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PubMed1981

Clinical implications of serum digoxin concentrations.

Factors influencing serum digoxin concentrations, and the relation of these levels to classical electrocardiographic (ECG) and clinical manifestations of toxicity, were assessed in a series of 463 consecutively hospitalized patients of mean age 58 years. The majority of patients were receiving beta-acetyldigoxin or beta-methyldigoxin. Age, sex, creatinine clearance, and weight-corrected dose collectively explained less than 7% of overall variability in serum digoxin concentrations; creatinine clearance, which declined significantly with age (r=-0.36, p less than 0.001) was the most important of these determinants. ST-segment depression was present in the majority of patients and became more common at higher serum digoxin concentrations. However, PR interval, QRS durations, QT interval, or the presence of AV block were not associated with serum levels. Among 75 patients with atrial fibrillation, ventricular rate did not decline with increasing digoxin concentrations. The presence of gastrointestinal, neuromuscular, or psychiatric symptoms classically attributed to digitalis toxicity was not associated with serum digoxin concentration. Serum levels of digoxin appear to be of limited value in assessing the degree of digitalization.

Acetyldigoxins↗
PubMed1995

Digoxin-induced ventricular arrhythmias in the guinea pig heart in vivo: evidence for a role of endogenous catecholamines in the genesis of delayed afterdepolarizations and triggered activity.

The mechanisms of digoxin-induced ventricular arrhythmias were studied in vivo using a novel experimental model. Anesthetized guinea pigs were instrumented with custom-made electrode catheters which enabled the monitoring and recording of right atrial, right ventricular, and His bundle electrograms, midmyocardial monophasic action potentials (MAP), and systemic arterial blood pressure. Intravenous digoxin induced ventricular arrhythmias ranging from ventricular premature contractions (VPCs) to ventricular fibrillation (VF). These were associated with delayed afterdepolarizations (DADs) observed on the MAP recordings. The severity of the arrhythmias depended on the dose of digoxin. Short bursts of ventricular pacing neither terminated nor suppressed episodes of ventricular tachycardias (VTs). A direct relationship existed between the paced ventricular cycle length and the coupling interval between the last paced beat and the first ectopic beat (r = 0.913, P < 0.001, n = 10) and between the amplitude of the DADs and the pacing rate (r = 0.972, P < 0.05, n = 7). The increased contractility (LV dp/dt) and heart rate evoked by isoproterenol (0.1 microgram/kg) did not induce DADs in the absence of digoxin. Verapamil terminated the digoxin-induced VTs in 15 of 16 animals and abolished the associated DADs in 7 of 7 animals. Adenosine terminated the VTs in 15 of 19 animals and abolished the DADs in 8 of 10 animals. Digoxin induced VT in only 1 of 6 animals treated with reserpine (5 + 5 mg/kg) 24 and 48h prior to experimentation. However, subsequent intravenous isoproterenol (0.2 micrograms/kg) induced VT and DADs, both of which were abolished by verapamil, in all 6 animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMedDate not supplied

Does digoxin still have a role in congestive heart failure?

The role of digoxin in the treatment of congestive heart failure is (CHF) being questioned. Digoxin continues to be the drug of choice for patients with atrial fibrillation in CHF. Large randomised trials have shown that digoxin (in addition to ACE inhibitors and diuretic) is beneficial in CHF due to systolic dysfunction, although it does not reduce mortality. Limited data suggest that digoxin benefit some, but not all patients with CHF due to left to right shunts. Digoxin does not benefit CHF due to diastolic dysfunction and it is not routinely recommended for prematures with patent ductus and CHF. The treatment with digoxin should be individualised.

Cardiotonic Agents↗
PubMedDate not supplied

Effect of cisapride and metoclopramide on digoxin bioavailability.

