortality rate of JMCTD seems to be in the same range as that of juvenile systemic lupus erythematosus, dermatomyositis and scleroderma. When compared with the other connective tissue diseases, however, mainly minor long-term problems are seen in the surviving patients.
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PMID:Course of mixed connective tissue disease in children. 945 80

Patients with homozygous beta-thalassemia are chronically transfused and, if not assiduously chelated, are at risk for cardiac dysfunction. Available data suggest that even in optimally chelated patients, cardiac pathology is abnormal secondary to iron deposition, fibrosis, hypertrophy, and the structural effects of chronic anemia. Evidence of myopericarditis may also be found. Cardiac performance is usually only subtly affected, primarily with diastolic abnormalities not routinely detected on echocardiograms or nuclear scan. In poorly chelated patients, severe heart failure occurs and is easily predictable but invariably fatal, despite treatment with diuretics, vasodilators, inotropes, and antiarrhythmics. Based on successful prevention of heart failure with ACE inhibitors in other forms of cardiomyopathy, we suggest multicenter trials to explore methods to stabilize cardiac function in patients at risk for iron-induced heart disease. Long-term adverse effects of iron deposition, diastolic dysfunction, and abnormal hormone regulation need to be quantitated in patients reaching their third and fourth decades when the potential for ischemic cardiac disease could compound cardiac dysfunction.
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PMID:Diagnosis and management of iron-induced heart disease in Cooley's anemia. 966 46

Cardiovascular emergencies in oncology patients include all of the usual cardiac problems, as well as complications of cancer and its therapy. Pericardial effusions and tamponade, cardiac masses, and extrinsic compression of the heart and great vessels by tumor masses, or fluid collections may all occur. Certain tumors may secrete mediators that are directly toxic to the heart; for example, catecholamines are secreted by pheochromocytomas and serotonin is secreted by carcinoid tumors. Tumors can also cause arrhythmias due to the mediators they secret or to direct mechanical irritation of the heart or pericardium. Cancer therapy is also associated with cardiac emergencies. Perioperative myocardial ischemia or infarction, as well as arrhythmias, may complicate surgery. Pericardial effusions and tamponade can follow surgery, radiation, or chemotherapy. Chemotherapy with anthracyclines, mitoxantrone, and trastuzumab may prompt acute and chronic heart failure. 5-Fluorouracil causes coronary spasm in some patients, leading to angina, myocardial infarction, arrhythmias, and/or sudden death. Cyclophosphamide, particularly in high doses, may produce acute myopericarditis. Radiation may cause acute pericardial disease and late sequelae such as myocardial infarction, acute valvular insufficiency, or effusive constrictive pericarditis. Endocarditis also occurs in cancer patients in association with vascular access devices and immune compromise. This review will discuss each of these complications of cancer and its therapy.
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PMID:Cardiovascular emergencies in the cancer patient. 1086 14

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


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