digoxin and Anemia

Anemia aggravates the disease course and the survival rate of chronic heart failure (CHF) patients. The purpose of the study was to investigate the level of erythropoietin (EPO) in CHF patients with anemic syndrome, with the aim to more accurately assess the severity of the disease and its treatment, depending on the anemia degree.. Patients with ischemic CHF of I-IV functional class (FC) with and without anemia were examined (total number of patients=208, patients with anemia=174). The EPO was determined using the enzyme-linked immunosorbent assay. Before treatment, the patients underwent the following medical therapy: angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, long-acting nitrates, diuretics, digoxin, and beta-blockers at individual doses. Depending on the plasma EPO level, the CHF patients with anemia were divided into four randomized groups in terms of treatment.. Normal erythropoietinemia was found in 36.2% of the CHF patients with anemic syndrome (I-III FC), hypoerythropoietinemia in 44.8% (III-IV FC), and hypererythropoietinemia in 18.96% (III-V FC). The EPO level in the blood plasma of the patients with I-II FC CHF with hypoerythropoietinemia, who were treated with methoxy polyethylene glycol-epoetin β (MEB), increased by 2.2 times. Combination therapy with disease-modifying drugs and MEB led to a significant increase in the plasma EPO level in the CHF patients with hypoerythropoietinemia.. It was shown that the EPO level in patients with CHF and anemia did not always drop. Hypererythropoietinemia in patients with CHF and anemia leads to an unfavorable treatment prediction. This necessitates the investigation of the EPO level in all patients with CHF before and after treatment, with the aim of correcting the anemic syndrome. The research showed that the combined therapy of patients with CHF and anemia using MEB medication and iron with regard to the EPO level in the blood plasma improved their overall physical condition, reduced heart failure symptoms and hospitalization frequency, and demonstrated a clear tendency to reduce the general mortality rate.

Topics: Adrenergic beta-Antagonists; Adult; Aged; Anemia; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Chronic Disease; Digoxin; Diuretics; Erythropoietin; Female; Heart Failure; Humans; Male; Middle Aged; Nitrates; Severity of Illness Index

Peripartum cardiomyopathy is rare in developped countries, but still frequent in Africa. It is defined as a heart failure occurring during peripartum, without any underlying etiology. Authors present 3 cases showing that heart failure before or after delivery may be due to causes which are frequent in the Sahelian area but generally misdiagnosed. Anemia, hypertension and rheumatic fever were the causes of heart failure in these 3 patients, but they were not apparent when the initial diagnosis was made. These observations emphasize that, despite the complex hypothesis trying to explain heart failure during the peripartum period, one should think about some frequent causes which can be misdiagnosed because of the pregnant state or the heart failure itself.

Topics: Adult; Africa, Northern; Anemia; Angiotensin-Converting Enzyme Inhibitors; Captopril; Cardiotonic Agents; Causality; Developing Countries; Digoxin; Diuretics; Echocardiography; Female; Furosemide; Heart Failure; Humans; Hypertension; Incidence; Pregnancy; Pregnancy Complications, Cardiovascular; Puerperal Disorders; Rheumatic Fever; Sudan

We tested whether digoxin would limit tissue hypoxia during severe anemia by improving peripheral O2 distribution or decreasing O2 demands. Hematocrit (Hct) was reduced in eight control and eight digoxin-treated pigs from 27-28% to 17-18, 11-12, and 7-8%. Whole body and hindlimb blood flow, O2 transport, O2 extraction, and O2 consumption and serum catecholamines (epinephrine and norepinephrine) were determined at each Hct. Arterial and femoral venous lactate and O2 deficit were obtained to reflect tissue hypoxia. Cardiac output was significantly greater (P less than 0.05) with digoxin, as expected, but there were no differences in hindlimb blood flow. Also, whole body and hindlimb O2 extractions were equal in both groups for similar levels of O2 transport, suggesting that digoxin did not alter the relationship of O2 flow to metabolism in regional circulations. As whole body O2 consumption fell, controls accumulated more (P less than 0.05) O2 deficit and arterial lactate than the digoxin group. Furthermore, the slope demonstrating the linear increase of lactate with respect to O2 deficit was much steeper in controls (y = 1.11 + 0.06x) than in digoxin (y = 1.36 + 0.02x), suggesting that there were differences in the degree of tissue hypoxia for comparable O2 deficit. This may be attributed to the marked differences in catecholamine response: epinephrine was higher in controls at Hct of 7-8% and norepinephrine was higher at Hcts of 11-12 and 7-8%. Digoxin may have inhibited the release of catecholamine or reduced the stimulus for catecholamine secretion during anemia. We speculate that digoxin markedly improved the balance between peripheral O2 supply and demand during anemia by inhibiting catecholamine thermogenesis, thereby decreasing O2 demands. This may explain some of the salutary effects of glycosides in high-output cardiac failure with normal ventricular function.

