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

In patients with mitral lesions and prevalence of stenosis and insufficient circulation of the I, II A and B stages clinical and functional indicators of the cardiac work were studied at three different altitudes, viz. with a low-mountain relief (760 m), middle-mountain relief (1650-2020 m) and in highland (3600-4200 m). In highland decompensated mitral incompetence was found to be characterized by a much higher incidence of such manifestations of the disease as vertigo, syncopal attacks, fits of distressed respiration, epigastral pulsation, positive venous pulse, a significant expansion of the heart to the right, accentuation and splitting of the II tone on the pulmonary artery, overloading of the right ventricle and atrium (according to ECG findings), the absence of peripheral edematization and fibrillation arrythmia, the presence of arterial and venous hypotension, highly intensive hyperventilation, a drop of PAO2 and PACO2. In patients-residents of low- and middle-mountain regions the severity of clinical and hemodynamic disorders depended on the stage of cardiac insufficiency, whereby in residents of the second region the disclosed deviations on the level of circulation proved more marked. It is shown that the correlation links between individual physiological variables become greatly disrupted parallel with progressively increasing severity of cardiac incompetence. In conditions prevailing in the middle and, especially, high altitude areas there are evident links between individual functional indicators which are absent in low-mountain areas. The above data bear evidence not only to the fact that with progressive severity of cardiac insufficiency the disrupted regulation of the circulation system becomes still more aggravated, but also to the presence of other compensatory mechanisms that are operative in mountain areas.
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PMID:[Diagnostic characteristics of cardiac insufficiency under mountain conditions]. 13 12

Under ether anesthesia electrocardiograms were derived from Syrian hamsters (strain BIO 8262) suffering from cardiomyopathy and muscular dystrophy. In addition, ventricular weights and body weight were determined. Young hamsters -- not yet showing morphological signs of the cardiomyopathy with the exception of possible left ventricular hypertrophy -- demonstrated only a longer ventricular activation time than normal hamsters. With the onset of cardiac necrotization left axis deviation in frontal plane projection and right bundle branch blocks are developing in the cardiomyopathic hamsters followed by first degree atrioventricular conduction defects. During the late stage of the cardiomyopathy left bundle branch blocks are additionally arising, while left ventricular hypertrophy is disappearing. Since no overt heart failure is occurring in this strain of cardiomyopathic hamsters, gradual development of high degree conduction defects is assumed to terminate their lives. The electrocardiographic pattern of the hamster cardiomyopathy fits partly into that of human primary as well as secondary cardiomyopathy. Nevertheless, it seems to form an entity of its own, as arrhythmias, higher degree atrioventricular conduction disturbances, typical signs of ventricular or septal hypertrophy, abnormal P and Q waves, ST segment and T wave changes are lacking.
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PMID:Electrocardiographic changes in cardiomyopathic Syrian hamsters (strain BIO 8262). 14 76

A case of chlorpropamide-induced, symptomatic hyponatremia in a diabetic patient is reported. The hyponatremia was associated with loss of appetite, nausea, and vomiting. These symptoms caused reduced food intake which provoked severe hypoglycemia with disturbed consciousness. The hyponatremia developed when the chlorpropamide doses were increased from 400 to 600 mg/day. Withdrawal of chlorpropamide was followed by remission of hyponatremia. Chlorpropamide-induced hyponatremia is a rare complication and is due to an antidiuretic effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of adiuretin in the tubuli of the kidney. This case report and the analysis of 18 published cases in the literature show the following characteristics for chlorpropamide-induced hyponatremia: (1) Hyponatremia is a rare complication in the treatment of diabetics with chlorpropamide. The patients typically are female and over sixty. The dosage of chlorpropamide usually was 500 mg daily or even more. (2) Hyponatremia is often unrecognized for a long time because the symptoms are not specific. The characteristic symptoms include loss of appetite, nausea, vomiting, abdominal pain, confusional state and, rarely, convulsions and coma. Recovery occurs spontaneously after withdrawal of the drug. (3) The incidence of this type of hyponatremia is increased in cases of preexisting tendency to water retention such as heart failure and renal failure, and in cases of diuretic therapy. In the light of these findings, the authors believe that chlorpropamide is no longer a drug of choice in the treatment of diabetic women, especially in cases of preexisting tendency to water retention and in diuretic therapy. In such cases, a sulfonylurea without antidiuretic effect is to be preferred.
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PMID:[Hyponatremia and hypoglycemia after treatment with chlorpropamide. Case histories with review of the literature on 18 cases of chlorpropamide induced hyponatremia]. 66 98

