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)

Leukaemia and its associated therapy result in pathophysiological peculiarities relevant to anaesthesia. Leukaemic patients suffer from anaemia, coagulation disorders, and the consequences of immunosuppression. In addition, some patients show infiltrations of the oropharynx, potentially resulting in difficult intubation and/or pharyngeal haemorrhage. Mediastinal masses can induce complete airway obstruction during general anaesthesia. Patients with a white blood cell count (WBC) greater than 100,000/mm3 (hyperleukocytosis) can suffer from the leukostasis syndrome with acute respiratory failure as well as cerebral vascular occlusions and bleeding due to increased blood viscosity and disturbed microvascular perfusion. Since this syndrome may be triggered by surgery, the WBC should be reduced prior to general anaesthesia in patients with hyperleukocytosis. To avoid development of the leukostasis syndrome, transfusion of packed red cells should be restricted in these patients. Hyperleukocytosis can simulate in-vitro hypoxaemia due to the excessive oxygen consumption of the mass of leukaemic blood cells during routine blood gas analysis. Therapy of leukaemia can lead to the tumor-lysis syndrome with hyperuricaemia, hyperphosphataemia, hyperkalaemia, hypocalcaemia, and hypoglycaemia, and may induce acute renal failure. Since drug interactions have only been evaluated for the combination of two or three drugs, interactions of cytotoxic agents with anaesthetics can hardly be predicted because of the large number of drugs simultaneously administered to leukaemic patients. The heart and lungs are target organs for the acute or chronic side effects of cytotoxic drugs, resulting in non-cardiogenic pulmonary oedema (e.g., cytosine-arabinoside), lung fibrosis (e.g., bleomycin), or arrhythmias and cardiac failure (e.g., adriamycin). The severity of these side effects depends on pre-existing organ disease and only in part on drug dosage. Only HLA- and CMV-compatible blood components should be administered to leukaemic patients. Hyperleukocytosis and the first days of cytotoxic treatment represent relative contraindications to general anaesthesia.
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PMID:[Pathophysiologic and anesthesiologic characteristics of patients with leukemia]. 152 54

An 11-month-old girl presented acute episodes of hypoglycaemia and hepatic encephalopathy reminiscent of Reye syndrome and 3-hydroxydicarboxylic aciduria. The patient showed peculiar clinical manifestations of severe sensory-motor neuropathy, pigmentary retinopathy, and cardiomyopathy. She died of cardiac failure. Pathological studies of peripheral nerve showed signs of axonal neuropathy and demyelination. Enzymatic studies in cultured fibroblasts showed a deficiency of mitochondrial long-chain 3-hydroxyacyl-CoA-dehydrogenase. Peripheral nerve involvement and retinal pigmentary degeneration have as yet not been described in patients with proven defects of mitochondrial beta-oxidation.
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PMID:Peripheral sensory-motor polyneuropathy, pigmentary retinopathy, and fatal cardiomyopathy in long-chain 3-hydroxy-acyl-CoA dehydrogenase deficiency. 153 53

In recent controlled trials using clinic-based manometry, thiazides and beta-blockers prevented cerebrovascular and coronary deaths in patients aged 60-79 years with cryptogenic hypertension (diastolic 90-119 mm Hg). Elderly patients should usually take low-dose thiazide with potassium replacement. beta-Blockers also postpone death, but may mask hypoglycaemia. Calcium blockers and low-dose angiotensin-converting enzyme (ACE) inhibitors appear preferable in diabetes, and thiazides or ACE inhibitors in heart failure or peripheral vascular disease. Maintaining average diastolic pressure at 80-84 mm Hg impairs function of the kidneys, and possibly the myocardium. Metabolic reactions worsen with age. Drug treatment should match individual daily function. By clinic manometry, the protection:risk ratio of antihypertensive treatment progressively decreases with age, reaching less than 1.0 in patients over 80-85 years. Twenty-four-hour ambulatory blood pressure information should guide treatment more reliably in patients greater than or equal to 60 years.
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PMID:Protection: risk ratio of antihypertensive drug treatment in the elderly. 159 Jun 63

