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)

A man aged 70, descendant of an apparently healthy family, showed disorientation, delusional ideas and rages at 66. Later there was slowly advancing deterioration with muteness, disorientation and dysphagia. He died of cardiac failure. There was the diffuse atrophy of the cerebrum, which was remarkably accentuated on both temporal lobes (poles, T2 and T3), where the loss of nerve cells and proliferation of astrocytes were found in the cortex and pallor and conspicuous fibrillary gliosis were noted in the white matter. These findings fundamentally suggest Pick's disease. On the one hand, numerous senile plaques and Alzheimer's neurofibrillary changes, suggestive of Alzheimer's disease (senile dementia), were observed throughout the cerebral cortex. On the other hand, a few inflated cells were also seen in the cingulate, superior frontal gyri and temporal lobes. Basilar artery was moderately atherosclerotic and cerebrovascular disorders were distributed throughout the cerebral cortex and basal ganglia, especially in the field of supply of middle cerebral artery. This case is similar to rare cases reported by Berlin (1949), Neumann (1949) and Oyanagi et al. (1975). The nosological situation as a disease entity remains to be determined.
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PMID:An autopsy case of atypical senile dementia with atrophy of the temporal lobes--a clinical and histopathological report. 66 3

A syndrome on four dairy farms in which calves up to two months of age died suddenly during a period of excitement usually precipitated by feeding was investigated. The description given by owners was that during, or shortly after milk feeding, the calves grunted, fell and died within one minute. Post mortem examinations revealed patchy myocardial pallor but no other lesions or evidence of infectious disease. Histopathological studies revealed peracute myocardial degeneration. Biochemical examinations have shown a selenium deficiency in in-contact calves and since this was corrected, no further cases have occurred. It is suggested that this is an additional manifestation of the selenium deficiency syndrome and that in certain circumstances, a deficiency of available selenium renders cardiac muscle vulnerable to stresses which induce severe peracute damage and leads to cardiac failure and sudden death.
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PMID:Sudden death in calves associated with acute myocardial degeneration and selenium deficiency. 71 69

A crude, whole-body extract of female or male heartworms was injected IV into 28 dogs with and 22 dogs without heartworm (HW) infection. The female HW extract caused shock in 22 of 24 dogs with and 12 of 20 dogs without HW infection. The male HW extract induced shock in 4 of 4 dogs with and 1 of 2 dogs without HW infection. Prevalence of shock caused by female HW extract was significantly (P < 0.05) higher in dogs with than without HW infection; shock developed 5 to 30 minutes after HW injection. These signs were observed: marked decrease in blood pressure; collapse (initial collapse); paleness of mucous membranes; weak heart sounds; dyspnea; skin coldness; intestinal hyperperistalsis, and defecation; increases in RBC count, serum total protein concentration, serum osmolality, serum Na and blood glucose concentrations; and decreases in neutrophil, eosinophil, and platelet counts. Alanine transaminase, alkaline phosphatase, and lactate dehydrogenase activities increased substantially from the time of initial collapse to 24 hours after HW injection. Of 39 dogs with shock, 29 recovered from initial collapse, but 5 of the 29 subsequently collapsed again (secondary collapse), with bloody diarrhea followed by death. Of these 39 dogs, 6 died during initial collapse without bloody diarrhea, and 4 were euthanatized during initial collapse. It was confirmed that HW extract had, in fact, induced shock. These clinical, hematologic, and biochemical findings were fundamentally similar to those associated with shock resulting from administration of drugs, such as diethylcarbamazine and milbemycin D, in microfilaremic dogs with HW infection.
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PMID:Clinical, hematologic, and biochemical findings in dogs after induction of shock by injection of heartworm extract. 787 76

A total of 4676 patients and 1759 patients were treated with lisinopril and nifedipine respectively in a post-marketing surveillance study conducted in general practice in the UK. Patients were followed up for 12 months. Most of the lisinopril patients had hypertension, but a small number (180) had heart failure. Most of the nifedipine patients had uncomplicated hypertension, but some (22.57%) had other cardiovascular disease with or without hypertension. Lisinopril and nifedipine were equally effective in reducing blood pressure. During the study, 1.5% of hypertensive patients assigned to lisinopril died compared with 1.8% of patients assigned to nifedipine, and 15.1% of lisinopril patients compared with 19.7% of patients in the nifedipine group withdrew because of adverse events. Cough, malaise and fatigue, nausea and vomiting were more frequent causes of withdrawal from lisinopril than nifedipine. Conversely, headaches, pallor and flushing, oedema and palpitations caused more frequent withdrawals from nifedipine. Anaemia was more often encountered on nifedipine treatment than on lisinopril. In hypertensive patients, the frequency of first-dose hypotension was similar on both treatments. Serious events occurred in 0.8% and 0.5% of patients given lisinopril and nifedipine respectively. Lisinopril was well tolerated by heart failure patients: 16 patients (8.88%) died and an incidence of 4.44% of serious adverse events was reported, a pattern to be anticipated in such patients; dizziness, giddiness, dyspnoea, cough, nausea and vomiting were the most frequent causes of withdrawal; the incidence of first-dose hypotension was low (2.22%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Post-marketing surveillance of lisinopril in general practice in the UK. 811 50

