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

Raised blood pressure is the strongest single risk factor for stroke in the general population. Diabetics are at increased risk of both hypertension and stroke. It is not clear if diabetes mellitus confers an excess risk of stroke that is independent of blood pressure. The authors examined the relation of diabetic status (personal history of diabetes and/or fasting plasma glucose greater than 7.8 mmol per liter) to stroke risk in a population-based cohort of 3,778 adults aged 50-79 years in Rancho Bernardo, California who were followed from 1972 for an average of 12 years. There were 232 stroke cases, 139 of which were ascertained from death certificates. Diabetics had higher mean systolic blood pressures, significantly so in females, and diabetics of both sexes were significantly more obese. Diabetics had greater univariate age-adjusted stroke mortality and morbidity rates than nondiabetics. The increased stroke rates were still apparent in diabetics after stratifying for systolic blood pressure. In multivariate analyses, the relative risks (RRs) for stroke mortality and morbidity associated with diabetes were not significantly changed in men (RR = 1.8) and women (RR = 2.2), after adjusting for the effect of risk factors including age, systolic blood pressure, cholesterol level, obesity, and smoking habits, and excluding persons with personal history of heart attack, heart failure, or stroke. These findings support the hypothesis that diabetes may confer excess risk of stroke independent of blood pressure.
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PMID:Diabetes mellitus: an independent risk factor for stroke? 338 20

The aim of the present study was to check whether equal, therapeutically relevant, positively inotropic doses of different adrenergic agents elicit equal inotropic and metabolic effects in 6 type I-diabetics as in 6 matched nondiabetic subjects. The effects of increasing doses of norepinephrine (NE)- and orciprenaline (0.12, 0.20, 0.33 microgram/kg min) on heart function (systolic time interval, heart rate, blood pressure) and on serum fatty acid (NEFA), glucose, lactate, pyruvate and insulin concentrations were recorded. In the therapeutic dose range, NE, and orciprenaline elicited in diabetics without clinical signs of any cardiovascular disease a diminished myocardial inotropic response (20-40%), less marked vascular effects (vasoconstriction, vasodilatation), but greater metabolic changes in right atrial blood (NEFA, pyruvate, lactate) compared to matched controls (p less than 0.05). The smaller increase of cardiac performance in diabetics to exogenous catecholamines cannot be explained by sympathetic cardiac denervation, since chronotropic beta 1-beta 2-stimulation with orciprenaline provoked nearly equal dose-dependent changes in diabetics and controls. It is suggested that the smaller positive inotropic effect during NE and orciprenaline infusion in type I-diabetics is a result first of all of alterations in myocardial energy turnover in diabetes due to reduced myocardial glucose utilization. It seems necessary to secure continuous myocardial glucose utilization and subnormal NEFA concentrations in the serum during the therapeutic application of inotropic adrenergic agents in severe cardiac failure and cardiogenic shock in diabetics.
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PMID:Interaction between glucose utilization and left ventricular heart function in type I-diabetics. 338 68

The impact of diabetes was prospectively studied during a 5-year period in 428 unselected and consecutive patients with acute cerebrovascular disease of whom 18% were diabetic. Cerebral infarction was more frequent in diabetics (81 vs 70%, p less than 0.02) whereas transient cerebral ischaemia was less frequent (4 vs 14%, p less than 0.01). Case fatality rate during hospitalization was higher in the diabetic than in the non-diabetic patients (28 vs 15%, p less than 0.02). Patients who died during hospitalization, diabetic as well as non-diabetic, had significantly higher blood glucose concentrations on admission compared with patients who survived. Hematocrit values were higher in the diabetic than in the non-diabetic patients (p less than 0.02). Diabetics had higher systolic blood pressure levels than the non-diabetics in the acute phase (p less than 0.005). The diabetic stroke patients more often had a history of hypertension, atrial fibrillation, heart failure and angina pectoris than non-diabetics stroke patients and diabetic control patients without stroke. Stroke patients, not known to be diabetic, had larger mean oral glucose tolerance test curve areas when compared with healthy controls but not when compared with hospitalized controls. We propose that diabetes increases the risk for stroke through other concurrent risk factors, cardiac disorders in particular.
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PMID:Clinical characteristics in diabetic stroke patients. 339 27

