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

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

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

Ischemic hepatitis is not an uncommon complication of reversible severe hypotension or cardiac failure. The prognosis usually is determined by the cause of the initial hypotension or cardiac failure, rather than the subsequent hepatic dysfunction. We report a retrospective analysis of nine patients with ischemic hepatitis in which previously unreported clinical and biochemical abnormalities are noted. The clinical and biochemical course of the patients were reviewed until recovery or death from ischemic hepatitis. All the patients had a rapid striking elevation of aspartate aminotransferase, and lactic dehydrogenase, with an equally rapid resolution of these parameters. Abnormal serum glucose levels occurred in six patients (none of whom had a prior carbohydrate intolerance). Insulin therapy was given to three patients for a limited period. Renal impairment was manifest in all nine patients, and it resolved spontaneously within 10 days. Altered mental status was detected in six patients; the changes reverted to normal within 7 days of their onset. A preexisting anemia (hemoglobin less than 11.0 g/dl) was noted on admission in four patients, and it did not appear to potentiate the manifestations of the hepatic ischemia. We conclude that ischemic hepatitis should be anticipated in all patients with a recent history of systemic hypotension. It should be considered in the differential diagnosis of patients with unexplained hepatitis; the early massive rise in lactic dehydrogenase, the rapid fall in transaminases, and the early mild/moderate renal failure strongly suggest ischemic hepatitis. Patients with ischemic hepatitis can manifest reversible renal failure, mental confusion, and hyperglycemia which may require insulin for its control.
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PMID:Ischemic hepatitis: widening horizons. 848 Jul 56

The discovery of insulin in 1922 aroused immediate clinical interest in its use in heart disease. In severe heart failure, insulin release is suppressed by the combined effect of poor pancreatic perfusion and by increased sympathetic activity. In these circumstances, myocardial metabolism of glucose may break down through the deficiency of insulin. Because of this, glucose, insulin and potassium solution (GIK solution) has been used in cardiopulmonary resuscitation. However, its mechanism is not yet fully known. This study was designed to determine the effect of insulin on cardiac muscle at various temperatures. The mechanical response of papillary muscle isolated from guinea pig ventricle was observed under various thermal conditions (23-37 degrees C). Twitch tension was increased by the administration of 0.2 I.U./ml insulin under each thermal condition. In all circumstances, the increase in contractile force was noted about 2 min after the administration of insulin. The effect of insulin on 20 preparations demonstrated the mean maximum contractile force was 226% ( +/- 34 S.D., n = 5) in 37 degrees C, 194% ( +/- 36 S.D., n = 5) in 30 degrees C, 190% ( +/- 30 S.D., n = 5) in 27 degrees C and 200% ( +/- 36 S.D., n = 5) in in 23 degrees C. The differences between different temperatures was not significant. The effect of insulin during depression Na-K pump by high concentration of ouabain (g-strophanthin, 10(-5) M) was also observed. Insulin (0.2 I.U./ml) was administered when the papillary muscle showed no response to electrical stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of isolated guinea pig myocardium to insulin therapy during normothermia and graded hypothermia. 242 78

Acute ischemic heart failure was induced in eight dogs by coronary embolization. Severe depression of the left ventricular (LV) performance was evidenced. At 15 min after the embolization procedure, dopamine was infused at a dosage sufficient to increase the maximum rate of LV pressure rise (LVdP/dtmax) by approximately 50%. The significant improvement in cardiac performance was obtained at unaltered myocardial oxygen consumption (MVo2). Dopamine infusion was concluded, and after a stabilization period 300 IU of insulin was injected. This was followed by the infusion of glucose and potassium to maintain levels. Insulin significantly improved the performance of the failing left ventricle at unaltered MVo2, but to a lesser extent than did dopamine. Additional dopamine infusion further significantly improved cardiac performance. The net effect of insulin and dopamine in combination as compared with dopamine alone was a significantly greater increase in stroke volume and cardiac output due to a more pronounced decrease in total peripheral resistance. Dopamine increased arterial concentrations and myocardial uptake of free fatty acids (FFA). The net metabolic effect of insulin and dopamine in combination as compared with dopamine alone was a shift in myocardial substrate uptake from FFA to carbohydrates.
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PMID:Hemodynamic and metabolic effects of dopamine and insulin during acute left ventricular failure in dogs. 242 68

Myocardial calcium uptake after isoproterenol (ISO) in the isolated, perfused heart was investigated at 24-h intervals after the injection of streptozocin (STZ) in rats. After 4 days, when hyperglycemia had persisted for 3 days, myocardial calcium uptake in response to this strong beta-adrenergic agonist fell significantly to the level of unstimulated hearts, which also was the level of propranolol-pretreated hearts exposed to ISO. Insulin, when given in vivo 60-90 min before perfusion, led to a complete normalization of this ISO response in diabetic rats (duration 8 days), while in vitro addition of insulin to the perfusate (0.1 U/ml) significantly increased, while not completely normalizing, the ISO-induced myocardial calcium uptake. Insulin, therefore, has a direct effect on this beta-adrenergic response in diabetic rats and streptozocin in itself does not cause the desensitization. Considering the essential role of this calcium transport for the electromechanical coupling in the heart, such metabolically induced changes in catecholamine sensitivity might hypothetically have relevance for the increased incidence of heart failure in diabetes.
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PMID:Abnormal myocardial calcium uptake in streptozocin-diabetic rats. Evidence for a direct insulin effect on catecholamine sensitivity. 388 96