Pharmacokinetics of digoxin were investigated in six healthy volunteers following one week of digoxin monotherapy 0.25 mg b.i.d., and during coadministration of metoclopramide 10 mg t.i.d. or cisapride 10 mg t.i.d.. Metoclopramide reduced the peak plasma concentration of digoxin from 1.5 +/- 0.2 ng/ml to 1.1 +/- 0.1 ng/ml (mean +/- SEM) (p = 0.05), cisapride lowered the peak concentration to 1.3 +/- 0.1 ng/ml (p = 0.14). Metoclopramide prolonged the time required to reach the peak concentration of digoxin from 2 hr to 2.7 hr (p = 0.17), cisapride did not. Digoxin AUC0-12 (743 +/- 79 ng/ml.min) was reduced by 12% on coadministration of cisapride (653 +/- 38 ng/ml.min, p = 0.22) and by 19% on coadministration of metoclopramide (605 +/- 34 ng/ml.min, p = 0.06). It is concluded that the gastrointestinal absorption of digoxin is reduced by both substances. Monitoring of the patient's clinical status should be recommended when metoclopramide and cisapride are coadministered.

Adult↗
PubMed2001

Population-based investigation of relative clearance of digoxin in Japanese neonates and infants by multiple-trough screen analysis.

OBJECTIVE: The steady-state concentrations of digoxin at trough levels were studied to establish the role of patient characteristics in estimating doses for digoxin using routine therapeutic drug monitoring data. METHOD: The data (n = 448) showing steady state after repetitive oral administration in 172 hospitalized neonates and infants were analyzed using Nonlinear Mixed Effect Model (NONMEM), a computer program designed to analyze pharmacokinetics in study populations by allowing pooling of data. Analysis of the pharmacokinetics of digoxin was accomplished using a simple steady-state pharmacokinetic model. The effects of a variety of developmental and demographic factors on the clearance of digoxin were investigated. RESULTS: Estimates generated using NONMEM indicated that clearance of digoxin (l.h-1) was influenced by the demographic variables of age, total body weight, serum creatinine, the coadministration of spironolactone, and the presence or absence of congestive heart failure. The interindividual variability in digoxin clearance was modeled with proportional errors with an estimated coefficient of variation of 32.1%, and the residual variability was 28.9%. In the validation set of 66 patients, the performance (bias, precision) of the final population model was good (mean prediction error -0.04 ng.ml-1; mean absolute prediction error 0.20 ng.ml-1).

Cardiotonic Agents↗
PubMed1984

Clinical effects of digoxin on sinus node and atrioventricular node function after pharmacologic autonomic blockade.

The effects of digoxin on sinus node and atrioventricular (AV) node function were studied in 18 patients (mean age 53.6 years) with normal intrinsic heart rates. Electrophysiologic testing was performed both during basal state and after autonomic blockade with propranolol and atropine. Full digitalization was achieved by intravenous administration of digoxin (0.02 mg/kg) given in three divided doses over a 24-hour period. The following day, after a basal recording, autonomic blockade was again induced and the study was repeated. During basal state, digoxin significantly prolonged the sinus cycle length (SCL) (p less than 0.01) and the AH interval (p less than 0.01). However, when the intrinsic sinus node functions were compared (i.e., the values obtained after autonomic blockade), digoxin did not produce significant changes in intrinsic SCL, corrected sinus node recovery time, and sinoatrial conduction time. No significant changes were noted even in the intrinsic AH interval and AV nodal refractory periods. These findings suggest that: (1) intravenous administration of digoxin in therapeutic doses does not produce any depression of the intrinsic functions of the sinus node and AV node; and (2) the depressant effects induced by digoxin during basal state appear to be mediated through the autonomic nervous system.

Adult↗
PubMed1985

Therapy of digoxin intoxication in dogs by specific hemoperfusion through agarose polyacrolein microsphere beads-antidigoxin antibodies.

