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

A case of chronic progressive heart failure in a bull, resulting from myocardial fibrosis, is reported. In view of the low concentration of copper in the liver, this condition is believed to be similar to that termed falling disease.
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PMID:[Myocardial fibrosis. A case of falling disease (author's transl)]. 115 58

Zinc, copper, and magnesium concentrations in hair were measured in groups of children varying in one condition--protein-energy malnutrition, ricketts, thalassemia, malignancy, cardiac failure, or after prolonged infection and in healthy controls. As compared with controls, copper and magnesium concentrations were low in all groups, whereas higher values were obtained for hair zinc. These results showed that a generalized copper and magnesium deficiency were observed in the southeastern part of Turkey. However, zinc deficiency couldn't be detected as far as the hair zinc values were concerned, although all of the subjects fell within the 50 percentile limits for their age-appropriate weights and heights.
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PMID:Zinc, copper, and magnesium concentrations in hair of children from southeastern Turkey. 170 58

The effect of copper deficiency on cardiac function and structure was studied in a strain of rats (SHHS/Mcc-cp) known to develop cardiac failure as adults. Restriction of dietary copper (less than or equal to 1 mg/kg vs. 6 mg/kg in adequate diets) at weaning in both sexes for a 6-wk period produced cardiac hypertrophy. Male rats developed more severe copper-deficiency symptoms than their female counterparts. In both sexes of copper-deficient rats, there was an increase in cardiac length, width, free ventricular wall thickness and septum thickness. Electrocardiographic tracings revealed greater QRS height among male copper-deficient rats. Heart rate also was substantially reduced in this group. The increased volume of myocardium occupied by mitochondria in the copper-deficient male rats might result in increased electrical resistance that would increase the QRS height; hypertrophy or anemia also could be contributory. Some male copper-deficient rats had prolongation of the QRS in a bundle branch block pattern. Maximal rates of rise and fall for left ventricular pressure were reduced in male copper-deficient rats. The gross histology indicated that this type of heart failure was more concentric than eccentric. The copper-deficient male rat may serve as a useful model for studying the concentric cardiac hypertrophy that occurs in humans.
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PMID:Copper deficiency in a genetically hypertensive cardiomyopathic rat: electrocardiogram, functional and ultrastructural aspects. 205 Dec 21

The authors made an autopsy study of 32 hearts from patients who died of acute myocardial insufficiency, rhythm disorders and heart ruptures at terms from 1 to 50 days. It was found that the infarction zone (IZ) showed an absolute lower content of copper that the noninfarction zone (NIZ). The relative content of copper in the IZ was lowest in patients who died of acute cardiac insufficiency. These data may be used in evaluation of destruction and healing processes in patients with myocardial infarction.
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PMID:[The copper content of the myocardium in the acute form of ischemic heart disease]. 208 88

Six neonates with aneurysms of the vein of Galen are described: five were associated with an intracerebral arteriovenous fistula and presented with heart failure in the neonatal period; one had hydrocephalus at birth. Two infants died from intractable cardiac failure within 48 hours of age and two from progressive hydrocephalus and cardiac failure at 8 months and 8 years respectively. Two of the infants had copper coil embolisation of the aneurysm--one has since died of an intracerebral haemorrhage. The diagnosis of an intracerebral arteriovenous fistula should be considered in any infant presenting with unexplained heart failure. Close attention to the volume of all arterial pulses, and the venous pulse in the neck as well as auscultation of the head for a cranial bruit may suggest the diagnosis, which can then be substantiated by cerebral ultrasound.
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PMID:Aneurysms of the vein of Galen. 233 30

3 cases of copper IUDs recovered during laparotomy from the sigmoid colon are presented. One woman was a 24-year old mother of 5 who had had 2 cesarean sections since the disappearance of her Cu-7 IUD in 1980. She had right upper quadrant abdominal pain for 1 year with gall bladder stones. The IUD was found lying 80% in the gut lumen. After colotomy she recovered. The 2nd woman was 31 years old, pregnant for the 4th time after failure of her IUD. She was experiencing a constant left iliac fossa ache. The IUD was shown to be extrauterine by ultrasound, could not be seen at laparoscopy, and was removed by colotomy. The 3rd woman was a 37-year old mother of 5, 19 weeks' pregnant, having a septic miscarriage on admission. She had labor induced, but the IUD was not expelled. Her pain worsened, and fever and tachycardia persisted. Emergency laparotomy revealed a perforated posterior uterine wall with the Cu-7 eroding the serosa of the sigmoid colon. It was removed but the defect was not repaired. She required a subtotal hysterectomy, and a second laparotomy with a temporary colostomy, and her recovery was complicated by pulmonary embolism and cardiac failure. These cases draw attention to the importance of proper management of patients with no visible IUD thread. Ultrasound, and if necessary x-rays and laparoscopy should precede laparotomy. Expulsion of an IUD is rarely unnoticed, nor should pregnancy with an IUD be assumed to be due to an expelled device.
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PMID:Recovery of the intrauterine contraceptive device from the sigmoid colon. Three case reports. 304 19