Protein energy malnutrition and infection are largely responsible for the very high postneonatal and toddler mortality ratios of developing countries. Availability of food is just one environmental factor in the aetiology of protein energy malnutrition--many others such as size at birth, infection and culture play a role. Diet needs as careful prescription as any other form of therapy, but in the severely malnourished child it is only one aspect of management; care is necessary to avoid or detect 6 complications: hypothermia, hypoglycaemia, encephalopathy, intractable diarrhoea, cardiac failure, and infection. Prevention should be incorporated within the child health services as a whole and delivered with them; however central government, and the food industry from farming to retailing, play an at least as important role as health care professionals.
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PMID:Protein energy malnutrition: problems and priorities. 195 28

A small-for-date infant presented at birth with severe non-immune hydrops, cardiac failure, metabolic acidosis and hypoglycaemia. Ultrasonography disclosed a cardiomyopathy. Initial therapy consisting of artificial ventilation, inotropes and diuretics resulted in partial disappearance of oedema without significant improvement in cardiac function. Episodes of hypoglycaemia recurred despite continuous glucose infusions. Total serum carnitine from cord blood was 1.65 nmoles/ml and was undetectable on day 20. Oral DL-carnitine supplements resulted in normoglycaemia, dramatic improvement in cardiac function and restoration of serum carnitine levels to normal values. The infant was thereafter maintained on carnitine therapy. Follow-up over 1 year showed moderate growth retardation and normal developmental milestones. In order to account for such a severe neonatal presentation of carnitine deficiency, a combination of defective pre- and postnatal carnitine supply with an inborn error of carnitine handling is considered. The present case illustrates the need for evaluation of carnitine status in fetuses and neonates presenting with hydrops associated with cardiac failure.
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PMID:Carnitine deficiency with cardiomyopathy presenting as neonatal hydrops: successful response to carnitine therapy. 210 50

High-flow cerebral arteriovenous fistulae are well known to present in the neonatal period with macrocephaly, cranial bruits and high-output cardiac failure. This report describes a newborn infant with such a clinical presentation, who had unilateral megalencephaly without macroscopic arteriovenous shunts. Ultrasound Doppler examination of the carotid and cerebral vessels showed diastolic flow, or a decreased pulsatility index, consistent with decreased intracranial vascular resistance. The ipsilateral cerebral arteries and veins were markedly enlarged at angiography and at post-mortem examination, but there was no arteriovenous malformation. The infant expired from high-output cardiac failure and hypoglycemia. It is postulated that the high-output cardiac failure was due to increased blood flow through the enlarged, dysplastic cerebral hemisphere.
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PMID:Unilateral megalencephaly associated with neonatal high output cardiac failure. 214 45

General considerations in planning therapy of heart failure include identification of the cause, rapidity of onset, and the age of the patient. Neonates and young infants with acute onset heart failure frequently develop acidaemia, respiratory compromise or failure, and metabolic derangements such as hypoglycaemia, hypocalcaemia or hypomagnesaemia. These complications require early recognition and urgent therapy. The diagnosis of heart failure in neonates with ductal dependent congenital cardiac lesions (such as coarctation of the aorta, hypoplastic left heart syndrome or pulmonary valve atresia) allows the early institution of alprostadil (prostaglandin E1) therapy to maintain patency of the ductus arteriosus, which stabilises these infants before surgical therapy. Classic therapy for infants with heart failure due to a large left-to-right shunt consists of salt restriction, diuretics and digoxin. If this treatment is inadequate an angiotensin converting enzyme (ACE) inhibitor (e.g. captopril) is added to therapy. The question then arises whether captopril and diuretics should be the initial therapy and digoxin added if this treatment fails. Acute heart failure may occur in the immediate postoperative period after cardiac surgery or may complicate acute overwhelming infections. Therapy consists of volume loading, vasodilator or inotropic agents. Heart failure due to various forms of chronic dilated cardiomyopathy usually responds to treatment with salt restriction, diuretics, digoxin and captopril. Acute deterioration requires treatment with vasodilators and/or inotropic agents. Heart failure in fetuses may occur from sustained supraventricular tachyarrhythmias, and may respond to treatment of the mother with antiarrhythmic agents such as digoxin or procainamide.
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PMID:New drug approaches to the treatment of heart failure in infants and children. 218 7

