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)

This report describes a case of severe acidosis with cardiac failure due to alcohol in a black man. Treatment with parenteral thiamine produced a prompt response. Thiamine deficiency should be recognized as an important cause of lactic acidosis.
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PMID:Acute pernicious or fulminating beriberi with severe lactic acidosis. A case report. 407 32

Clinical, biochemical and pathological findings are described in a 23-year-old male with a mitochondrial myopathy who had a high-output circulatory state and cardiomyopathy which resulted in cardiac insufficiency 22 years before presentation of the skeletal myopathy. Venous lactate levels were elevated and severe lactic acidosis developed at one stage of the illness. Electron microscopy of muscle tissue showed various mitochondrial abnormalities and accumulation of neutral lipids which was confirmed histochemically and by thin-layer chromatography. Marked improvement in the myopathy occurred after commencement of prednisone and thiamine and was maintained following withdrawal of these drugs. The metabolic defect in this case has not been defined, but an abnormality in the Kreb's over-production of lactate and lipid accumulation in muscle is postulated.
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PMID:Mitochondrial myopathy with cardiomyopathy, lactic acidosis and response to prednisone and thiamine. 693 88

Fetal and neonatal biophysical and biochemical changes were studied in four preterm infants who developed cardiogenic shock as a result of severe perinatal asphyxia. Fetal distress was documented by the presence of severe late and variable decelerations associated with decreased fetal heart rate variability. Severity of fetal acidosis was decumented by scalp and umbilical cord blood pH. Apgar scores at 1, 5, and 10 minutes were all equal to or less than 5. Although the clinical findings shortly after birth resembled respiratory distress syndrome, it was possible to make a primary diagnosis of cardiac failure with the recognition of cardiomegaly, hepatomegaly, electrocardiographic changes of myocardial hypoxia, decreased myocardial contractility, elevated central venous pressure, and severe lactic acidosis. The treatment of heart failure, including use of inotropic agents, resulted in rapid improvement in the clinical condition, with reversal of the abnormal findings within 24 to 36 hours. Concomitant with this improvement, the increase in arterial blood pressure was paralleled by increase in peripheral (toe) temperature.
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PMID:Cardiogenic shock associated with perinatal asphyxia in preterm infants. 718 61

In recent years, lactic acidosis has been described in association with metformin therapy in diabetics. We report a fatal case in an elderly diabetic patient with impaired renal function and cardiac insufficiency. The patient presented with an elevated plasma metformin concentration and a concomitant digitoxin intoxication.
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PMID:Lactic acidosis during metformin treatment in an elderly diabetic patient with impaired renal function. 725 70

A further case of pyruvate carboxylase deficiency, French type, with a particular clinical presentation and evolution is described. The initial neonatal symptoms started with respiratory distress, severe metabolic acidosis and a tendency to hypoglycemia. However, the clinical course was not rapidly deteriorating. At the age of 6 months he presented acute neurological symptoms, respiratory difficulty, lactic acidosis and hyperammonemia. Amino and organic acid abnormalities strongly suggested pyruvate carboxylase deficiency, which was confirmed by enzymatic studies in cultured fibroblasts and liver necropsy. Progressive deterioration and bronchopneumonia with cardiac failure and renal insufficiency led to death. Anatomic-pathologic studies revealed periventricular cysts and diffuse hypomyelination. Prenatal diagnosis of a further sibling was performed. The neonatal clinical presentation, biochemical abnormalities, and the presence of periventricular cysts suggested a French phenotype. However, the clinical course was less severe, suggesting a residual enzymatic activity and a possible milder mutation.
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PMID:An atypical French form of pyruvate carboxylase deficiency. 750 91