The importance of metals in normal and pathologic cardiovascular function has been recognized. Significant derangements in myocardial Ca2+, Mg2+, and Cu2+ have been reported in ischemic heart injury. We studied 3 groups of hearts: 1) fifteen specimens obtained from patients who had no heart disease, 2) nine specimens from patients who had expired from cyanotic congenital heart disease, and 3) ten specimens from patients who had expired from acute rheumatic heart disease with carditis and severe heart failure. None of the patients had undergone cardiac surgery. Left ventricular lateral wall Mg2+, Ca2+, Cu2+, and Zn2+ contents were measured by atomic absorption spectrometry. The results showed a significant decrease in myocardial Mg2- (Group I 177.06 +/- 32.71; Group II 155.66 +/- 14.79; Group III 149.00 +/- 13.29, p less than 0.05 and p less than 0.01, respectively), and Cu2+ contents (Group I 3.22 +/- 0.37; Group II 2.94 +/- 0.22; Group III 2.56 +/- 0.32, p less than 0.02 and p less than 0.001, respectively), and a rise in myocardial Ca2+ content (Group I 36.06 +/- 10.72; Group II 43.22 +/- 7.01; Group III 46.30 +/- 4.85, p = not significant, and p less than 0.01, respectively). The myocardial Zn2+ content did not change significantly (Group I 26.53 +/- 3.99; Group II 26.00 +/- 4.15; Group III 26.40 +/- 3.53). The myocardial Mg2+/Ca2+ ratio was reduced markedly in both groups (Group I 5.328 +/- 1.879; Group II 3.685 +/- 0.735; Group III 3.135 +/- 0.291, p less than 0.001 for both Groups II and III vs Group I). The latter results correlated closely with the myocardial Mg2+/Ca2+ ratios reported in experimental models in peri-infarction zones. Thus, the myocardium of patients who had expired from cyanotic congenital heart disease and acute rheumatic carditis is jeopardized by ischemia, with metal contents similar to the border areas in myocardial infarction.
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PMID:Myocardial metal content in patients who expired from cyanotic congenital heart disease and acute rheumatic heart disease. 717 80

Changes in the blood content of trace elements (E)--copper, zinc and iron--have been studied in 10 patients with ischemic heart disease subjected to cardiopulmonary bypass surgery. It has been shown that blood TE concentrations decreased considerably during surgery. Variability in blood TE levels could be accounted for by hemodilution caused by the administration of colloids and crystalloids that contained no TE under study. These solutions were used initially for filling assisted circulation device. However, it is noteworthy that the degree of hemodilution was not the only reason for the changes in blood TE content, as despite hematocrit normalization it was only blood iron content that returned to preperfusion level. It has been demonstrated that copper and zinc blood concentrations were considerably lower in patients developing heart failure in the early postperfusion period than in those with an uncomplicated postoperative period. It has been shown that the nature and degree of changes in copper, zinc and iron levels in the coronary sinus blood during heart surgery can be assessed by changes in their arterial blood content.
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PMID:[Changes in the content of microelements--copper, zinc and iron--in the blood of patients following cardiopulmonary bypass]. 823 30

Dietary copper restriction in rats results in cardiomyopathy. In rats fed copper-restricted diets from weaning for 5 to 8 weeks, a concentric hypertrophy is apparent, whereas postweaning copper restriction does produce cardiomyopathy without apparent hypertrophy. Both sets of circumstances appear to affect the integrity of the basal laminae of cardiac myocytes and capillaries. In rats fed copper-restricted diets from weaning, decreases in cytochrome c oxidase are related not only to copper's role as a coenzyme, but also to a marked decrease in the nuclear encoded subunits of the enzyme complex. Decreased levels of the delta-subunit of ATP synthase have been observed. However, such aberrations in mitochondrial enzymes, as well as morphologic alterations, apparently do not affect cardiac levels of ATP. This review suggests mechanisms of cardiac adaptation and initiation factors leading to cardiac hypertrophy. We present a hypothetical working model explaining the events leading to cardiac failure in the copper-deficient rat heart based on the present body of knowledge, and compare the pathology with other models of cardiomyopathies.
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PMID:A unified perspective on copper deficiency and cardiomyopathy. 837 91

The moose (Alces alces L.) in an acid rain affected region in south-west Sweden has developed a complex disease with numerous clinical signs, most of which are consistent with those of secondary copper (Cu) deficiency and/or molybdenosis in cattle and sheep. The clinical signs of the moose disease reported to date include diarrhoea, anorexia, emaciation, achromotrichia, alopecia, sudden heart failure and osteoporosis. Findings at necropsy included mucosal oedema, atrophied lymphoid tissues of the mucous membranes of the alimentary tract, neuropathy, neuronal degeneration and uni- or bilateral corneal opacity. In a study of clinically healthy animals from the affected region in Sweden over a 12-year period (1982-1994), the hepatic Cu concentration decreased by 50% and the liver and kidney cadmium (Cd) concentration decreased by 25-35%, while the molybdenum (Mo) concentration increased by 20-40%. These changes are probably related to an increase in the pH of the soil and water in the moose environment and a consequent change in the uptake of these elements by the plants consumed by the moose. It is noteworthy that the occurrence of the disease in the mid 1980s coincided with increased liming undertaken to counteract the noxious effects of acid rain in this region. Clinical signs and lesions of the moose disease resemble those reported for Cu deficiency and/or molybdenosis in cattle and sheep. To elucidate the complex, multi-faceted clinical signs of the moose disease, the clinical signs and necropsy findings are discussed in relation to the biochemical functions of certain well-known Cu-dependent enzymes, e.g. depigmentation of hair due to depressed tyrosinase activity, osteoporosis by depressed lysyl oxidase activity, sudden heart failure due to decreased activity of lysyl oxidase, cytochrome c oxidase and Cu/Zn-superoxide dismutase; in addition, mucosal lesions and ulcerations due to loss of activity of diamine oxidase as well as of lysyl oxidase and cytochrome c oxidase. It is concluded from the present findings that the moose disease is most probably a Cu deficiency and/or a molybdenosis-type syndrome.
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PMID:'Mysterious' moose disease in Sweden. Similarities to copper deficiency and/or molybdenosis in cattle and sheep. Biochemical background of clinical signs and organ lesions. 949 61


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