A traumatic transection of the upper descending thoracic aorta, undiagnosed, was complicated on the tenth day by an acute obstruction of the descending thoracic aorta. The upper body hypertension resulted in generalised convulsions and cardiac failure with pulmonary oedema. The lower body ischemia resulted in paraplegia, acute ischemia of the lower limbs, liver failure and anuria. An emergency revascularisation of the lower body was achieved by axillary-bifemoral bypass. The improvement of the clinical status allowed complete repair of the aortic transection two days after the extra-anatomic revascularisation. This case emphasizes the severity of the cases with impaired blood flow to the lower body and the benefit of the extra-anatomic bypass in pathology of the upper descending thoracic aorta when complete repair of the aortic transection is associated with an extremely high risk.
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PMID:[Traumatic rupture of the aortic isthmus revealed by acute obstruction of the descending thoracic aorta]. 128 8

Fifty patients of grade III & IV malnutrition with diarrhoeal dehydration were rehydrated using the WHO recommended ORS. Serum sodium and potassium levels were estimated at admission and 24 hours later. Forty seven patients were successfully rehydrated orally. In 7 patients the level of dehydration at initial assessment was overestimated. Periorbital edema developed in 25.5% of the patients rehydrated. No patient had cardiac failure or convulsions during therapy. Though persistent hyponatremia and hypokalemia were found in 10.6% and 19.15% cases respectively after rehydration, the incidence decreased as compared to the pre-hydration levels and was comparable to that found in malnourished children without diarrhea who served as controls in the present study. Oral rehydration was discontinued in three patients due to development of excessive vomiting in one case and paralytic ileus in two. Thus WHO ORS can be used safely in children with severe malnutrition but constant monitoring is required.
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PMID:Oral rehydration therapy in severely malnourished children with diarrheal dehydration. 139 64

An hydropic infant was delivered at 32 weeks gestation by emergency Caesarean section for acute polyhydramnios. A diagnosis of cardiac rhabdomyomata was made on echocardiography. The baby survived 10 days, during which time repeated episodes of supraventricular tachycardia occurred. She eventually died of cardiac failure following an episode of septicaemia, convulsions and aspiration pneumonia. Necropsy showed multiple cardiac rhabdomyomata and numerous cerebral germinal layer and periventricular white matter nodules. This case stresses the importance of clinical investigations and perinatal necropsy in non-immune hydrops fetalis (NIHF) in determining the causes of clinical presentation and the underlying pathology.
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PMID:Tachyarrhythmia, cardiac rhabdomyomata and fetal hydrops in a premature infant with tuberous sclerosis. 160 81

The clinical spectrum of toxic effects and serum concentrations after ingestion of carbamazepine were studied in 82 pediatric patients. Serum carbamazepine level was related to the depth of coma (p less than 0.001), convulsions (p = 0.002), hypotension (p less than 0.001), and the requirement for mechanical ventilation (p less than 0.001). In 10 patients in deep coma with a Glasgow Coma Scale (GCS) of 3-4, the mean serum level was 213 mumol/L (range 143 to 343); seizures, ventilatory failure, or hypotension caused by myocardial failure and conduction defects were observed. In four of these, large doses of inotropic agents were required, one patient was treated with plasmapheresis, and two died--one of cardiac failure and one of aspiration pneumonitis. In 27 patients with moderate coma (GCS 5-8), the mean serum level of carbamazepine was 112 mumol/L (range 63 to 176); convulsions were observed in two patients in this group. In 45 patients whose conscious state was mildly depressed or normal (GCS 9-15), the mean serum level was 73 mumol/L (range 37 to 128); additional effects were drowsiness (80%), ataxia (53%), nystagmus (38%), vomiting (17%), and dystonia (7%). I conclude that patients with serum carbamazepine levels of approximately 100 mumol/L require close observation, whereas those with levels greater than 150 mumol/L may require intensive life support.
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PMID:Acute toxic reaction to carbamazepine: clinical effects and serum concentrations. 164 Mar 2

