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

The plasma level of the immunoreactive insulin and the blood level of sugar on an empty stomach and following carbohydrate provocation were determined in 31 patients with congestiva heart failure due to ischaemic heart disease. In 26 of them the plasma levels of adrenalin and noradrenalin were also studied. After 30-35 days of active therapy 15 patients were reexamined. The immunoreactive insulin plasma level was determined by the Hales and Randle technique, that of catecholamines-flowmetrically by the trioxyindol method after Vendsalu modified by E. Sh. Matlina. Carbohydrate metabolism disorders that manifested themselve in fasting hyperglycemia and in changing tolerance of glucose were noted in 13 of the 31 patients, examined. In the majority of patients with congestive heart failure insulin secretion was reduced both after fasting and after glucose administration. The improvement of the patients state in response to the employed therapy was accompanied by an increasing insulin secretion. One of the causes of the inhibition of insulin secretion in patients with congestive heart failure consisted in hypercatecholaminemia that was noted in most of the examined cases. The obtained data prove the necessity of a careful control of carbohydrate metabolism in patients with congestive heart failure and of a more active employment of insulin for their treatment.
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PMID:[Levels of immunoreactive insulin and catecholamines in the blood plasma of patients with congestive heart failure]. 115 39

Experimental hyperthyroidism was produced in guinea pigs by daily intraperitoneal injection of l-thyroxine (T4) in various doses (0.7, 0.35, 0.175, and 0.07 mg/kg/day) for 7 days. Controls received solvent only. The following metabolites were determined in heart muscle (freeze-stop technique, enzymatic tests): Pi, adenosine tri-, di-, and monophosphates (ATP, ADP, AMP), creatine phosphate (CP), glucose 6-phosphate (G-6-P), fructose diphosphate (FDP), pyruvate, and lactate. Thyroxine induced a dose-related decrease of CP and a corresponding increase of Pi even in the lowest dose used in this study (0.07 mg/kg) and became more pronounced with increased doses. No remarkable changes of adeninenucleotides (ATP, ADP, AMP) were observed. G-6-P and FDP levels were markedly elevated in all dosages. Besides other possible effects (thyroxine-induced activation and induction of enzymes) the dose-related decrease of CP and increase of Pi may be due to the increasing contractility. In the physiological and pathophysiological range of thyroxine doses (T4 less than 20 mug%) high energy phosphates stores are dose-related decreased but not to a critical level. In the toxic range heart failure as a consequence of a deficit of CP may occur.
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PMID:Dose-relation of thyroxine-induced changes in myocardial energy stores. 121 45

Hearts from chronically adrenalectomized (ADX) cats deprived of any steroid support for 9-12 days were isolated and perfused in a Langendorff apparatus at a constant pressure of 95 mm Hg. The perfusion medium was Krebs-Henseleit buffer with either 10 mM glucose or 0.4 mM palmitate complexed to 3 percent albumin. Labeled 14C substrate was used and the transient rate of glucose and palmitate uptake was measured. Oxygen consumption and [14C] palmitate incorporation into CO2, and heart lipids were also measured. ADX hearts showed an enhanced glucose uptake rate compared with controls, 65 +/- 11.3 mumoles/gm to 16.2 +/- 6. However, the qO2 was not significantly different from control hearts. Palmitate uptake, O2 consumption, and 14CO2 were significantly lower in ADX hearts perfused with fatty acid as the energy substrate. Fatty acid uptake decreased from 9.7 +/- 1.0 to 3.6 +/- 1.1 and lipid fractions in the heart showed significant decreases in [14C] palmitate incorporated into triglycerides (p less than 0.001) and monoglycerides (p less than 0.01). The ADX heart does not appear to have any impairment to glucose uptake but does show an impairment to fatty acid uptake. Because the heart uses lipid as the primary energy source, the impairment probably is not the primary factor responsible for cardiac failure in adrenal insufficiency because of its capability of using other available substrates for energy.
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PMID:Glucose and palmitate uptake in the myocardium of isolated hearts from adrenalectomized cats. 125 83

