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)

Fifty-eight children with laryngotracheobronchitis (LTB) were studied. Many were malnourished, or in the post-measles state, or had some lower respiratory tract or cardiac involvement. In these patients, factors helpful in assessing the need for relief of airway obstruction by tracheal intubation have been evaluated. A set of indications for intubation, which includes clinical and arterial blood gas features of LTB is suggested. Cognisance of complications of disease, where present, has also been taken. If cyanosis or muscular hypotonia or unawareness is present, intubation is urgently needed. When two of the following occur together, the need for intubation has arisen: (a) pulse rate greater than 170/min and respiratory rate greater than 55/min; (b) paCO2 greater than 37 mmHg; (c) paO2 less than 50 mmHg; and (d) a complication (cardiac failure or severe lower respiratory tract infection).
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PMID:Indications for intubation in laryngotracheobronchitis in black children. 23 52

The symptoms of the tourniquet syndrome (hypotonia, tachycardia, postischemic edema, hypercaliemia, metabolic acidosis, myoglobinuria, renal insufficiency) could be observed after embolectomy of saddle embolism in 37 patients. 19 patients died postoperatively; heart insufficiency was demonstrated by autopsy in 14 patients. The pathophysiology of heart failure in tourniquet syndrome was studied in dog experiments after unilateral and bilateral hind limb ischemia. The development of shock turned out to be more severe after bilateral ischemia--comparable to saddle embolism--than after unilateral ischemia. The course of heart failure after recirculation could be referred to hypercaliemia, hypermagnesiemia, metabolic acidosis and hemoconcentration. The prophylaxis of the tourniquet syndrome can be practised by knowing the pathogenesis.
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PMID:[The tourniquet-syndrome--a severe complication after embolectomy of saddle embolism (author's transl)]. 108 27

The case of surgical treatment of a 44-years old female with a double atrio-ventricular accessory pathway and mitral stenosis was described. Fast ventricular rates due to conduction through the accessory pathways during atrial fibrillation in course of mitral stenosis caused severe heart failure, occasionally with deep hypotonia. Combined treatment with prajmaline and propafenone blocked conduction through accessory pathways. The ventricular rate slowed from approx. 200/min to 150/min. Addition of digoxin slowed the ventricular rate down to approx 80-100/min. There were no signs of preexcitation. Treatment with diuretics and vasodilators was continued. The state of patient improved. Echocardiographic and hemodynamic evaluation revealed: mitral stenosis (orifice - 75 mm2) with moderate regurgitation, small aortic and tricuspid regurgitation. The coronary arteries were normal. On the base of the ECG recordings during atrial fibrillation both accessory pathways were localized on lateral and posterior parts of the left free wall. The patient was operated on. Both atrio-ventricular by-pass tracts were dissected using Sealy's method in Cox modification and then mitral valve prosthesis Medtronic-Hall 27 mm was implanted. Prajmaline and propafenone were discontinued and preexcitation did not recovered. The sinus rhythm was restored by electroversion. The patient had no overt heart failure on discharge from the Institute.
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PMID:[Dissection of the accessory conduction pathways with simultaneous mitral valve surgery]. 227 77

Five cases of infant glycogen storage disease of the heart are reported. Their ages ranged from 2 to 7 months. They all presented with generalized hypotonia and respiratory tract infections. Four of the diagnosis were proven by skeletal muscle biopsy and enzymatic assay of alpha-1,4-glucosidase. All 5 infants had clinical signs of cardiac failure, cardiomegaly shown by chest X-ray, short PR intervals, severe left or bi-ventricular hypertrophy shown on electrocardiograms, increased thickness of the right and left ventricular walls and interventricular septum both on M-mode and two-dimensional echocardiograms and angiocardiograms. Four of them died during the follow-up period with a mean age at death of 7.5 months.
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PMID:Clinical analysis of five infants with glycogen storage disease of the heart--Pompe's disease. 345 1

We examined a 14-month-old boy with severe muscular hypotonia and weakness. Loss of tendon reflexes were noted at age 2 months. Right-sided heart failure and dyspnea during sleep developed at age 4 months. Muscle biopsy revealed selective hypoplasia of type II fibers and normal type I fibers. Intercostal and diaphragmatic muscles showed similar changes at necropsy and probably accented the respiratory failure.
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PMID:Congenital myopathy with type II muscle fiber hypoplasia. 234 10