Near infrared spectroscopy (NIRS) is a noninvasive technique of monitoring tissue oxygen saturation by detecting changes in tissue absorbance of two wavelengths (850 and 760 nm) reflecting the relative oxygenation of hemoglobin and myoglobin. Aim of the present study was to determine whether changes in skeletal muscle oxygen saturation during incremental exercise detected by NIRS can reflect an impared oxygen delivery and an early onset of anaerobic metabolism in patients with chronic heart failure (CHF). We studied 19 subjects (mean age 43 +/- 16 years). Seven patients had a history of CHF with a diagnosis of ischemic cardiomyopathy (Group A) and 12 were healthy sedentary (Group B). All patients had a history of dyspnea on exertion (NY-HA II), peripheral edema, pulmonary rales and cardiac gallop sounds over the last 6 months. They were in sinus rhythm and stable clinical condition in the last 3 months. They were well matched regarding age, sex and body surface area. All subjects performed an incremental work rate test in a ramp pattern on a upright cycle ergometer until volitional fatigue. Gas exchange was measured breath by breath with a metabolic chart. Muscle oxygenation was determined, transcutaneously, during the exercise test over the vastus lateralis muscle with NIRS. At peak exercise, work rate, VO2, anaerobic threshold (LAT), heart rate and systolic blood pressure were significantly lower in Group A compared to Group B (92 +/- 28 vs 232 +/- 17 watts; 14 +/- 2 vs 21 +/- 2 ml/kg/min; 868 +/- 225 vs 1317 +/- 354 ml/min; 149 +/- 7 vs 172 +/- 18 b/min; 145 +/- 18 vs 195 +/- 21 mm Hg, respectively; p < 0.0001 for all). In both groups, as work rate increased, tissue oxygenation initially either remained constant near resting levels or decreased. In both groups, muscle oxygenation decreased more steeply near the work rate where lactic acidosis (LAT) was detected. However, patients with CHF had an earlier acceleration in muscle deoxygenation compared to the other group, indicating a premature onset of anaerobic metabolism. Moreover, Group A had a flatter increase in both heart rate and systolic blood pressure and a steeper slope of oxygenation profile at all matched workloads compared to normals (Group A: -0.13 +/- 0.03 ml/min; Group B: -0.06 +/- 0.015 ml/min; p < 0.0001). The LAT correlated with the work rate at which the rate of tissue O2 desaturation accelerated (r = 0.94; p < 0.0001).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Near infrared spectroscopy and changes in skeletal muscle oxygenation during incremental exercise in chronic heart failure: a comparison with healthy subjects. 764 20

Patients with mitochondrial disease may present to the Intensive Care Unit (ICU) with a variety of neurological and general medical disorders. Eleven patients were admitted to a neurological ICU between 1970 and 1992 because of respiratory insufficiency, status epilepticus and/or metabolic encephalopathy associated with mitochondrial disease. Respiratory impairment occurred in eight patients and was associated with nocturnal hypoventilation due to respiratory muscle weakness, aspiration due to bulbar weakness and abnormalities of central control leading to a reduced CO2 drive, irregular respiratory patterns and sleep apnoea. Seven patients received continuous respiratory support during the acute illness; three were subsequently weaned to domiciliary ventilation, and four died. Five patients had stroke-like episodes, which in two were recurrent. Four patients developed tonic-clonic grand mal epilepsy associated with myoclonic fits (2 patients), absences (2), focal fits (1) and status epilepticus (2). Encephalopathy was associated with recurrent lactic acidosis (2 patients), cardiac failure (2), hyponatraemia (2), renal abnormalities (3) and complete heart block (1). Although rare, mitochondrial disease should be considered in any patient with unexplained respiratory failure, intractable epilepsy, lactic acidosis or recurrent stroke.
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PMID:Management of mitochondrial disease on an intensive care unit. 776 70