Acute ischaemic heart failure was induced in 13 dogs by coronary embolisation. Severe dysfunction of the left ventricular (LV) performance was shown by a significant increase in LV end-diastolic pressure and significant decreases in maximum rate of LV pressure rise (LVdP/dtmax), stroke volume and cardiac output. 300 IU of fast-acting insulin was injected as a bolus dose in 7 dogs 90 min after the embolisation procedure. This was followed by infusion of glucose and potassium to maintain normal blood levels. After 15 min, insulin had significantly improved the performance of the failing left ventricle. Total peripheral resistance was decreased. Myocardial blood flow was significantly increased while myocardial oxygen consumption was unchanged. After beta receptor blockade with propranolol 0.5 mg kg-1 given intravenously, the improvement in cardiac performance was reduced, heart rate decreased, and a concomitant decrease in myocardial blood flow and oxygen consumption was recorded. Compared with values before treatment, the net effect of combined insulin and beta receptor blockade was unchanged LVdP/dtmax, LV end-diastolic pressure and cardiac output, significantly increased stroke volume and decreased heart rate, and moderately reduced total peripheral resistance and mean aortic blood pressure. Myocardial blood flow was unaltered, while myocardial oxygen consumption was significantly reduced. In the control group of 6 dogs propranolol was given before insulin, and similar haemodynamic alterations were found.
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PMID:Haemodynamic effects of insulin and beta receptor blockade during acute left ventricular failure in dogs. 351 26

Diuretics are among the most widely prescribed drugs, especially for the elderly with cardiac failure or hypertension. Progressive structural and functional changes occur in the kidneys after the fourth decade, leading to impairment of the ability of the kidneys to handle sodium, water and solutes. The renal reserves of the elderly are about half those of the young. In addition, the renin-aldosterone system shows reduced activity in old age. The pharmacokinetics and pharmacodynamics of diuretics in the elderly are reviewed, and the influence of congestive cardiac failure is emphasised with regard to the kinetics of diuretics and the deleterious effect of diuretic-induced hypokalaemia and hypomagnesaemia on the pharmacology of digoxin. Guidelines are suggested for the use of diuretics in the elderly, including the avoidance of unnecessary use, the careful choice of diuretic used, the need for small initial doses, and the prevention of hypokalaemia. The place of potassium-sparing agents for the elderly and adverse effects of diuretics, either mechanical, metabolic or toxic are discussed. Mechanical problems are related to the rate and volume of urine produced, and the resulting effects on bladder function and on blood volume. Although toxic effects are relatively rare, metabolic effects include electrolyte changes, impairment of glucose tolerance, and increased serum uric acid and lipids. Most of these adverse effects are preventable by careful management; the consensus is that they are not of sufficient clinical significance to outweigh the long record of efficacy and safety of diuretic therapy in the elderly. Diuretics will, and should, continue to be used extensively in elderly patients with hypertension and/or cardiac failure.
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PMID:The elderly patient. A special case for diuretic therapy. 352 88

Intestinal ischemia shock was induced either by temporary occlusion of the three splanchnic arteries for 40 min (SAO-shock) or by temporary occlusion of the portal vein for 35-40 min (PVO-shock). In both types of shock, life can be considerably prolonged (5-8-fold) by treatment with rat plasma plus glucose. Eventually, death is caused by heart failure due to hyperkalemia (plasma K+ concentration greater than 10 mmol/l). The amount of K+ causing this hyperkalemia is estimated at roughly 10% of the total body K+. Acidosis, low blood pressure, reduced kidney function, and disintegration of erythrocytes in the gastrointestinal (GI) tract probably are of no or minor importance in causing this extreme hyperkalemia. No indication was found that the liver, the skeletal muscles, or the erythrocytes release K+. Although the K+ concentration of the contents of the GI tract as well as the K+ transport by the portal vein were increased, the source of the excess K+ remains obscure. Removal of the contents of the stomach and small intestine, followed by flushing of the gastrointestinal tract, may have a favorable effect on the course of plasma K+ (and plasma glucose) concentration, indicating that toxic products from the damaged intestines may be important lethal factors.
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PMID:Studies on hyperkalemia as a cause of death in intestinal ischemia shock in rats. 373 7

Hypoglycaemia with manifest clinical symptoms has been observed in four patients with cardiac insufficiency after infiltration of high doses of lidocaine prior to surgery. The depressing influence of lidocaine on blood glucose levels has also been seen in six out of 12 patients to whom a pacemaker was implanted in local anaesthesia. The interaction between hepatic glucose- and lidocaine-metabolism could possibly be responsible for this effect. Therefore the evaluation of blood glucose level and iv. administration of glucose is advisable in patients with systemic toxic reactions following lidocaine overdosage to avoid unnecessary symptomatic therapy.
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PMID:[Hypoglycemia caused by lidocaine overdosage]. 374 49