Topics: Anemia; Animals; Biological Availability; Biological Transport; Catecholamines; Digoxin; Hematocrit; Hemodynamics; Hindlimb; Hypoxia; Lactates; Lactic Acid; Oxygen; Oxygen Consumption; Swine

Chronic inflammatory diseases are often associated with decreased red blood cell (RBC) mass. The cytokines cachectin/tumor necrosis factor-alpha (TNF) and interleukin 1 (IL 1) are produced by monocytes/macrophages in response to many inflammatory stimuli and have been implicated in the anemia of chronic disease. This study was undertaken to evaluate the mechanisms by which cachectin/TNF, IL 1, or endotoxin induce anemia. Hematologic parameters and RBC kinetics were quantitated in rats given chronic sublethal quantities of either recombinant human cachectin/TNF, recombinant human IL 1 alpha, or Salmonella endotoxin for 7 days. Cachectin/TNF or endotoxin treatment resulted in a 25 or 31% decrease, respectively, in total RBC mass, whereas RBC mass was unchanged by IL 1 administration. Anemia associated with either chronic cachectin or endotoxin administration was characterized by normal mean corpuscular volume, mean corpuscular hemoglobin content, and reticulocyte numbers. [59Fe]RBC survival was significantly shortened in animals given cachectin, IL 1 or endotoxin, but the magnitude of the response was greatest in cachectin/TNF-or endotoxin-treated rats. Although cachectin/TNF-IL 1-, or endotoxin treatment resulted in similar hypoferremia and shortened plasma iron half-life, endotoxin or cachectin/TNF treatment (but not IL 1) significantly reduced the incorporation of plasma 59Fe into newly synthesized RBCs. We conclude that chronic cachectin/TNF administration produces anemia by decreasing RBC synthesis and reducing the life span of circulating RBCs. An endogenous cachectin/TNF response during inflammatory disease may contribute to an associated anemic state, whereas the modestly reduced red cell life span induced by IL 1 does not lead to a net reduction in RBC mass, presumably owing to a preserved RBC synthetic rate.

Topics: Anemia; Animals; Blood Proteins; Cardenolides; Digoxin; Erythrocyte Aging; Erythrocyte Indices; Erythrocytes; Half-Life; Hematocrit; Hemoglobins; Interleukin-1; Iron; Male; Rats; Rats, Inbred Strains; Recombinant Proteins; Salmonella; Saponins; Tumor Necrosis Factor-alpha

Systolic time intervals were measured from simultaneous high speed recordings of the electrocardiogram, phonocardiogram, and carotid artery pulse in 15 men with chronic severe anaemia not in heart failure and with a normal heart size, and in 15 normal men. Heart rates, electromechanical systole (QS2), pre-ejection period index (PEPI), left ventricular ejection time index (LVETI), and the ratio of pre-ejection period to left ventricular ejection time (PEP/LVET) did not differ significantly in the two groups. After the intravenous administration of frusemide in 10 of the anaemic patients, the pre-ejection period index was prolonged, the PEP/LVET ratio increased, heart rate increased, and the left ventricular ejection time index shortened. Intravenous digoxin did not alter the QS2 interval and heart rate significantly in the anaemic subjects. Left ventricular function in chronic severe anaemia as measured by systolic time intervals does not differ from that of normal controls. The effect of frusemide on the systolic time intervals is explained as an effect of the fall in preload, bringing cardiac function further down on the ascending limb of the Frank-Starling curve. Other related studies are discussed.

Topics: Adult; Anemia; Chronic Disease; Digoxin; Furosemide; Humans; Male; Middle Aged; Myocardial Contraction; Systole

Topics: Anemia; Anti-Bacterial Agents; Cardiomyopathies; Diet, Sodium-Restricted; Digoxin; Diuretics; Heart Defects, Congenital; Heart Failure; Humans; Infant; Infant, Newborn; Myocarditis; Palliative Care; Respiratory Tract Infections; Rest; Tachycardia, Paroxysmal

Topics: Anemia; Atrial Fibrillation; Black People; Blood Pressure; Cardiac Catheterization; Cardiac Output; Digoxin; Electrocardiography; Endomyocardial Fibrosis; Heart Rate; Heart Ventricles; Hemodynamics; Hemoglobinometry; Humans; Oxygen; Pericarditis, Constrictive; Strophanthins; Uganda

Topics: Anemia; Blood Pressure; Blood Pressure Determination; Blood Urea Nitrogen; Blood Volume; Cardiac Catheterization; Cardiac Output; Cardiovascular System; Dialysis; Digoxin; Drug Therapy; Glomerulonephritis; Guanethidine; Humans; Methyldopa; Peritoneal Dialysis; Pyelonephritis; Renal Dialysis; Urine

Topics: Anemia; Anemia, Pernicious; Blood Transfusion; Deficiency Diseases; Deglutition Disorders; Digoxin; Diuretics; Esophagoscopy; Geriatrics; Hematinics; Humans; Iron; Plummer-Vinson Syndrome; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Anemia; Anemia, Hypochromic; Animals; Digitalis; Digitalis Glycosides; Digitoxin; Digoxin; Dogs; Epinephrine; Heart; Potassium