The usefulness of a new biocompatible, specific immunosorbent, Agarose-Polyacrolein Microsphere Beads--Antidigoxin antibodies (APAMB-AD) for hemoperfusive removal of digoxin in digoxin intoxicated dogs is described. The sorbent contains antidigoxin antibodies covalently bound to polyacrolein microspheres, 0.2 micron in diameter. Thousands of microspheres are matrix-encapsulated in cross-linked agarose to form beads 500 to 800 micron in diameter. The sorbent removes digoxin specifically, leaving other components of the blood intact, in contrast to the nonspecific sorbents (charcoal and ion exchange resins) currently in use. Digoxin-intoxicated dogs looked ill, vomited, and their ECGs showed malignant arrhythmias which were reversed during the first hour of hemoperfusion. By 2 hours of hemoperfusion, the ECG tracings returned to the preintoxication state. Up to 27% of the total body digoxin burden was removed. The sorbent is biocompatible. Neither the formed elements nor a battery of the routinely assayed soluble components of the blood or complement (C'4) were altered significantly during the hemoperfusion trials. The dogs tolerated the hemoperfusion well and all survived the intoxication. Nonhemoperfused dogs or dogs whose blood was hemoperfused through beads lacking antidigoxin did not survive the digoxin intoxication.

Acrolein↗
PubMed1987

Vasodilators as first-line therapy for congestive heart failure: a comparative hemodynamic study of hydralazine, digoxin, and their combination.

Although digitalis and vasodilators both enhance cardiac performance in patients with congestive heart failure, their relative efficacy is unknown. Accordingly, the acute hemodynamic effects of intravenous hydralazine (0.15 mg/kg), digoxin (1.0 mg), and the hydralazine-digoxin combination were evaluated in 14 normotensive heart failure patients at sitting rest, nine of whom were also studied during submaximal upright bicycle exercise. Hemodynamic responses at rest and exercise were similar. Cardiac output and stroke volume rose with both agents, the increase in cardiac output with hydralazine exceeding that with digoxin at rest. Left and right ventricular filling pressures declined equally. Systemic arterial mean pressure and total systemic vascular resistance fell with hydralazine, while, with digoxin, systemic arterial mean pressure increased and total systemic vascular resistance was unchanged. The hydralazine-digoxin combination produced increases in cardiac output and stroke volume that were greater than with either drug alone, and that equalled the sum of the drugs' individual effects; reductions in ventricular filling pressures were similar to the single-drug interventions. Thus, hydralazine is at least as effective as digoxin in improving cardiac function over the short term. Vasodilators may constitute an acceptable alternative to digitalis as initial therapy for congestive heart failure, except where a reduction in systemic arterial pressure is potentially deleterious. Use of combined treatment produces greater increases in cardiac output than with either drug alone, but requires risking the toxicities of two agents.

Aged↗
PubMed1988

Low- and medium-dose diltiazem in chronic atrial fibrillation: comparison with digoxin and correlation with drug plasma levels.

The safety and efficacy of diltiazem were compared with digoxin maintenance therapy for control of ventricular response in 19 patients with chronic atrial fibrillation. The relationship between drug plasma levels and cardiovascular effects was also investigated. After 7 days of combined therapy with diltiazem (60 mg three times a day in 10 patients and four times a day in nine patients) and digoxin (0.125 mg/day in two patients and 0.250 mg/day in 17 patients), the 24-hour mean heart rate derived from ambulatory ECG recording was reduced by 16.3% in comparison with digoxin therapy alone; the serum digoxin level was not significantly changed (1.06 +/- 0.43 vs 1.05 +/- 0.61 ng/ml). After a standardized bicycle exercise test (50 watts for 3 minutes), maximal heart rate was reduced by 19.9%, diastolic blood pressure was decreased by 8.9%, and systolic pressure-rate product was decreased by 12.5%. Diltiazem plasma levels (mean 120.9 +/- 63.3 ng/ml) were linearly correlated with percentage variations in maximal heart rate, diastolic blood pressure, systolic blood pressure, and pressure-rate product during exercise. Eighteen patients in succession discontinued digoxin therapy; after 14 days of diltiazem alone, the 24-hour mean heart rate returned to control values of digoxin therapy, whereas maximal heart rate and pressure-rate product during exercise were significantly reduced (-17.2% and -14.1%, respectively), with no changes in blood pressure. Diltiazem plasma levels (135.0 +/- 83.2 ng/ml) showed a linear correlation with the percentage of reduction in maximal heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1976

Favorable effects of oral maintenance digoxin therapy on left ventricular performance in normal subjects: echocardiographic study.