Angiotensin-converting enzyme (ACE) inhibitors are established in the treatment of hypertension and heart failure; both conditions are complicated by resistance to insulin-mediated glucose disposal. The defect in essential hypertension is both tissue and pathway specific, i.e., confined to nonoxidative (glycogen synthetic) routes of intracellular glucose utilization in skeletal muscle, whereas heart failure and non-insulin-dependent diabetes mellitus (NIDDM) are associated with more widespread abnormalities of carbohydrate and lipid metabolism. Thus, the mechanisms of the insulin resistance in hypertension, NIDDM, and heart failure are fundamentally different, so metabolic responses to drug therapy may not be the same in all insulin-resistant states. There have been conflicting reports about the effects of ACE inhibitors on insulin sensitivity and glycemic control. A number of studies, both with captopril and with enalapril, have shown small increases in insulin sensitivity, and there is evidence that this is due to enhanced glucose uptake into skeletal muscle. The interpretation of these studies, however, is often compromised by poor trial design, lack of full placebo data, various indirect measurements of insulin sensitivity, and heterogeneous patient populations in whom the biochemical mechanisms of insulin resistance (and drug responses) may not be the same. Overall, there probably is a modest class effect of ACE inhibitors that enhances insulin-mediated glucose disposal; the mechanism of this effect is likely to be a combination of increased muscle blood flow, local renin-angiotensin system blockade, and elevated kinin levels.
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PMID:Angiotensin-converting enzyme inhibitors and insulin sensitivity: metabolic effects in hypertension, diabetes, and heart failure. 128 42

Insulin resistance and hyperinsulinemia is now recognized in non-insulin-dependent diabetes, essential hypertension, obesity, atherosclerotic heart disease, dyslipidemia, heart failure, and in heavy smokers. Several mechanisms have been proposed to explain hyperinsulinemia, insulin resistance and its relationship to hypertension; reduced sodium excretion, activation of the sympathetic nervous system, increased activity of the sodium/hydrogen pump, and stimulation of cellular growth. Some of the nonpharmacological methods to control hyperinsulinemia are of benefit in the management of hypertension, most notably weight loss, exercise program, and reduced salt intake. High-fiber and reduced-protein diets also reduce hyperinsulinemia. Thiazide diuretics can result in insulin resistance, and insulin secretion may be inhibited, possibly associated with concomitant hypokalemia. beta-Blockers result in some reduction of glucose tolerance and mask some of the features of hypoglycemia. Angiotensin-converting enzyme (ACE) inhibitors and alpha-receptor blockers do not effect insulin resistance; probably the same is true for calcium antagonists. Although the effect on risk factors should not be discounted, it is the effect of treatment on hard end points, cerebrovascular accidents, myocardial infarction, or death that is most important. Evidence in hypertension is at present restricted to diuretics and beta-blocking drugs.
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PMID:Hypertension and insulin resistance. 128 47

The method of surface fluorometry with indo-1 allows the simultaneous quantitative recording of changes in free intracellular calcium ([Ca2+]i) transients during the cardiac cycle and haemodynamic parameters and ECG. Using this method, recent studies gave further insight into acute and chronic changes in [Ca2+]i during disease (e.g. heart failure, ischaemia, arrhythmias), as well as pharmacologic interventions. The failing myocyte is characterized by small calcium transients and elevated end-diastolic [Ca2+]i concentrations. Without an adequate delivery of substrate to the mitochondria (pyruvate, but not glucose) the cardiomyopathic heart muscle is no longer capable of maintaining its [Ca2+]i homeostasis. In healthy hearts, positive inotropic agents lead to an increase in developed pressure commensurately with the percentage changes in amplitude of the [Ca2+]i transients, while the end-diastolic [Ca2+]i levels seem to depend on the activation of cAMP. In failing hearts the latter finding may explain the different behaviour of end-diastolic [Ca2+]i and haemodynamics during perfusion with various catecholamines, more likely stimulating alpha- and/or beta-adrenoceptors. Further studies analysed [Ca2+]i during ischaemia or showed the importance of changes of [Ca2+]i in the genesis of premature beats and the initiation of tachyarrhythmias, in particular ventricular fibrillation. The present overview underlines the comprehensive role of calcium homeostasis in the pathophysiology of contraction and relaxation of the heart muscle.
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PMID:[Importance of intracellular calcium homeostasis for contraction and relaxation of the heart muscle]. 131 68

We studied the hemodynamic and metabolic effects of the novel class III antiarrhythmic agent dofetilide (UK-68,798) in acute ischemic heart failure. In pentobarbital-anesthetized dogs, heart failure was induced by microembolization of the area supplied by the main left coronary artery until a stable left ventricular (LV) end-diastolic pressure of 27 +/- 2 mm Hg was achieved. Embolization depressed LV systolic pressure, LV dP/dtmax, LV dP/dtmin, and cardiac output. None of these parameters were changed following i.v. infusion of dofetilide 5, 10, or 25 micrograms/kg, during spontaneous and paced cycle length of 300 ms (n = 9). Heart rate decreased by 12 +/- 8, 19 +/- 7, and 21 +/- 7 beats/min (p less than 0.05), while QT time increased by 23 +/- 7, 33 +/- 9, and 40 +/- 10 ms (p less than 0.05) after 5, 10, and 25 micrograms/kg, respectively. Ventricular effective refractory period increased from 128 +/- 10 to 153 +/- 11 ms after 25 micrograms/kg (n = 4). Arterial concentration and net myocardial uptake of glucose, lactate, and free fatty acids were not significantly influenced by dofetilide. In conclusion, dofetilide, at doses that prolonged repolarization, was devoid of cardiodepressive effects in acute ischemic heart failure.
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PMID:Class III antiarrhythmic action and inotropy: effects of dofetilide in acute ischemic heart failure in dogs. 137 91

