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PubMed1995

Evaluation and comparison of the TDxII, Stratus, and OPUS digoxin assays.

Three automated immunoassays for digoxin in serum were evaluated--Abbott TDxII, Baxter Stratus, and Behring OPUS. The accuracy and precision of the assays were assessed by weighed-in controls and an external quality control program. Coefficients of variation of all methods in serum were < or = 10% at weighed-in concentrations of digoxin of 1 and 2.5 micrograms/L. Accuracy relative to weighed-in concentrations of 1 and 2.5 micrograms/L ranged from 98 to 126% for all methods. Comparative results from patient samples showed little difference between the TDxII and Stratus and a greater difference observed between the TDxII and OPUS assays. The detection of digoxin-free samples containing digoxin-like immunoreactive substances (DLIS) in neonatal cord blood, pregnant patients, and liver and renal recipients by each assay was then assessed. The TDxII exhibited the highest incidence of DLIS. This is evident in neonatal cord blood in which 40.4% of samples tested positive. In comparison, the extent of DLIS detected by Stratus was less and OPUS exhibited no DLIS in any of the groups studied. A case study of a patient treated with anti-digoxin Fab fragments (Digibind) also was included for analysis by each method. Fourteen hours after Digibind administration, the TDxII registered a digoxin concentration of 49.5 micrograms/L compared with 3.73, 1.80, and 2.49 micrograms/L for Stratus, OPUS, and ultrafiltered TDxII methods, respectively. The results indicate that to determine the concentration of digoxin after the administration of Digiband, the OPUS or fluorescence polarization immunoassay (FPIA)-ultrafiltered samples by TDxII are the assays of choice.

Adult↗
PubMed1997

Diffusion characteristics of placental preparations affect the digoxin passage across the isolated placental lobule.

Our aim was to evaluate the isolated placental lobule to study maternofetal transplacental digoxin transfer and accumulation in placental tissue in vitro. Digoxin passage across the isolated lobule of 10 human placentas was calculated from repeated fetal and maternal perfusate samples, and placental tissue digoxin concentrations were measured at the end of the experiments. To determine the degree of overlap of the fetal and the maternal circulation, the antipyrine clearance was used. Digoxin disappearance from the maternal circuit was not significantly affected by the degree of overlap. In contrast, the increase of digoxin in the fetal compartment was significantly higher in "well-perfused" placentas (antipyrine clearance > 1.60 ml/min; n = 5) than in "malperfused" placentas (antipyrine clearance < 1.50 ml/min; n = 5) (end-feto to initial maternal digoxin ratio 0.44 +/- 0.08 vs. 0.30 +/- 0.08; p < 0.05), whilst the accumulation in placental tissue was higher in the latter group (0.45 +/- 0.07 vs. 0.62 +/- 0.10 ng/mg protein; p < 0.05). We conclude that the isolated placental lobule is suitable to quantify transplacental digoxin transfer in vitro, but the diffusion characteristics of each preparation have to be considered.

Anti-Arrhythmia Agents↗
PubMed1997

Cross-reactivity of TDX and OPUS immunoassay systems for serum digoxin determination.

The properties of the widely used TDX Analyzer and recently developed OPUS Immunoassay System were compared using 403 serum specimens taken from patients who did or did not take digoxin. Of the 210 specimens from patients not treated with digoxin, a false- positive digoxin concentration was detected in 15 specimens (7%) by TDX and in only 2 specimens (1%) by OPUS because of the cross-reactivity with structurally similar drugs. Potassium canrenoate, digitoxin, deslanoside, and methyldigoxin exhibited marked concentration-dependent cross-reactivity in the TDX assay method, whereas deslanoside and methyldigoxin only showed cross-reactivity with the antibody used in the OPUS method. Although a poor correlation was observed between these two methods for the determination of 193 samples from patients treated with digoxin, the correlation was remarkably improved (r = 0.914) and the slope approximated unity when excluded the data from patients who were treated concurrently with the cross-reactive compounds. In routine TDM of digoxin, the authors experienced two cases in which cross-reactivity of the assay system caused a clinical problem. Concurrent administration of intravenous canrenoate apparently interfered with the digoxin assay by TDX, but this problem was solved by using the OPUS system. The authors found OPUS more useful for monitoring serum digoxin concentrations in patients because of its superior specificity.

Anti-Arrhythmia Agents↗
PubMed1978

Comparison of digoxin and medigoxin in normal subjects.