Left ventricular performance was assessed with echocardiography in 10 normal subjects before and during maintenance therapy with digoxin (0.5 mg/day orally) in the basal state and after acute pressure loading with intravenously administered phenylephrine. During digoxin therapy, despite a decrease in mean heart rate of 5 beats/min in the basal state, mean left ventricular ejection fraction increased from 74 +/- 2 to 79 +/- 1 percent (standard error, P less than 0.03); percent shortening of a left ventricular minor dimension increased from 37 +/- 2 to 41 +/- 1 percent (P less than 0.04) and the mean rate of left ventricular dimension shortening increased from 5.66 +/- 0.22 to 6.31 +/- 0.23 cm/sec (P = 0.05). During acute pressure loading with phenylephrine there was no change in mean heart rate after digoxin and mean ejection fraction increased from 69 +/- 3 to 75 +/- 2 percent; mean percent shortening increased from 33 +/- 2 to 38 +/- 2 percent; mean rate of shortening increased from 5.46 +/- 0.32 to 6.48 +/- 0.33 cm/sec and mean normalized rate of shortening increased from 1.11 +/- 0.06 to 1.29 +/- 0.05 sec-1 (all P less than 0.01). In a few subjects the response to digoxin did not coincide with the mean data for the whole group. This variability was largely due to difficulties in exactly matching heart rate between the control and digoxin studies. These data (1) support the concept that long-term oral digoxin therapy exerts a positive inotropic effect on the normal left ventricle, and (2) demonstrate the usefulness of echocardiography in nonivasive assessment of the effects of drugs on left ventricular performance.

Adult↗
PubMed1979

Effects of digoxin on sinus nodal function before and after vagal blockade in patients with sinus nodal dysfunction: a clue to the mechanisms of the action of digitalis on the sinus node.

To increase the limited knowledge of the effects of digitalis on sinus nodal function in patients with sinus nodal dysfunction and to initiate an investigation into the mechanisms underlying its effects, 34 patients with sinus nodal dysfunction were studied. Twenty patients underwent determination of sinus cycle length, estimated sinoatrial conduction time and maximal corrected sinus recovery time before and after the administration of 0.75 mg of intravenous digoxin. For the group, sinus cycle length did not change, sinoatrial conduction time increased insignificantly and maximal corrected sinus recovery time shortened; however, individual variation occurred. The effects of acute digitalization appeared to predict the effects of chronic digitalis administration on sinus nodal function in the eight patients who subsequently continued to take digoxin. Fourteen patients received digoxin after vagal blockade with atropine. After vagal blockade, digoxin lengthened sinus cycle length, sinoatrial conduction time and maximal corrected sinus recovery time. The effects of digoxin administered after atropine could be antiadrenergic, direct, or both, and are opposite to those induced by atropine alone. Because these effects are similar to those of vagotonia yet are not apparent when the vagi are unblocked, digoxin may have direct excitatory, adrenergic or previously unrecognized vagolytic effects on sinus nodal function in man and their manifestation may be dependent on heart rate or autonomic tone.

Adult↗
PubMed1983

Postmortem digoxin tissue concentration and organ content in infancy and childhood.

The concentration of digoxin in tissues and the content of the drug in various organs are reported in 36 infants and children. Sixteen received the drug on a short-term basis and 20 on a long-term basis. The drug was given intravenously to 12, orally to 17, and by intramuscular injection to 7. The study was conducted to determine distribution of digoxin in infants and children and to examine the forensic implications related to digoxin overdosage. Upper therapeutic concentration thresholds for digoxin were established in various tissues. These are different for preterm and full-term neonates than for older children and adults; for example, adult and neonatal values for postmortem blood specimens are 8 and 15 ng/ml, and for ventricular myocardium are 250 and 450 ng/g, respectively. The chronically digitalized premature infant retains in most tissues a considerably larger fraction of digoxin than more mature infants and children. This is in accord with previously demonstrated lower renal digoxin levels in premature infants attributed to their reduced ability to excrete this drug.

