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)

We performed right ventricular endomyocardial biopsies in 23 patients with dilated cardiomyopathy aged 45 +/- 14 years. All patients had congestive heart failure of unknown etiology dating up to one year before the procedure (57% less than 3 months). NYHA functional class was II in 5, III in 12 and IV in 6 patients. All patients had evidence of systolic dysfunction and a dilated left ventricle (LV diastolic dimension 68 +/- 11 and systolic dimension 55 +/- 11). Definite evidence of myocarditis, based on findings of inflammatory infiltrate and cellular damage, was found in 6 patients (26%), borderline myocarditis in 9 and abnormalities consistent with dilated cardiomyopathy in 8. The incidence of myocarditis here reported is lower than previously figures based on findings of more than 5 lymphocytes per high power field. In this series, clinical and functional aspects of heart failure did not differ in patients with or without evidence of myocarditis.
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PMID:[Incidence of myocarditis in patients with dilated cardiomyopathy]. 213 22

We studied the expression and distribution of atrial natriuretic polypeptide in the ventricles of 27 autopsied children with Kawasaki disease. Fourteen of the children had died in the acute stage of the disease. Three without any coronary artery aneurysms died due to myocarditis, while 11 with coronary artery aneurysms also had myocarditis but died of coronary heart disease. Histologic evidence of acute myocardial infarction was noted in three children who died of coronary heart disease. In the 14 children with acute-stage deaths, no abnormal expression of atrial natriuretic polypeptide was noted in the ventricles, despite the presence of heart failure in seven of them for 2 to 22 days before death. The other 13 patients had coronary artery aneurysms and died in the healed stage. In three patients with granulation tissue and congestive heart failure, myocytes in foci around the granulations were moderate to markedly positive for atrial natriuretic polypeptide. These three patients died over 8 days after the onset of their first myocardial infarct. Of 10 patients with old myocardial infarction, four had a history of congestive heart failure. They demonstrated moderate or marked atrial natriuretic polypeptide expression in extensive regions around sites of massive fibrosis, and foci of slight expression in the inner third of the noninfarcted region of the ventricle. In the other six patients without congestive heart failure, there was slight or moderate expression in foci around sites of massive fibrosis. We concluded that the expression of atrial natriuretic polypeptide appeared more than 1 week after the onset of acute myocardial infarction in the ventricles of children with Kawasaki disease who died in the healed stage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression and distribution of atrial natriuretic polypeptide in the ventricles of children with myocarditis and/or myocardial infarction secondary to Kawasaki disease: immunohistochemical study. 214 84

Specific-pathogen-free white leghorn chickens were inoculated at 1 day of age with avian leukosis virus (ALV, RAV-1). All chickens in Expt. 1, killed 33 or 64 days postinoculation, had focal chronic lymphocytic or lymphoplasmacytic myocarditis. Among those held beyond 33 days, eight of 22 developed lesions in the myocardium that resulted in a chronic circulatory syndrome (CCS) typical of right-sided heart failure. Chickens in Expt. 2 were held for 210 days, and 21% of 125 developed CCS. In Expt. 2, ALV particles were found by electron microscopy in myocardium of 100%, 72%, and 89% of inoculated chickens that developed CCS, lymphoid leukosis, or that had no gross lesions, respectively. These findings were in accord with the immunoperoxidase staining of tissue sections for group-specific antigen of ALV. In areas of extensive virus replication, there were often abnormal virus particles and also round bodies, which may have been remnants of host-cell membranes formed in the budding process. In contrast to findings in hearts, the spleens were usually negative for virus and viral antigen.
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PMID:Chronic myocarditis and circulatory syndrome in a White Leghorn strain induced by an avian leukosis virus: light and electron microscopic study. 215 91

85 cases of virologically proved viral myocarditis were followed up for 96.45 +/- 23.7 months for a better understanding of the late prognosis of this disease. Among these cases, 63 (74.1%) were cured, 14 (16.5%) remained with sequelae, 8 (3.5%) became chronic and 5 (5.9%) of the patients died. Most of the abnormal findings, i.e. physical signs, x-ray, ECG and UCG changes, originally existing on admission of the survived patients disappeared. The clinical features of the chronic cases resemble those of cardiomyopathy. The main causes of death were heart failure and sudden death. In order to reduce mortality, sequelae and chronicity, the importance of early virological examination, early clinical diagnosis and early and persistent treatment are stressed.
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PMID:[Late prognosis of viral myocarditis]. 216 32

The hearts of eight patients aged 22 to 67 years (mean, 41 years) who died during or within 4 days of interleukin-2 (IL-2) based immunotherapy for treatment of renal cell carcinoma or melanoma were studied at necropsy. Death resulted from combined cardiorespiratory failure in two patients, sepsis in four patients, acute myocardial infarction in one patient, and myocarditis in one patient. Transmural left ventricular necrosis was present in one of the two patients with significant atherosclerotic coronary artery narrowing. Noninfectious myocarditis was present in five patients: the inflammatory infiltrate was lymphocytic in four and composed of a mixture of eosinophils and lymphocytes in one. Although treatment-related deaths associated with high-dose IL-2 therapy are uncommon (1.5% in 652 consecutive patients), the potential for significant myocardial ischemia or myocarditis exists, and careful monitoring for arrhythmias or myocardial failure is warranted.
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PMID:Myocarditis or acute myocardial infarction associated with interleukin-2 therapy for cancer. 220 2