An algorithm has been developed to provide predictable control of blood glucose for 48 h following acute myocardial infarction. In 29 diabetic patients intravenous infusion of soluble insulin was started upon admission to hospital and the rate adjusted hourly on the basis of bedside capillary glucose estimations. Insulin infusion rates related to glycaemia were higher in obese patients and those with severe cardiac failure. For all patients mean admission glucose levels were reduced from 18.3 +/- 5.9 mmol l-1 to 9.1 +/- 3.3 mmol l-1 at 4 h and to 8.8 +/- 2.5 mmol l-1 at 6 h. Mean glucose concentrations for 48 h after admission were 8.2 +/- 1.3 mmol l-1 for all patients. Admission glucose levels were slightly higher in patients with severe, compared to those without or mild, cardiac failure (P less than 0.1), but levels over the following 48 h were similar. Doubling insulin infusion rates before meals did not achieve tighter glycaemic control. Hypoglycaemia (glucose less than 3 mmol l-1) occurred on 11 occasions in six patients; only two episodes were symptomatic and only two episodes occurred when the insulin rates were doubled before meals. This algorithm produced tighter glycaemic control than previously published protocols, particularly in patients with severe cardiac failure. Hypoglycaemia is uncommon and the algorithm easy to administer by nursing staff.
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PMID:An algorithm for tight glycaemic control in diabetic infarct survivors. 142 42

We studied the haemodynamic and metabolic effects of the novel class III antiarrhythmic agent almokalant (H 234/09) in acute ischaemic heart failure at a dose prolonging ventricular repolarization. In pentobarbital anaesthetized dogs, heart failure was induced by microembolization of the area supplied by the main left coronary artery until a stable left ventricular end-diastolic pressure (LVEDP) of 32 +/- 2 mmHg was achieved. Embolization depressed LV dP/dt(max), LV dP/dt(min), left ventricular systolic pressure (LVSP) and cardiac output. After intravenous infusion of almokalant (0.35 micrograms/kg) LV dP/dt(max) and LV dP/dt(min) were not significantly changed at paced cycle length of 300 msec., whereas LVSP and aortic pressure decreased both at spontaneous and paced cycle length of 300 msec. LVEDP remained unchanged. Heart rate decreased from 185 +/- 7 to 167 +/- 5 beats/min., and corrected QT-time (QTc) increased from 9.5 +/- 0.3 to 10.4 +/- 0.5 msec. Arterial concentration and net myocardial uptake of glucose, lactate and free fatty acids were not significantly influenced by almokalant. In conclusion, almokalant at a dose prolonging ventricular repolarization had no negative inotropic effect in acute ischaemic heart failure.
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PMID:Class III antiarrhythmic action and inotropy: effects of almokalant in acute ischaemic heart failure in dogs. 143 22

Patients with congestive heart failure (CHF) have impaired peripheral vasodilation during exercise. Hyperosmolality is one local stimulus that produces vasodilation during exercise in normal subjects. This study addressed the hypothesis that vasodilation to hyperosmolal stimuli is impaired in patients with CHF. Forearm blood flow responses to intrabrachial artery infusions of isoosmolar (280 mosm/kg) and hyperosmolal (480 and 660 mosm/kg) solutions of saline and glucose were compared in 9 patients with CHF and 13 normal subjects. Forearm blood flow was measured by strain gauge plethysmography. In the normal subjects, hyperosmolal infusions of 480 and 660 mosm/kg increased forearm blood flow by 3.12 +/- 0.40 and 6.80 +/- 0.67 ml/min/100 ml forearm volume, respectively (both p < 0.001 compared with isoosmolal infusions). In contrast, in the patients with CHF, these infusions increased forearm blood flow by 2.19 +/- 0.44 and 4.06 +/- 0.92 ml/min/100 ml forearm volume (p < 0.05 normal vs CHF). The impaired forearm blood flow responses in heart failure occurred despite significantly greater (p < 0.05, normal vs CHF) increases in venous osmolality (17.3 +/- 6.5 vs 9.6 +/- 1.3 mosm/kg for the 660 mosm/kg infusion). There were no differences between groups in forearm venous hematocrit, calcium, and sodium or potassium changes during hyperosmolal infusions. It is concluded that peripheral vasodilation to hyperosmolal stimuli is impaired in patients with CHF.
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PMID:Impaired forearm vasodilation to hyperosmolal stimuli in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy or to ischemic cardiomyopathy. 144 84


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