Adolescent↗
PubMed1989

Comparison of enalapril versus digoxin for congestive heart failure.

A multicenter, randomized, double-blind, parallel-group trial was conducted to compare the effects of enalapril and digoxin on clinical signs and symptoms, as well as exercise capacity, in 142 patients with congestive heart failure classified as mild to severe (New York Heart Association functional classes II to IV). The patients received optimal treatment with digitalis and diuretics for 2 to 4 weeks. Thereafter, they were randomly assigned to receive either enalapril plus diuretics (n = 72) or digoxin plus diuretics (n = 70). After 8 weeks of treatment, a significant improvement in classification was observed in 22 of 63 patients (35%) in the enalapril group and in 17 of 61 (28%) in the digoxin group (difference not significant [NS]). Similarly, duration of exercise increased in both groups (p less than 0.005; p = NS between groups). Blood pressures decreased in the enalapril group (from 129 +/- 19/80 +/- 10 to 121 +/- 20/78 +/- 11 mm Hg; p less than 0.001), but not in the digoxin group (from 134 +/- 19/82 +/- 12 to 138 +/- 19/85 +/- 10 mm Hg; NS). Serum creatinine and electrolytes did not exhibit any significant change from baseline values, except for serum potassium, which increased slightly in the enalapril group (from 4.24 +/- 0.48 to 4.43 +/- 0.49 mmol/liter; p less than 0.05) and decreased slightly in the digoxin group (from 4.28 +/- 0.47 to 4.18 +/- 0.40 mmol/liter; p less than 0.05). Adverse events were reported in 13 patients (5 withdrawals) in the enalapril group and in 7 patients (2 withdrawals) in the digoxin group (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗
PubMed1991

Effect of digoxin on ST-segment changes detected by ambulatory electrocardiographic monitoring in healthy subjects.

Digoxin causes false-positive ST depression during exercise stress testing, but it is unknown if digoxin produces ST depression during ambulatory electrocardiographic monitoring. Fifty healthy volunteers underwent both exercise stress testing and ambulatory electrocardiographic monitoring before and after 14 days of digoxin (0.25 mg/day) administration. Significant ST depression was defined as greater than or equal to 1 mm of horizontal or downsloping ST depression 80 ms after the J point lasting for greater than or equal to 60 seconds. During therapy, 13 subjects (26%) had at least 1 episode of ST depression and 5 subjects (10%) had multiple episodes of ST depression detected by ambulatory monitoring. Ten subjects (20%) had ST depression that occurred during exercise that was detected by both stress test and ambulatory monitoring. Three subjects (6%) had ST depression that was detected on the ambulatory recording only at times other than during the stress test. Stratification of demographic and clinical variables did not predict digoxin-induced ST depression. Thus, digoxin causes false-positive ST depression detected by ambulatory monitoring. The incidence is similar to that observed during stress testing, but also occurs at heart rates lower than that achieved during stress tests. Ambulatory electrocardiographic monitoring will be less useful in the noninvasive assessment of coronary artery disease in patients receiving digoxin.

Adult↗
PubMed1993

Effectiveness and costs of digoxin treatment for atrial fibrillation and flutter.