Metabolic effects of pharmacological doses of insulin were studied during acute ischaemic heart failure in 7 dogs. Severe depression of left ventricular performance was induced by embolization of the left main coronary artery with 50 micron plastic microspheres. This was followed by a significant reduction in myocardial blood flow and oxygen consumption. After a period of stabilization of the haemodynamic and metabolic variables, 300 IU of insulin free of glucagon and calcium was injected as a bolus dose. Glucose and potassium were given to maintain their plasma concentrations. Insulin significantly improved performance of the failing left ventricle. Myocardial blood flow was significantly increased, whereas myocardial oxygen consumption was unchanged. Insulin significantly reduced arterial concentrations and myocardial uptake of free fatty acids, while myocardial uptake of glucose and lactate showed a non-significant increase. In conclusion, pharmacological doses of insulin significantly improve cardiac pump function without increasing myocardial oxygen consumption during acute ischaemic left ventricular failure in dogs. This may be partly related to reduced myocardial uptake of free fatty acids relative to that of glucose.
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PMID:Metabolic effects of high doses of insulin during acute left ventricular failure in dogs. 389 51

Diabetes mellitus (DM) was induced in 10 lambs by giving alloxan (150 mg/kg). Two to 4 days later, mean values for glucose were 748 mg/dl, and for arterial pH 7.25 (acute group). Two additional lambs were studied after 3 mo of DM (chronic group). Data were compared with 7 controls (glucose 128 mg/dl, pH 7.36). Left ventricular (LV) performance was assessed from function curves and measurements of LV dP/dtmax. Stroke volume ejected at LV end-diastolic pressure of 5 cmH2O (SV5) was calculated from regression analysis of each curve. SV5 averaged 2.83 +/- 0.34 ml in controls and 2.90 +/- 0.23 ml in the acute diabetics (not significant). Mean values for LV dP/dtmax also did not differ. A significant correlation was found between SV5 and LV weight (P less than 0.001). SV5 was normalized as ml/100 g LV, and average values for the three groups were identical. Insulin (10 U/kg) caused a progressive fall in SV5 in diabetics with severe acidosis (pH 7.00), but not in those with less acidosis (pH 7.28). In nondiabetics given lactic acid (pH 7.01), SV5 fell to 60% of initial values 1 h after insulin. Acidemic animals not given insulin showed no reduction in LV performance in the same time interval. Adrenergic support is necessary to prevent cardiac failure associated with acidosis. The present findings are ascribed to inhibition by insulin of catecholamine inotropic action on myocardium.
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PMID:Effects of insulin on ventricular function in diabetic lambs with acidosis. 679 34

Frequent abnormalities of left ventricular function were detected in 212 established diabetic patients using non-invasive techniques. Diabetics without angina or heart failure (n = 185) were significantly different from normal subjects (n = 50) in beat-to-beat variation, ratio of pre-ejection period to left ventricular ejection time, pre-ejection period index, isovolumic relaxation time, and interval from minimal dimension to mitral valve opening. Diabetics with angina (n = 18) were similar to control subjects with angina (n = 25); they showed a significant dimension change during the isovolumic period as compared with other diabetics and normals. Sixteen diabetics without angina also showed outward motion during the isovolumic period (incoordinate relaxation) and 13 had abnormal systolic time intervals. Four diabetics suffered a myocardial infarction during the study period; all had previously shown incoordination. Comparison of diabetics with a diastolic blood pressure below 100 mmHg and between 100 and 125 mmHg showed that the latter had a thicker posterior wall; the enlarged systolic dimension and reduced fractional shortening were the result of the inclusion of five of the 11 diabetic subjects with heart failure in the hypertensive group. Insulin-dependent diabetics tend to have more pronounced abnormalities of left ventricular function than those not requiring insulin. Patients selected from a diabetic clinic frequently have impaired left ventricular function, and ventricular hypertrophy, when present, in primarily caused by hypertension.
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PMID:Left ventricular function in diabetes mellitus. I: Methodology, and prevalence and spectrum of abnormalities. 700 55

The objective of this study was to investigate the existence of abnormalities of insulin sensitivity in patients with chronic heart failure. Glucose metabolism and insulin resistance were assessed in 10 male patients with severe, chronic heart failure and in 10 matched control subjects. Glucose, insulin and C-peptide concentration profiles were measured following a 0.5 g.kg-1 intravenous glucose tolerance test. Insulin sensitivity (inversely related to insulin resistance) was estimated by minimal modelling analysis of the glucose and insulin profiles. Heart failure patients had similar mean fasting plasma glucose concentration to controls but a significantly greater mean fasting plasma insulin concentration (P = 0.002) and C-peptide concentration (P = 0.02). Plasma glucose response profile was similar in the two groups but the incremental plasma insulin response profile of the heart failure group was significantly greater (P = 0.004). Mean insulin sensitivity was 73% lower in the heart failure patients (P = 0.003). These findings show that patients with severe chronic heart failure are hyperinsulinaemic and insulin resistant compared with a matched health group. This insulin resistance and hyperinsulinaemia may contribute to the progressive deterioration in myocardial function and associated clinical features of fatigue and reduced exercise tolerance seen in heart failure. Interventions designed to overcome or reduce insulin resistance warrant further investigation.
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PMID:Insulin resistance in chronic heart failure. 783 69


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