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

The case of a 27 year old patient with IgG-lambda-myeloma is reported. Examination revealed hypercalcemia and acute renal failure. The patient died of heart failure two days after diagnosis. Autopsy revealed an extensive calcification of the inner organs, in particular the heart.
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PMID:[Fulminating course of IgG plasmacytoma at a young age]. 308 20

An acute tolerance test per os using calcium (Ca) lactate at a dose of 0.25 mmol of Ca per kg of body mass (calcium tolerance test--CTT) was performed twice in healthy persons (HP) and in patients with chronic heart failure (CHF) of various degrees: before and after 3-day administration of the same dose of Ca lactate. The "double" CTT made it possible to detect in HP and CHF a "phenomenon of adaptation" to Ca excess in the body based probably on changes in the activity of calcium-regulating hormones. It was manifested in less marked and prolonged tolerance hypercalcemia and a more rapid and effective calciuretic reaction, and probably in decreased intestinal absorption of Ca. It pointed to reversibility of Ca metabolic derangements even in severe CHF and a possibility of their non-medicamentous correction.
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PMID:[Assessment of the calcium homeostatic state using the double calcium tolerance test]. 324 51

Cardiac autotransplantation (excision and reimplantation) is a unique model that isolates totally the cardiac afferent and efferent neural pathways and results in hemodynamic misadaptability to many provocative tests. Since the cardiovascular response to acute hypercalcemia is modulated by numerous factors among which the autonomic innervation plays a major role, the hemodynamic response to bolus administration of calcium gluconate was compared in normal and cardiac autotransplanted dogs. Twenty-two animals underwent an autotransplantation while a sham procedure was performed in 18 animals. Each dog was equipped with an electromagnetic flow probe positioned around the ascending aorta and with central venous and aortic catheters. Hemodynamic data were collected daily during 1 month, before and during rapid intravenous administration of calcium gluconate (0.90 mEq). Baseline hemodynamic studies indicate that for both groups myocardial failure is evident in the immediate postoperative period; despite progressive recovery, the autotransplants always show lower cardiovascular performance. Calcium administration elicits transient positive inotropism, which is more important in presence of myocardial failure; this is true for both control and autotransplanted dogs. In the early postoperative period, hemodynamic adaptability to this stress is impaired in the autotransplants. However, long-term results indicate that minimal differences subsist over time in response to calcium administration, and when they are observed, they result from interferences in baroreceptor regulation and reflexes.
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PMID:Acute hypercalcemia and cardiac autotransplantation in dogs: long-term hemodynamic adaptability. 353 97

Since the hemodynamic consequences of acute hypercalcemia are altered by numerous interferences we have evaluated the role of peroperative myocardial ischemia on the adaptability to rapid calcium increment. Twenty-two dogs served as control and 16 were submitted to 1 hour of myocardial ischemia along with topical myocardial cooling. Each animal was equipped with blood flow transducer positioned around the ascending aorta and with central venous and aortic catheters. During each study 0.90 mEq of calcium was rapidly injected and hemodynamic data were recorded until base-line resetting. This experimental protocol was carried out 3 hours postoperatively and then daily during one month. Base-line hemodynamic data indicated the presence of myocardial failure in the experimental group in the immediate postoperative period only. Rapid calcium administration elicited transient positive inotropic response, widening of the arterial pulse pressure, reflex bradycardia and no evidence of peripheral vasoconstriction. In the early postoperative period (3 hours after surgery) the failing myocardium is more sensitive to the inotropic effect of hypercalcemia. Twenty-four hours after surgery both groups of animals have the same hemodynamic response to this stress; thereafter for both groups this response gradually decreased and finally stabilized by the 6th to 10th day after surgery. Acute hypercalcemia bears hemodynamic consequences that are amplified early after peroperative myocardial ischemia. However in long term this surgical component widely used clinically does not interfered with the cardiovascular adaptability to this pharmacological stress.
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PMID:[Cardiovascular adaptability to acute hypercalcemia in the dog. The role of peroperative myocardial ischemia]. 383 Apr 46