Sickle cell disease is transmitted as an autosomal recessive trait. Symptoms of pallor, fever, abdominal and joint pain, and swelling of the liver, spleen, hands and feet first appear near the latter part of the first year of life. Intravascular sickling affects all organs. For clinical and therapeutic purposes, exacerbations may be classified as vasoocclusive or pain, aplastic, hemolytic or sequestration crisis. In addition to infection, complications include severe pain, cerebrovascular accidents, cholelithiasis, bone infarction, heart failure, hypotension and priapism. The most common cause of early childhood death is septicemia or meningitis due to Streptococcus pneumoniae. Complications may be reduced or prevented by early diagnosis through newborn screening, patient education, routine immunizations, administration of folic acid, pneumococcal and influenza vaccinations, penicillin prophylaxis, and early diagnosis and aggressive treatment of complications.
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PMID:Common problems in sickle cell disease. 781 Apr 78

A 78 year-old male presented with a bilateral pyramidal syndrome, urinary incontinence and mild intellectual slowing. He died seven months after onset of the neurological signs from cerebral infarct and heart failure. Neuropathological examination showed predominant involvement of the cerebral white matter including diffuse myelin pallor, astrocytic gliosis and small necrotic foci. Polyglucosan bodies were diffuse in the cerebral cortex, white matter, brainstem, cerebellum and proximal part of the cranial nerves. In these latter, some polyglucosan bodies were found within myelinated axons but the inclusions mostly involved astrocytic processes. This case is characteristic of the polyglucosan body disease. It is compared with the autopsy and biopsy cases previously reported in the literature.
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PMID:[Polyglucosan body disease]. 839 Aug 20

The history and findings at autopsy of a 9-year-old female with I-cell disease are reported. She manifested gargoyle face, progressive psychomotor retardation, and increased serum levels of lysosomal enzymes with decreased activities in peripheral blood lymphocytes. She received a bone marrow transplantation from her HLA-mismatched father when she was 8 years old. Rejection followed, and 9 months later, she died of cardiac failure secondary to aortic regurgitation. The characteristic inclusion bodies, ultrastructurally corresponding to double-membranous lamellar vacuoles and empty single membrane-bound vacuoles, were identified in dermal fibro blasts, macrophages, glomerular epithelial cells, cardiomyocytes and smooth muscle cells. Pale bodies, faintly eosinophilic cytoplasmic globular inclusions immunoreactive for plasma proteins, were observed in hepatocytes and renal collecting tubular epithelial cells. Enzyme histochemical analyses were performed for N-acetyl-beta-glucosaminidase, beta-glucuronidase, nonspecific esterase and acid phosphatase. Decreased activities of the acid hydrolases and their diffusion in the cytoplasm were seen in Kupffer's cells. Ultrastructural localization of acid phosphatase activity suggested the labilization of the lysosomal membrane. The abnormality in the intracellular transport of the acid hydrolases into the lysosomes in I-cell disease is briefly reviewed and discussed.
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PMID:I-cell disease: report of an autopsy case. 879 67

We reported about a rare case of painless Stanford type A acute aortic dissection with the only complaints being numbness and paleness in the right arm. A 68-year-old male who hed been treated in another hospital under the diagnosis of acute occlusion of the right subclavian artery was referred to our hospital because of severe heart failure and shock. After being admitted to our hospital, the patient was diagnosed as Standford type A acute aortic dissection with transesophageal echocardiography and underwent an emergency graft replacement of the ascending aorta and total aortic arch. The postoperative course was uneventful and the patient was discharged without any complications.
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PMID:[A case of painless Standford type A acute aortic dissection complicating acute occlusion of the right subclavian artery]. 952 30

We report the case of a 32-year-old woman who was admitted at hospital because of ortho-dyspnea, arrhythmia, and paleness. Clinical examination showed continuous arrhythmia, systolic heart murmur, enlargement of spleen and liver, and pathologic hematological parameters, thus indicating an intravasal hemolysis (elevated HBDH, bilirubin, and reticulocytes; reduced hemoglobin and haptoglobin levels), and bone-marrow-smears showed a typical cytomorphology of CDA III. The patient's diagnosis was heart failure caused by mitral valve insufficiency due to congenital atrioseptal defect associated with congenital dyserythropoietic anemia type III (CDA III).
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PMID:Congenital dyserythropoietic anemia type III associated with congenital atrioseptal defect has led to severe cardiac problems in a 32-year-old patient. 1091 87

Heart failure during the immediate period of an acute myocardial infarction constitutes a major insult to this pathology; since, once installed, it is associate to ventricular dysfunction and expansion of the left ventricle. It can appear either early or delayed. Subsequent to the acute insult, the myocardium is subjected to diverse changes in its anatomical conformation and to diastolic and systolic alterations, which will affect the hemodynamic constants of the patient. Changes in the parietal ventricular architecture as well as at the neurohumoral level will also occur. The clinical signs of heart failure are: dyspnea, pallor, tachycardia, diaphoresis, cold skin, oliguria, somnolence, and gallop, which can be observed at the very beginning of the coronary occlusion. Its clinical identification, through in-hospital studies supported by adequate hemodynamic monitoring, is of utter relevance since it will lead to appropriate and fast treatment. The groups of patients with acute myocardial infarction with high risk for the development of cardiac failure are: patients with extensive Q wave infarction, diabetic, patients over 65 years of age, and those with a history of previous myocardial infarction(s). The cornerstone of treatment must be focused on reducing the myocardial ischemia, which can be achieved through the use of modern therapeutics and, given the case, pharmacological agents, coronary intervention procedures, or cardiac surgery must be taken into account. At present it is known that angiotensin converting enzyme inhibitors, betablockers, inotropics, are useful to improve ventricular function in patients with acute myocardial infarction.
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PMID:[Heart failure in acute myocardial infarction]. 1200 71


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