The sulphonylureas and the biguanides are widely used as adjuncts to dietary measures in the treatment of non-insulin-dependent (type 2) diabetes mellitus (NIDDM). Adverse effect profiles differ markedly between the sulphonylureas and biguanides, reflecting differences in chemical structure and mode of action. Sulphonylureas are generally well tolerated, although pharmacokinetic differences between these agents have important clinical implications. The main adverse effect associated with sulphonylureas is hypoglycaemia. This effect is a predictable consequence of the principal pharmacological effect of these drugs, i.e. sensitisation of the islet beta-cell to glucose, resulting in enhanced endogenous insulin secretion. Sulphonylurea-induced suppression of hepatic glucose production may cause profound and protracted hypoglycaemia, especially in elderly patients, in individuals with intercurrent illnesses and reduced caloric intake, or when taken in combination with other compounds with hypoglycaemic potential, e.g. alcohol (ethanol). Sulphonylureas with a longer duration of action, notably chlorpropamide and glibenclamide (glyburide), are more liable to induce serious hypoglycaemia, particularly when drug elimination is reduced by renal impairment. Other drugs such as salicylates may potentiate the actions of sulphonylureas, thereby increasing the risk of hypoglycaemia. Biguanide therapy is associated with alterations in lactate homeostasis which under certain clinical circumstances may result in fatal lactic acidosis. Phenformin is associated with a markedly greater risk of lactic acidosis than metformin. Phenformin has been withdrawn in many countries for this reason. All biguanides must be avoided in patients with renal impairment, hepatic dysfunction and cardiac failure--conditions where drug accumulation or disordered lactate metabolism may predispose to lactic acidosis. Phenformin should not be given to individuals who exhibit a severe, genetically conferred hepatic defect of hydroxylation which impedes metabolism of this drug. Less seriously, the biguanides are associated with a relatively high incidence of gastrointestinal adverse effects which limit compliance. Acarbose, a competitive inhibitor of intestinal alpha-glucosidases, has recently been introduced. In contrast to the sulphonylureas and biguanides, acarbose has not been associated with life-threatening adverse effects. This reflects the low systemic absorption of the drug and, predictably, its principal unwanted effects are gastrointestinal disturbances resulting from iatrogenic carbohydrate malabsorption.
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PMID:Comparative tolerability profiles of oral antidiabetic agents. 784 43

A 17-year-old male with mitochondrial myopathy was transferred to our hospital because of respiratory distress and a rapidly deteriorating level of consciousness. He had a markedly increased cardiac output with low systemic vascular resistance and decreased arteriovenous oxygen difference. Severe lactic acidosis, rhabdomyolysis and acute renal failure were also present. He was treated in the intensive care unit with continuous hemofiltration and hemodialysis. This case demonstrates that cardiac failure in mitochondrial encephalomyopathy may be caused by myocardial abnormalities as well as by reduced systemic vascular resistance secondary to disturbed oxidative metabolism.
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PMID:High-output heart failure in mitochondrial myopathy: a fulminant form with severe lactic acidosis and rhabdomyolysis. 801 76

Acute alcohol ingestion can affect life expectancy and is directly responsible for 3,500 deaths per year. Acute lung diseases are mainly caused by pneumococci, Gram negative bacilli and anaerobic germs, and are often due to multiple microbes. In this case, evolution toward abscess can be feared. Septicaemia and enterobacterial peritonitis are frequently observed in cirrhotic patients. Ethanol, hypokaliemia and hypophosphoraemia also lead to rhabdomyolysis. Rhabdomyolysis can be complicated with acute renal failure and hyperkaliaemia. Alcoholic ketoacidosis and the hypoglycaemia favored by prolonged inadequate nutrition, are corrected by infusion of glucose solutions. Hyponatraemia can be complicated by convulsions and central pontine myelinolysis. Minor forms of alcoholic hepatitis remiss after stopping alcohol intoxication. The major forms can evolve toward fatal encephalopathy; treatment with corticosteroids improves the prognosis in severe hepatitis. The cardiac failure with lactic acidosis in shoshin beriberi rapidly evolves to collapsus; treatment is based on emergency administration of vitamin B1. Management of patients in acute alcohol episodes requires great vigilance. Careful clinical examination and biological tests should eliminate severe somatic complications before concluding to simple alcoholic intoxication.
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PMID:[Severe somatic complications of acute alcoholic intoxication]. 813 83


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