A 28-year-old male patient suffering from Wegener's granulomatosis died suddenly with signs of cardiac failure after clinical symptoms had basically subsided under chemotherapy. Autopsy revealed pulmonary granulomata, necrotizing vasculitis of the lungs and kidneys, focal and segmental necrotizing glomerulonephritis, and diffuse granulomatous and necrotizing giant cell myocarditis. Histological confirmation of inflammation of the heart in Wegener's disease has rarely been reported. Although cardiac involvement in Wegener's granulomatosis sometimes is suspected, it is usually thought to have no major impact on the course of the disease. By its dramatic clinical and morphologic presentation this case illustrates that the heart, in addition to the lungs and kidneys, may determine the outcome of the idiopathic granulomatous vasculitis of Wegener.
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PMID:Severe granulomatous giant cell myocarditis in Wegener's granulomatosis. 221 15

The causes, clinical indications and diagnosis and differential diagnosis of cardiac disorders which may lead to cerebral symptoms are illustrated on the basis of a review of the present day level of scientific research. Principally involved are cerebral ischaemias arising from cerebral embolisms or from reduction of cardiac output in cardiovalvular and myocardial disorders. The incidence of all embolisms of cardiac origin makes up 10% of all ischaemic cerebral infarcts, with auricular fibrillation, irrespective of its origin, mitral stenosis, myocardial infarct, mitral insufficiency and combined mitral valve defects, and, in younger patients, mitral valve prolapse, being, in this order of frequency, of primary clinical significance. The other cardiovalvular and myocardial disorders have, in comparison, a relatively low incidence of cerebral embolisms. Haemodynamically induced cerebral ischaemias frequently occur in the form of complications following acute cardiac arrest, in myocarditis and in case of primary cardiomyopathies resulting from cardiac insufficiency or complicating bradyarrhythmia. They are clinically apparent in the form of syncope, and other impairments of consciousness of various levels of seriousness with and without indications of cerebral origin, extending up to coma. In view of the high incidence of 25% of acute cerebral ischaemias in cases of cardiac disease, not only neurological but also detailed cardiological investigation is vital in all cases for a correct diagnosis and for the selection of a suitable course of treatment. Cerebral complications in bradyarrhythmia and endocarditis are discussed in the context of a review of the relevant literature together with consideration of their epidemiology, aetiology, pathophysiology and clinical profile. Pathological sinus-bradycardia, bradyarrhythmia absoluta, sinu-atrial and atrio-ventricular blockages, carotid-sinus and sick-sinus node syndrome, paroxysmal atrial tachycardia, AV-node tachycardias, and auricular fibrillation and flutter, taken as a whole, lead to cerebral complications affected patients in 5 to 10% of afflictions of the central nervous system occur in 50% of patients suffering from complete AV blockage and, at a not precisely definable frequency, in patients suffering from other bradyarrhythmias. In addition to transitory, uncharacteristic symptoms such as dizziness, vertigo, impairment of vision and balance, presyncope, syncope and Adams-Stokes syndrome dominate the clinical profile. Endocarditis, with an incidence of 0.01 to 0.05% in the overall population, results in central nervous system complications in 12 to 25% of cases on average.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Heart diseases as a cause of cerebral symptoms and syndromes]. 222 59

Clinical signs of heart failure developed in two cardiac transplant recipients and were interpreted initially as graft rejection. Morphologic examination of explanted hearts revealed myocarditis with abscess formation and necrosis consistent with a bacterial process; Listeria monocytogenes was isolated from myocardial tissue in the first case and from blood in both. The first patient also developed signs of meningoencephalitis, but the second had no signs of infection outside the heart. Antimicrobial therapy and retransplantation were successful in eradicating listeriosis. The differential diagnosis of heart failure in cardiac transplant recipients includes infectious myocarditis due to L. monocytogenes.
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PMID:Listerial myocarditis in cardiac transplantation. 223 24

The pathologic study of the cardiac lesions in 25 persons who died of AIDS were studied from autopsies. Most of these patients were intravenous drug abusers (14 cases). Heart failure was symptomatic and lead to death in 4 cases. This study showed histological abnormalities in 76% of the cases. We observed 12 myocarditis. In 6 cases, pathogenes were found: Toxoplasma gondii (2), Cryptococcus neoformans (2), Candida (1), Aspergillus (1). A lymphocytic myocarditis was observed in 6 hearts. By immunohistochemical technique, we could distinguish 2 toxoplasmic myocarditis, and in 4 cases, solitary cysts in the myocardium without inflammation. The remaining lesions comprised respectively: 3 lymphocytic pericarditis, 2 marastic endocarditis and 1 dilated myocardiopathy.
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PMID:[Cardiac lesions in acquired immunodeficiency syndrome (AIDS). Apropos of an autopsy series of 25 cases]. 225 24

Mucocutaneous lymph node syndrome, Kawasaki disease, is a potentially fatal pediatric disease characterized by prolonged high fever, conjunctivitis, stomatitis. myocarditis, aseptic meningitis and coronary artery vasculitis. We present peritonsillar abscess as a previously unreported otolaryngologic symptom and presentation of Kawasaki disease. A previously healthy 7-year-old boy required hospitalization for a peritonsillar abscess. Despite adequate surgical drainage and appropriate intravenous antibiotics, the patients' systemic symptoms persisted. After the week of hospitalization, the child was transferred to the intensive care unit with acute myocarditis, heart failure and severe arthritis. The diagnosis of Kawasaki disease was confirmed with echocardiographic evidence of coronary artery aneurysms and the development of the characteristic hand and foot desquamation. The patient's symptoms resolved with salicylates and intravenous gamma globulin therapy. He was discharged in good condition after 3 weeks of hospitalization. This is the first report of Kawasaki syndrome presenting with peritonsillar abscess. Although we discuss a unique presentation of this disease. Kawasaki syndrome often exhibits other otolaryngologic findings early in its course. A literature review of the clinical characteristics, pathogenesis and therapy of this disease is presented.
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PMID:Peritonsillar abscess in Kawasaki disease. 226 96


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