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

Self-limited edema is a well-recognized complication of insulin therapy. However, progression to overt cardiac failure has only recently been reported in one patient with pre-existing heart disease. This report describes the first case of insulin-induced cardiac failure in a patient without underlying heart disease. Current trends toward intensive insulin therapy for rapid near-normalization of blood glucose levels will increase the recognition of this entity. Careful follow-up of so-called "self-limited" insulin edema is encouraged, and the early institution of diuretic therapy is advocated in elderly patients to prevent the development of overt cardiac failure.
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PMID:Insulin-induced cardiac failure. 401 1

To investigate the role of the autonomic nervous system in controlling insulin secretion 13 normal subjects and 5 patients with heart failure underwent insulin secretion tests. Alpha-adrenergic stimulation and beta-receptor blockade significantly depressed the secretion of insulin in response to intravenous tolbutamide in normal subjects, while both alpha-blockade and beta-stimulation significantly increased the insulin secretion response in both normal subjects and patients in heart failure. Parasympathetic stimulation and blockade had no significant effect on the insulin secretion response. These findings suggest that drugs that block the alpha-adrenergic receptors or stimulate the beta-adrenergic receptors by their ability to counteract the insulin suppression resulting from increased sympathetic nervous activity may play a vital metabolic part in the deranged metabolism of the failing heart in addition to their direct haemodynamic benefits.
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PMID:Autonomic control of insulin secretion and the treatment of heart failure. 439 68

Beta-adrenergic receptor blocking agents have been receiving attention as first-line agents for the treatment of hypertension. However, a number of significant side effects of these drugs have been brought to light. The most important of these--increases in "atherogenic" lipid concentrations--may place treated persons at risk of coronary artery disease and myocardial infarction. Other side effects, including bronchospasm, heart failure, cold extremities, reduced insulin secretion and central nervous system effects, may preclude their use in many patients. However, because several major trials have shown that controlling blood pressure reduces the incidence of coronary heart disease and stroke, the use of antihypertensive therapy is likely to increase and to continue for longer periods. The physician must prescribe an agent with the fewest and most minor side effects. Alternatives to beta-blocking drugs, such as the alpha-receptor blocking agent prazosin, should be considered and evaluated because of the limiting side effect profile of beta blockers.
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PMID:Beta-adrenergic receptor blocking drugs in hypertension. With special reference to their use as initial therapy. 614 20

In order to limit the spread of myocardial infarction, 56 patients with acute myocardial infarction, admitted to hospital within 10 hours after the attack, for two days received continuous intravenous drip infusion of glucose-insulin-potassium mixture (GIP) containing: 300 ml glucose, 50 U common insulin, 60 meqv potassium chloride per 1 1 of the solution, at the rate of 1 ml/kg/hour. A control group of 48 patients were given saline solution at the rate of 20 drops/minute for the same duration of time. In the GIP-treated group, the frequency of cardiac rhythm disorders and clinical signs of heart failure was significantly lower. In spite of a certain improvement in the clinical pattern of the disease, hospital mortality rates did not differ statistically between the treated and control patients. GIP treatment did not reduce the spread of myocardial infarction, as evidenced by electrocardiographic charting and routine assays of serum CPK activity.
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PMID:[Effect of a glucose-insulin-potassium mixture on the size and clinical course of myocardial infarct]. 633 81

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

The hemodynamic, hormonal and electrolyte effects of prenalterol, a synthetic selective beta 1 agonist, were studied in six patients with New York Heart Association functional class II and III heart failure. Prenalterol was infused incrementally at 60, 120 and 240 nmol/min, each rate for 24 hours, producing steady-state plasma prenalterol levels of 52 +/- 3, 121 +/- 6 and 194 +/- 9 nmol/1, respectively (mean +/- SEM). Hemodynamic and hormonal measurements were performed before, during and after prenalterol administration under conditions of constant body posture and a regulated intake of dietary sodium and potassium. Prenalterol induced a statistically significant increase in cardiac index (from 2.6 +/- 0.2 to 3.1 +/- 0.3 1/min/m2), with parallel increases in stroke index (from 28 +/- 2 to 34 +/- 2 ml/beat/m2). Forearm blood flow measurements increased (from 2.9 +/- 0.5 to 4.1 +/- 0.6 ml/min/100 g), while calculated systemic vascular resistance fell, as did pulmonary capillary wedge pressure (from 13.7 +/- 1.6 to 10.5 +/- 1.7 mm Hg). The drug did not alter heart rate, arterial pressure, right heart pressures or the frequency of ventricular premature beats. Prenalterol increased plasma renin activity (from 2.9 +/- 0.8 to 6.6 +/- 1.8 nmol/1/hour), angiotensin II (from 59 +/- 12 to 89 +/- 22 pmol/1), urinary aldosterone excretion (from 41 +/- 10 to 78 +/- 34 nmol/day) and plasma insulin (from 10.6 +/- 2.2 to 19.8 +/- 3.9 mU/1). Circulating catecholamines, cortisol, glucose, glucagon or pancreatic polypeptide did not change. Dose-response studies in five patients showed dose-dependent increments in hemodynamic variables, while hormonal changes plateaued at the second dose level. We conclude that prenalterol infusion augments myocardial contractility, reduces systemic vascular resistance, and stimulates insulin release and the renin-angiotensin-aldosterone system.
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PMID:Hemodynamic, hormonal and electrolyte responses to prenalterol infusion in heart failure. 682 3