The vein of Galen malformation is a rarely recognized cause of congestive heart failure in the newborn. This report describes a newborn who developed severe cardiac failure in the second week of life. An aneurysm of the vein of Galen was noted on the computerized tomography scan, confirming the clinical diagnosis of cerebral arteriovenous fistula. The vascular abnormality was well shown by cerebral arteriography. At the age of four weeks, surgery was carried out by clipping the afferent arteries. The patient is non a three years old infant with moderate developmental delay and hypotonia.
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PMID:[Aneurysm of the vein of Galen with neonatal cardiac insufficiency. Success of early neurosurgical treatment]. 365 18

We describe 8 patients with muscle carnitine deficiency, 7 males and 1 female, varying in age from 5 days to 64 years. Seven had decreased muscle strength and all had increased lipids droplets in the muscle biopsy. The symptoms began in the first days of life in three cases, in childhood in two, in adult life in two, while one case was free of symptoms at age 64 (heterozygote?). Some patients had difficulty chewing, dysphagia, hypotonia and splenomegaly; one patient had a fluctuating clinical course. All had elevated serum enzymes, mainly creatine-kinase. The electromyogram showed primary muscle involvement in one case, denervation in two, "mixed" features in two and was not done in three. The muscle biopsy, beside lipid storage, showed denervation in four, chronic myopathy in four and type II fiber atrophy in one. In two cases, histological findings suggested infantile spinal muscle atrophy. One patient appeared to have a systemic form of carnitine deficiency, with severe myocardial involvement and died of heart failure before treatment was initiated. A discussion about clinical findings, metabolism and therapeutic aspects of muscle carnitine deficiency is made.
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PMID:[Muscle carnitine deficiency: report of 8 cases with clinical, electromyographic, histochemical and biochemical studies]. 409 39

Four infants with Down syndrome developed cor pulmonale and heart failure in association with chronic upper airway obstruction. Features of the sleep apnea syndrome were conspicuous; namely, noisy breathing with retraction, cyanosis and frequent apnea during sleep, and daytime lethargy and somnolence. The clinical picture masqueraded as cyanotic congenital heart disease. Arterial blood gas analyses revealed alveolar hypoventilation, especially during sleep. The nature of the obstructive element was variable. Adenoidectomy provided partial relief in one patient, and tonsillectomy and adenoidectomy resulted in temporary improvement in two others. Three patients were markedly benefitted by tracheostomy. Functional inspiratory pharyngeal closure was demonstrated fluorographically in one patient. Infants with Down syndrome may be predisposed to upper airway obstruction by virtue of hypoplasia of facial and oropharyngeal structures and generalized hypotonia. Additional obstructive elements may be contributed by hypertrophied lymphoid tissue, excessive secretions, and glossoptosis. Removal of the obstructive element is helpful, but functional obstruction may only be relieved by tracheostomy.
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PMID:Alveolar hypoventilation and cor pulmonale associated with chronic airway obstruction in infants with Down syndrome. 645 3

We report two patients with Opitz trigonocephaly syndrome. Both children showed the pattern of abnormal findings characteristic of this syndrome, including trigonocephaly, upslanted palpebral fissures, inner epicanthic folds, broad alveolar ridges, small chin, short neck with loose skin, muscular hypotonia and cardiac defect. An 8-week-old girl had multiple gingival frenula, brachydactyly, syndactyly of toes and anal stenosis in addition, while a boy who died at 28 h from cardiac failure showed multiple joint contractures, cryptorchidism and renal cortical cysts.
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PMID:Optiz trigonocephaly syndrome: report of two cases. 669 65

An infant with hypotonia, gross cardiomegaly and heart failure is described. Angiocardiography revealed a hypertrophic restrictive cardiomyopathy. The diagnosis of type II glycogenosis was confirmed by the total absence of alpha-1,4-glucosidase in cultured skin fibroblasts. It is now possible to offer prenatal diagnosis by amniocentesis to women at risk of having affected children.
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PMID:Angiocardiographic and enzyme studies in a patient with type II glycogenosis (Pompe's disease). A case report. 677 81


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