Clinical outcomes and costs associated with the use of digoxin in atrial fibrillation and flutter were evaluated in a prospective, observational study at 18 academic medical centers in the United States. Data were collected on 115 patients (aged > 18 years) with atrial fibrillation or flutter who were treated with digoxin for rapid ventricular rate (> or = 120 beats/min). The median time to ventricular rate control (i.e., resting ventricular rate < 100 beats/min, decrease in ventricular rate of > 20%, or sinus rhythm) was 11.6 hours from the first dose of digoxin for all evaluable patients (n = 105) and 9.5 hours for those only receiving digoxin (n = 64). Before ventricular rate control, the mean +/- SD dose of digoxin administered was 0.80 +/- 0.74 mg, and a mean of 1.4 +/- 1.8 serum digoxin concentrations were ordered per patient. Concomitant beta-blocker or calcium antagonist therapy was instituted in 47 patients (41%); in 19 of these, combination therapy was initiated within 2 hours. Adenosine was administered to 13 patients (11%). Patients spent a median of 4 days (range 1 to 25) in the hospital; 28% spent time in a coronary/intensive care unit and 79% in a telemetry bed. Loss of control (i.e., resting ventricular rate returned to > 120 beats/min) occurred at least once in 50% of patients and was associated with a longer hospital stay (p < 0.05). Based on 1991 data, the estimated mean hospital bed cost for patients with atrial fibrillation or flutter was $3,169 +/- $3,174.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1983

Hemodynamic effects of combined digoxin and dopamine administration in postoperative patients with cardiac dysfunction.

In 10 patients with postoperative cardiac dysfunction which required dopamine for inotropic and hemodynamic support, we observed the cardiovascular effects of short-term digoxin administration. The average dosage of dopamine was 7.45 micrograms/kg per minute and was maintained while the patients were given 1 mg of digoxin over 8 hours. The dosage of dopamine was then tapered over the next 4 hours. We observed a significant increase in the cardiac index (4 hours) and a reduction in the heart rate (8 hours) before the dopamine dosage was reduced. After a reduction in dopamine dosage to 2.28 micrograms/kg per minute, these effects persisted. No significant changes were noted in systemic vascular resistance or pulmonary artery diastolic pressure during digoxin administration. These results indicate that the inotropic effects of dopamine and digoxin are additive when given in combination and that digoxin can be used to significantly reduce the dopamine dosage in patients with postoperative cardiac failure. Thus, the combination of an acute inotropic agent, dopamine, and a chronic inotropic agent, digoxin, appears to be clinically useful in postoperative cardiac dysfunction.

Cardiac Output↗
PubMed1975

Radioimmunoassay of digoxin in renal failure: a comparison of different commercial kits.

Six commercially available kits for radioimmunoassay of digoxin were compared. When serum from patients with chronic renal failure on maintenance digoxin therapy was analysed, important discrepancies in the results obtained with the 6 kits were found in some of these patients. However, recovery of digoxin added to serum of a healthy volunteer, was within acceptable limits and comparable for the 6 kits. In patients with renal failure not taking digoxin but several other medications, digoxin estimations gave results close to zero. The affinity of the antibodies for some metabolites of digoxin was also assessed: important differences between the kits were found.

Adult↗
PubMed1986

Effects of BAY K-8644 on inotropic and arrhythmogenic actions of digoxin.

Myocardial intracellular 'Ca2+ overload' may be involved in the direct arrhythmogenic actions of cardiotonic steroids. This proposal was examined by determining if the sensitivity of guinea-pig atrial muscle to digoxin-induced arrhythmias was affected by BAY K-8644, a 1,4-dihydropyridine derivative which promotes Ca2+ influx via slow channels. BAY K-8644 significantly reduced both the time required for a given concentration of digoxin to produce arrhythmias and the amount of digoxin bound to atrial muscle at the onset of arrhythmias. In addition, BAY K-8644 increased the maximum developed tension observed in the presence of digoxin before the onset of arrhythmias. Similar results were obtained with increasing concentrations of buffer Ca2+. In contrast, A23187, a Ca2+ ionophore, enhanced the sensitivity to digoxin-induced arrhythmias without affecting maximum developed tension. These results suggest that increases in intracellular Ca2+ enhance cardiac sensitivity to digoxin-induced arrhythmias and that the arrhythmogenic action may involve Ca2+ overload at a pool other than that which activates contractile proteins.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