In a cholestatic infant showing hypoglycemia and cardiac failure, non-ketotic medium-chain dicarboxylic aciduria was disclosed by urinary organic acid analysis. As urinary excretion of long-chain fatty acids was also increased, a defect in beta-oxidation of long-chain fatty acids appeared likely. To try to improve this abnormality, carnitine supplements were given, which led to the complete resolution of clinical and laboratory abnormalities. This is the first reported case of a cholestatic infant who responded to carnitine supplementation. Deficiency of carnitine palmitoyl transferase was suspected as the underlying cause.
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PMID:Transient carnitine-responsive medium-chain dicarboxylic aciduria in an infant with cholestasis, hypoglycemia and cardiac failure. 251 1

To define the mechanisms of unexpected cardiac arrest in advanced heart failure, we reviewed the causes of cardiac arrest as established from electrocardiographic monitoring and from clinical and autopsy data in patients hospitalized for cardiac transplantation evaluation and management of advanced heart failure (mean left ventricular ejection fraction, 0.18 +/- 0.08) who were stable while on vasodilator and diuretic therapy such that hospital discharge to home was anticipated. Twenty-one cardiac arrests occurred in 20 of 216 (9%) such patients during a 4-year period. Heart failure was due to coronary artery disease with prior myocardial infarction in 13 patients and nonischemic cardiomyopathy in seven patients. The rhythm at the time of arrest was severe bradycardia or electromechanical dissociation (BA/EMD) in 13 (62%) patients. The precipitating cause of the BA/EMD arrest was coronary artery thrombosis or embolism in two patients, pulmonary embolism in one patient, hyperkalemia in two patients, and unexplained hypoglycemia in one patient. In seven of 13 (54%) patients, a precipitating cause of the bradycardia arrest could not be established. Only eight of 21 (38%) arrests were due to ventricular tachycardia or fibrillation (VT/VF), and all occurred in patients with prior myocardial infarction (p = 0.02 vs. BA/EMD arrests). Two VT/VF arrests were due to acute or recent infarction, and one patient had hyperkalemia. The patients who suffered a BA/EMD arrest were similar to those who had a VT/VF arrest in age, ventricular arrhythmia history, ventricular function, and serum potassium levels. Serum sodium levels were lower in patients with BA/EMD arrests (129 +/- 3 vs. 133 +/- 4 meq/l, p = 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diverse mechanisms of unexpected cardiac arrest in advanced heart failure. 259 30

Nine normal subjects and 6 coronary patients (aged 26 to 53 years) who had survived myocardial infarction more than 3 years before and showed no clinical signs of heart failure, obesity, hypertension and diabetes mellitus, while having normal glucose tolerance test values, were exposed to the insulin test in combination with physical stress in the presence of clinically manifest hypoglycemia. Plasma and erythrocyte glucose and immunoreactive insulin, and urinary excretion of catecholamines were measured. Coronary patients showed considerably increased erythrocyte immunoreactive insulin levels, recorded immediately upon discontinuation of exercise, while their sympathoadrenal hormonal activation was less significant, as compared to normal subjects. The combination of the insulin test and exercise in coronary patients with normal glucose tolerance values helps to detect disturbances of regulatory mechanisms at the erythrocyte level and can be used as an adjuvant method for the assessment of latent carbohydrate metabolic disorders.
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PMID:[Characteristics of hormonal regulation in patients with ischemic heart disease after the insulin test combined with physical load]. 266 6


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