1 The properties of a recently introduced digitalis glycoside, 4-beta-methyl digoxin (medigoxin) were compared to those of a standard digoxin preparation. Using a radioimmunoassay (RIA) technique, serial plasma levels were recorded for 8 h following a single oral dose in five fasting volunteer subjects, and urinary glycoside elimination was measured for 4 consecutive days after dosage by use of a modification of the RIA method. 2 It was found that this RIA was suitable for plasma level measurement of both digoxin and midigoxin by reference to appropriate standard curves. Comparison of the plasma level profiles of these two drugs showed that medigoxin was very rapidly absorbed with peak levels occurring within 15--30 min, while digoxin produced peak levels after 45--75 min. The area under the plasma level-time curve produced by medigoxin was also consistently greater than that produced by digoxin, even though the medigoxin dose used was smaller. Quantitative comparison of these areas after adjustment to compensate for differing doses showed that medigoxin is considerably more biologically available than digoxin under study conditions (ratio 1.6 +/- 0.25:1), and comparison of quantitative urinary elimination suggested that medigoxin is eliminated in the urine to a lesser extent than digoxin and therefore it undergoes more metabolism and/or hepato-biliary elimination.

Adult↗
PubMed1983

Serum digoxin determination in outpatients--need for standardization.

1 Blood samples were taken from 30 outpatients for serum digoxin analysis before and after 5 min-4 h of rest in the supine position. 2 The digoxin concentration increased significantly during rest and a steady-state concentration was reached after approximately 2 h of rest. 3 The mean increase in serum digoxin after 2 h of rest was 23% with a considerable range, i.e. 0-75% (0-0.6 nmol/l). 4 On the analogy of a previous finding of a decrease in serum digoxin concentration during exercise in healthy subjects ingesting digoxin, the present results suggest that everyday physical activity affects the serum digoxin concentration. Standardized rest in the supine position prior to collecting blood samples from outpatients is therefore necessary for reliable serum digoxin determinations.

Aged↗
PubMed2006

Multiple doses of the antimuscarinic agent solifenacin do not affect the pharmacodynamics or pharmacokinetics of warfarin or the steady-state pharmacokinetics of digoxin in healthy subjects.

AIMS: Solifenacin succinate is used for the treatment of overactive bladder (OAB). The potential for pharmacokinetic and/or pharmacodynamic interactions between solifenacin and warfarin or digoxin was investigated. METHODS: The solifenacin-warfarin study was a two-period crossover trial conducted in healthy males. Subjects received warfarin on the 10th day of 16 days of dosing with either solifenacin or placebo. The solifenacin-digoxin study was an one-sequence crossover trial conducted in healthy males and females. Following a phase-in period for digoxin, solifenacin was administered concomitantly with the drug on days 9-18. RESULTS: The AUC(PT; 0-168 h) following a single dose of warfarin was unchanged in the presence of solifenacin [point estimate = 1.005; 90% confidence interval (CI) 0.98, 1.02)]. The AUC(0-infinity) values for both warfarin enantiomers were also unchanged. A small increase in the C(max) of digoxin was observed during treatment with solifenacin, but for AUC(ss,tau) and C(max) the 90% CI fell within the prespecified interval of 0.80-1.25. Combined administration of solifenacin and warfarin or digoxin was well tolerated. CONCLUSIONS: Since the pharmacokinetics and pharmacodynamics of a single dose of warfarin and the steady-state pharmacokinetics of digoxin were not affected by coadministration of solifenacin in healthy subjects, the need for dosing adjustments for digoxin and/or warfarin does not seem warranted.

Administration, Oral↗
PubMed1991

Steady-state concentrations and dosage of digoxin in relation to kidney function in hospitalized patients over 70 years of age.