Two patients with Di George syndrome are presented. Diagnosis was done at ages 4 months and 16 days respectively. Their main clinical symptoms were hypocalcemic convulsions, unusual facies (hyperthelorism, low set prominent ears, micrognathia, short philtrum) and cardiac malformations (vascular ring with right aortic arc, aberrant left innominated artery and ligamentum arteriosus in one of them and Tetralogy of Fallot with pulmonary valve atresia in the other). The first patient is now a 3.5 year old boy, his vascular ring was repaired and he has hypoparathyroidism but no clinical nor laboratory evidence of cellular immunodeficiency. The other patient had evidence of heart failure at her second week of life, she died at age sixteen days and, at necropsy, Fallot's tetralogy with pulmonary valve atresia, closed ductus arteriosus, histologically normal ectopic thymus and absent parathyroid glands were demonstrated. We postulate that these cases correspond to partial forms of Di George syndrome.
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PMID:[Di George syndrome]. 184 46

An 83-day-old male infant had convulsions, hypertrophic cardiomyopathy, and lactic acidosis. Cranial computed tomography revealed low-density areas in both parieto-occipital lobes and in the left temporal lobe. Muscle biopsy did not reveal ragged-red fibers, but abnormal mitochondria were found in the capillary endothelial cells as well as in the muscle fibers. At 5 months of age, the patient developed purpura on the soles and palms. Skin biopsy showed degeneration of the endothelial cells with abnormal mitochondria in the arterioles and capillaries. Myelinated nerves in the skin had vacuolated axons with swollen mitochondria, and their myelin sheaths showed vacuolation. At 9 months of age, he died of heart failure, and autopsy revealed abnormal mitochondria in the myocardium but not in the coronary vessels. Our findings indicate that the symptoms of the mitochondrial encephalopathy, myopathy, lactic acidosis, and strokelike episodes (MELAS) syndrome cannot be fully explained by the mitochondrial angiopathy alone.
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PMID:MELAS of infantile onset: mitochondrial angiopathy or cytopathy? 186 30

Thirty out of 287 patients (10.4%) admitted to hospital for infective endocarditis between December 1970 and January 1990 had neurological complications. Twenty-three patients had native valve infectious endocarditis and 7 had prosthetic valve endocarditis. The clinical features were characterized by the frequency of aortic valve involvement (23 out of 30) and other complications, especially cardiac failure (16 cases) and peripheral vascular manifestations (7 cases). The commonest organism was the staphylococcus (53% of identified organisms) but the number of negative blood cultures was high (50% of cases). The neurological complication was often the presenting symptom of the endocarditis (19 cases) but it occurred after bacteriological cure in 4 cases. The complications observed were cerebral ischemia (16 cases), cerebral haemorrhage (11 cases), coma (2 cases), and one peripheral neuropathy causing a Claude Bernard Horner syndrome. These complications presented with hemiplegia in 17 cases, a meningeal syndrome in 8 cases, a convulsion in 1 case, a Von Wallenberg syndrome in 1 case, and a Claude Bernard Horner syndrome in 1 case. Twelve patients had a transient or permanent neurological coma. Cerebral CT scan showed ischemic lesions in 7 cases and haemorrhagic lesions in 10 cases. Carotid angiography demonstrated mycotic aneurysms in 6 patients. Twelve patients died: the cause of death was neurological coma (7 cases), low cardiac output (4 cases) and haemorrhagic shock (1 case). Four patients underwent neurosurgery: 3 for clipping a mycotic aneurysm and 1 for drainage of an intracerebral haematoma. Poor prognostic factors were: coma, cardiac failure, cardiac valve prosthesis and, above all, the extent and multiplicity of the neurological lesions. The authors propose the following measures to improve the prognosis: early surgery in cases of large and/or mobile vegetations especially when the infecting organism is a staphylococcus and when a systemic embolism has occurred; routine CT scanning and/or digitised cerebral angiography in all patients with infective endocarditis to detect surgically accessible mycotic aneurysms.
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PMID:[Neurologic manifestations of infectious endocarditis]. 201 89


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