There is an increasing use and variety of beta-adrenoceptor blocking agents (beta-blockers) available for the treatment of hyperthyroidism. Recent comparative studies suggest that atenolol (200mg daily), metoprolol (200mg daily); acebutolol (400mg daily), oxprenolol ( 160mg daily), nadolol ( 80mg daily) and timolol (20mg daily) produce a beneficial clinical response equal to that seen with propranolol ( 160mg daily). Most beta-blockers reduce resting heart rate by approximately 25 to 30 beats/min, although a lesser reduction is seen with those possessing intrinsic sympathomimetic activity such as oxprenolol and pindolol. While earlier studies employing large doses of intravenous propranolol concluded that beta-blockade reduced myocardial contractility, more recent non-invasive studies suggest that the predominant cardiac effect is on heart rate. In patients with cardiac failure, beta-blockers may, however, produce a profound fall in cardiac output. Nevertheless, in combination with digoxin they may be useful in controlling the atrial fibrillation of thyrocardiac disease. beta-Blockers improve nervousness and tremor (although to a lesser extent with cardioselective agents) and severe myopathy, and they also reduce the frequency of paralysis in patients with thyrotoxic periodic paralysis. There is often subjective improvement in sweating but usually no major effect on eye signs. Recent studies show a 10% reduction in oxygen consumption/basal metabolic rate with long term oral use of selective or nonselective beta-blockers. In addition, many agents (propranolol, metoprolol, nadolol and sotalol but not acebutolol, atenolol or oxprenolol) reduce circulating tri-iodothyronine (T3) concentration by between 10 and 40%, although the clinical significance of this effect (if any) is not established. beta-Blockers may also have endocrinological effects on gastrin, cyclic AMP, catecholamines and other hormone levels. Given in adequate dosage, propranolol has been shown to control thyrotoxic hypercalcaemia. Minor side effects (nausea, headaches, tiredness, etc.) are quite common but overall beta-blockers are well tolerated by the thyrotoxic patient. The major use of these drugs is in symptomatic control while awaiting definitive diagnosis or treatment. As an adjunct to antithyroid drugs or radioactive iodine, beta-blockers will produce a satisfactory clinical response in the weeks to months before these forms of therapy produce a euthyroid state. beta-Blockers are more convenient than antithyroid drugs in the control of patients receiving therapeutic radioiodine, in that continuous therapy and assessment of biochemical response is possible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of beta-adrenoceptor blocking drugs in hyperthyroidism. 614 1

The natural history of acute rheumatic fever (ARF) in adults has been studied from an analysis of 23 patients together with a review of a further 466 published cases. In contrast to the picture in juvenile ARF, in our patients (average age 55 yr), only arthritis (83%) and carditis (35%) were major criteria for the diagnosis. All patients had at least 3 minor criteria. To summarize, 39% of the patients, average age 56 yr were seen in their initial attack of ARF. In those patients with a previous history of rheumatic fever, the mean interval between the index attack and the first illness was 20.5 yr. Contact with young children appeared to be an important predisposing factor. None had an ESR of less than 50 mm in the first hour, even in the presence of cardiac failure. Findings in the acute illness included anemia (70%), hyperglobulinemia (70%), urinary sediment (66%), and hypercalcemia in 7 out of 12 cases. The response to treatment was good and only 1 patient of 13 followed-up developed a new valvular lesion. A survey of the literature shows that attacks of ARF may occur at any age; death in the acute episode is rare and occurs only in patients with severe preexisting valvular disease with congestive failure. The problem of diagnosing active carditis in the presence of rheumatic heart disease (RHD) is discussed. While juvenile ARF may be overdiagnosed, the diagnosis may be missed in the adult rheumatic patient whose cardiac state inexplicably deteriorates. In such patients evidence for a preceding streptococcal infection should be sought. Patients with a high risk of developing ARF include those with carditis in previous attacks, with preexistent RHD, and with several children in the family. These factors should be considered when advising on the duration of antibiotic prophylaxis.
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PMID:Acute rheumatic fever in adults over the age of 45 years: an analysis of 23 patients together with a review of the literature. 729 18

Typical symptoms of acute myocardial infarction led to admission of a 66-year-old female. Creatine kinase (CK) was 720 U/l on admission and together with CK-MB of 108 U/l fitted the clinical picture. The ECG showed complete left bundle branch block. The patient died a few hours later in cardiac failure. Massive hypercalcaemia of 6.2 mmol/l and hyperphosphataemia of 1.6 mmol/l suggested acute primary hyperparathyroidism already clinically which later could be verified by a parathormone level of more than 100 000 ng/l ("C-terminal assay"). At necropsy chief cell adenoma of the epithelial bodies was found, typical changes of primary hyperparathyroidism in the skeleton and kidneys, and disseminated calcifications and fresh necroses of cardiac muscle. The coronaries were normal. This is the first clinical report of fatal acute primary hyperparathyroidism due to hypercalcaemia-induced myocardial necroses.
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PMID:[Calcium induced necroses of cardiac muscle causing death in acute hyperparathyroidism (author's transl)]. 735 14