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

Clinical pattern and complications of the disease were studied in 62 heparin-treated patients with large-focal myocardial infarction as compared to a control group of 59 patients treated with a polarizing mixture of glucose, insulin, potassium, analgetics and tranquilizers. The changes of the necrotic area and lesion were assessed on the basis of precardiac charting. The results obtained were correlated to the data on central hemodynamics, heart contractility and pumping function, gaseous exchange and acid-base balance. Heparin-treated patients showed a smaller rate of fatal outcomes, although primary ventricular fibrillation and heart failure prevailed in the mortality pattern in both groups. Heparin treatment improved central hemodynamics, contractility and pumping function of the heart, and gaseous exchange, while prestress decreased simultaneously, which is the optimum effect for patients with acute myocardial infarction. Precardiac charting data showed heparin treatment to be associated with a more rapid reduction in the depth of the ischemic lesion. The advantages of continuous intravenous heparin infusion are demonstrated.
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PMID:[Effectiveness of heparin in patients with acute myocardial infarction]. 716 20

A 68-year-old female on two-year chronic hemodialysis for chronic renal failure due to chronic pyelonephritis, was admitted to hospital for weakness, dulled sensorium and dizziness. On examination the patient was in a state of circulatory collapse, the electrocardiogram showed an accelerated idioventricular rhythm and laboratory analysis revealed extreme hyperkalemia (K+ 10.1 mmol/l). There were no common causes of shock, such as hypovolemia, sepsis, heart failure and presence of vasodilator drugs. The patient was treated with calcium gluconate, sodium bicarbonate and sodium chloride (to oppose the effects of hyperkalemia on the cell membrane to minimize cardiac and neuromuscular toxicity), insulin and dextrose (to increase the transport of K+ from the extracellular to the intracellular compartment), and hemodialysis (to remove K+ from the body). At the end of the hemodialysis session, the patient was in a clinically good condition, blood pressure was 160/90 mm Hg and the serum K+ concentration was normal. The case appeared to suggest that extreme hyperkalemia may have direct effects on vascular resistance, causing hypotension and shock.
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PMID:A life-threatening complication of extreme hyperkalemia in a patient on maintenance hemodialysis. 748 41

From 1975 to 1993, our University Hospital performed 2789 graft procedures. During the same period, 12 poisoned, "brain-dead" patients were considered as organ donors. The toxic substances involved were: methaqualone (n = 1), benzodiazepine alone (n = 1), benzodiazepine plus tricyclic antidepressants (n =1), tricyclic antidepressants alone (n = 1), barbiturates (n = 2), insulin (n = 2), carbon monoxide (n = 1), cyanide (n = 1), methanol (n = 1), and acetaminophen (n = 1). From these intoxicated persons, 32 organ transplants were obtained, but only 23 could be followed for 1 month and only 20 for 1 year. The outcome at 1 month was favorable in 20 of the 23 patients. Two heart transplant patients died with 24h after grafting from stroke and acute heart failure, respectively. Preoperative hepatic encephalopathy was not corrected after grafting and was directly responsible for the death of a liver transplant patient. After 1 year, 15 of the 20 recipients were still alive. Chronic hepatic graft rejection led to a fatal outcome in one recipient and to second grafting in another. Finally, one recipient died from delayed neoplasia. Based on our experience, organ procurement may be considered in a few select cases of acute poisoning. Attention should, however, be drawn to possible graft damage due to some poisons.
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PMID:Outcome following organ removal from poisoned donors: experience with 12 cases and a review of the literature. 762 77


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