The relation between metabolic and functional derangement in various cardiomyopathies has not been well characterized. This information was specifically sought in a spontaneous cardiomyopathic model. Metabolic and hemodynamic parameters were obtained in glucose-perfused beating hearts of 180-200-day-old cardiomyopathic Syrian hamsters and age-matched healthy animals. This period in the cardiomyopathic hamster lifetime is intermediary between the necrotic phase and the appearance of heart failure. We used 31P nuclear magnetic resonance spectroscopy to analyze energy metabolites and intracellular pH. Cardiomyopathic hamsters had significantly higher mole fraction values for inorganic phosphate, lower phosphocreatine mole fraction as well as lower phosphocreatine/inorganic phosphate and adenosine triphosphate/inorganic phosphate ratios. Analysis of pH indicated the presence of regions of increased acidity within the heart of myopathic hamsters. Cardiomyopathic hamsters also had significantly lower left ventricular pressure, coronary flow, and myocardial oxygen consumption. Separate groups of normal and myopathic hamsters were given verapamil for 24 hours (one injection of 4 mg/kg s.c. followed by 1.2 g/l in drinking water). Verapamil-treated myopathic hamsters had evidence of markedly improved mitochondrial function when compared with untreated animals. Left ventricular pressure and coronary flow rose to normal levels. Replacing glucose by pyruvate in the perfusate of myopathic hamsters results in a marked increase in left ventricular pressure, coronary flow, and oxygen consumption with a moderate rise in phosphocreatine. Thus, 180-200-day-old cardiomyopathic hamster heart is characterized by evidence of decreased mitochondrial function, by areas of increased acidity within the heart, and by reduced left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of the hereditary Syrian hamster cardiomyopathy by 31P nuclear magnetic resonance spectroscopy: improvement after acute verapamil therapy. 381 56

The metabolic, hormonal and haemodynamic effects of oral pirbuterol, a new beta 2-adrenoceptor agonist, were studied acutely (n = 19) and after 3 months treatment (n = 11) in patients with severe heart failure receiving chronic frusemide therapy. In the acute study fasted patients (n = 10) showed reductions in plasma K+ (P less than 0.005) and cortisol (P less than 0.01) and increases in plasma glucose (P less than 0.005), insulin (P less than 0.01), lactate (P less than 0.005) and pyruvate (P less than 0.0025). These acute changes were less in unfasted subjects (n = 9). Maximal increase in stroke volume occurred at approximately half the plasma pirbuterol concentration required for maximal effect on plasma insulin. Treatment with pirbuterol for 3 months was associated with sustained increases in stroke volume and fasting plasma glucose and insulin, but there was loss of all other acute metabolic effects. Despite concurrent frusemide and digoxin therapy acute hypokalaemia caused no adverse effects. Hypokalaemia did not occur with chronic pirbuterol administration.
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PMID:Differences between acute and long-term metabolic and endocrine effects of oral beta-adrenoceptor agonist therapy with pirbuterol for cardiac failure. 382 94

In the performance of heart-lung preparations, after 4-8 hours, it is an usual feature to have multiple microinfarctions, and, finally, heart failure and ventricular fibrillation. We have studied glucose, triglycerides and conjugated fructose consumption by the heart-lung preparation and found a very fast glucose depletion (30 to 90 minutes to glucose 0, starting with glucose 120 mg/dl). The depletion has been slower for triglycerides and even slower for conjugated fructose. Ventilation with pure oxygen has not modified itself the coronary deterioration, but if a Biostator has been used in order to maintain the glucose levels at 100-110 mg/dl., the isolated heart-lung does not deteriorate in 16-24 hours, nor show electrical signs of coronary impairment; after this time, the respirator is disconnected and the preparate discarded. The above mentioned experiments demonstrated the need of artificial control of glycemia in isolated organ experiments and suggest the convenience to use more widely the artificial pancreas (Biostator in our case) for better treatment no only in diabetic or pancreatic patients, but also in many circumstances in which the glucose utilization is impaired.
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PMID:Glucose stabilization and coronary infarction with artificial pancreas in heart-lung preparation. 387 Jun 21


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