A patient with an intermediate state of human T lymphotropic virus type I (HTLV-I) infection and in whom autopsy showed multiple organ failure (MOF) associated with extensive metastatic calcification in systemic organs is described. A 56-year-old man presented with signs and symptoms of advanced cardiac insufficiency, respiratory disturbance and renal failure. Serologically, the anti-human T lymphotropic virus type I (HTLV-I) antibody titer and the levels of both calcium and parathyroid hormone-related peptide (PTHrP) were distinctly elevated. These data suggested a diagnosis of adult T cell lymphoma/leukemia (ATLL). However, examination of a peripheral blood sample revealed only a few atypical lymphoid cells (3%) associated with mild leukocytosis (white blood cell count, 13.7 x 10(3)/mm3). Lymph node swelling was systemic but mild, with some nodes up to 10 mm in diameter. The patient died of MOF. Adult T cell leukemia/lymphoma was unable to be diagnosed definitively because of the short duration of laboratory abnormalities and because of the discrepancy between the laboratory data and the magnitude of lymphoproliferation in both the lymph nodes and peripheral blood. At autopsy, the most conspicuous finding was extensive metastatic calcification in the multiple organs, including the heart, lungs, kidneys, tongue, liver, pancreas, spleen and systemic arterial walls. Very small numbers of medium-sized atypical lymphoid cells admixed with small reactive lymphocytes were identified in multiple organs, with no evidence of massive infiltration. Molecular analyses could not detect monoclonal integration of HTLV-I provirus DNA or monoclonality of T cell lineage cells. Parathyroid hormone-related peptide was demonstrated in the cytoplasm of the atypical lymphoid cells on immunohistochemical examination. The bone trabeculae generally showed distinct evidence of resorption associated with marked proliferation of osteoclasts. These findings suggested that the hypercalcemia in the present case was categorized as humoral hypercalcemia of malignancy rather than local osteolytic hypercalcemia.
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PMID:Multiple organ failure associated with extensive metastatic calcification in a patient with an intermediate state of human T lymphotropic virus type I (HTLV-I) infection: report of an autopsy case. 964 62

Cardiac abnormalities as a sign of hyperparathyroidism are common. A spectacular pitfall of peracute extended myocardiac hypercalcemia is reported. The history of a 30-year-old woman included symptoms such as insufficiency of the kidneys since childhood, secondary hyperparathyroidism, and hemodialysis for approximately 4 years. After kidney transplantation, the patient died from progressive heart failure. Three days before she died, CT showed a nearly white heart, and myocardial scintigraphy revealed a total infarction. The autopsy revealed a heart of normal size but with a weight of 590 g and with nearly bony texture. The histologic examination showed extended calcifications of the entire myocardium, thus explaining these findings. Laboratory photographs and electron microscopic images will be demonstrated. The metabolic pathogenesis of tertiary hyperparathyroidism and calciphylaxis is discussed. "Malignant" progression after kidney transplantation is stressed.
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PMID:Acute hypercalcemia of the heart ("bony heart"). 1135 Nov 91

The 4q-Syndrome: Here we report four cases of interstitial and terminal deletions of the long arm of chromosome 4. Case 1 is a 16 month old boy with del(4)(q12q21) who has soft dysmorphic features, tetralogy of Fallot, and severe developmental delay. Case 2 is a male infant with the same deletion and congenital cardiomyopathy. He suffered severe birth asphyxia and died at the age of 6 months. His father was found to have a complex chromosome 4 rearrangement. Case 3 is a female infant with del(4)(q33) who died of aspiration pneumonia. She was mildly dysmorphic and presented with heart failure and hypercalcaemia. Case 4 is a 8 month old girl who has del(4)(q33) and Pierre-Robin sequence. So far about 70 patients with microscopically visible deletions of chromosome 4q have been described. Although they vary in their phenotypes, they have several features in common. We suggest to use the term 4q-syndrome for all macrodeletions of the long arm of chromosome 4.
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PMID:The 4q-Syndrome. 1183 1


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