Steady-state serum digoxin concentrations were determined and related to renal function in 62 hospitalized patients 70-93 years of age. Renal function was assessed by serum creatinine concentration, and creatinine clearance was estimated by a formula employing the serum creatinine concentration and adjusting for body weight, sex and age. The steady-state digoxin concentration was inversely related to the estimated creatinine clearance. As there was no correlation between serum creatinine and age, a simplified estimation of creatinine clearance capacity, disregarding age and sex and allowing only for body weight and serum creatinine, was applied. It is suggested that this simplified calculation is suitable for bedside use. If the body weight/serum creatinine ratio is less than 0.5 (kg x 1/mumol), approximately one-third of our patients would have digoxin concentrations that are close to or above the upper reference limit (2.6 nmol l-1) at the maintenance dose of 0.13 mg digoxin daily. A digoxin dose of 0.07 mg daily thus appears to be suitable for many patients aged greater than 70 years when the body weight/serum creatinine ratio is less than 0.5, and also when the serum creatinine level is normal or only slightly elevated. The half-life of digoxin in serum was determined in 12 patients for whom digoxin treatment was withdrawn due to clinical signs of intoxication, and these half-lives were markedly prolonged: 3.5-6 days at a body weight/serum creatinine ratio of 0.5-0.3. The seven patients with prolonged half-lives had serum creatinine concentrations in the range of 80-140 mumol l-1.

Aged↗
PubMedDate not supplied

Pharmacokinetics of tritiated ouabain, digoxin and digitoxin in guinea-pigs.

1. Elimination rates of tritiated ouabain, digoxin and digitoxin after single intravenous administrations were investigated in guinea-pigs, the total radioactivity in whole blood being traced for a period of up to 2 weeks. 2. In the initial rapid phase of elimination between 2 and 30 min following intravenous glycoside administration, the concentration decline of radioactivity in the blood was found to be identical for the three glycosides investigated, this part of the elimination curve displaying a hyperbolic shape. 3. During this early elimination phase, rapid metabolic degradation and excretion of digoxin had already taken place. The maximum concentration of radioactivity in the bile was reached 4 min following intravenous administration of 3H-digoxin. The positive inotropic response occurred in the cat heart-lung preparation 1.5 min after intravenous injection of a therapeutic dose of digoxin, indicating a quick occupation of binding sites in the tissues. 4. The biological half-lives of tritiated ouabain, digoxin and digitoxin averaged 11 h, 2.5 days and 4.1 days, respectively, as determined by the terminal exponential elimination phase, in guinea-pigs. This terminal phase was attained 6-12, 7-24, and 24-48 h after administration of ouabain, digoxin and digitoxin, respectively. 5. The findings reveal that in guinea-pig, as has been demonstrated in man, the elimination rates of the three glycosides increase according to their hydrophobic properties. 6. The biological half-lives of tritiated ouabain, digoxin and digitoxin obtained in the guinea-pig closely resemble those found in healthy man.

Animals↗
PubMed1990

Relationship between systemic and coronary vascular responses to digoxin and concurrent drug therapy with verapamil/beta-adrenoceptor antagonists in humans.

1. In 24 patients who were undergoing coronary arteriography for the assessment of ischaemic heart disease, the relationship between the systemic and coronary vascular responses to acute intravenous digoxin administration (500 micrograms) and concurrent drug therapy with the calcium antagonist verapamil (group I) or a beta-adrenoceptor antagonist (group II) or neither of these agents (group III) was examined. 2. Systemic vascular resistance (SVR) tended to rise rapidly after digoxin injection in patients in groups II and III, and tended to decline initially in patients in group I; however, these differences were not statistically significant (variance ratio [VR] = 0.77). 3. No significant differences were observed in coronary vascular responses to acute digoxin administration between the three groups of patients (VR = 0.34). 4. For the entire group of 24 patients, no statistically significant digoxin-induced effects on resistance could be demonstrated in either the systemic or coronary circulations, although in individual patients vasoconstrictor effects were observed. 5. We conclude that acute intravenous administration of digoxin does not consistently cause systemic or coronary vasoconstriction in patients with ischaemic heart disease. Variability in vasomotor responses to digoxin is not clearly related to concurrent drug therapy with verapamil or a beta-adrenoceptor antagonist. The observation that systemic vascular resistance tends to increase in the first few minutes after digoxin injection should be addressed in future studies.

Adrenergic beta-Antagonists↗
PubMed1986

Glucose uptake and binding of digoxin to skeletal muscle.

Physical exercise induces increased uptake of both digoxin and glucose in exercising skeletal muscle. Glucose uptake could be a regulatory factor for the digoxin binding to skeletal muscle, since in dogs, insulin and glucose infusion have been reported to increase the uptake of digoxin in muscle. In the present study on eight healthy digitalized subjects (0.5 mg digoxin daily) the uptake of glucose in skeletal muscle was achieved by infusion of 6 mg/kg body weight/min glucose, 0.004 IE/kg body weight/min insulin and 300 micrograms/h somatostatin. Serum and skeletal muscle digoxin levels were analysed before and during the infusion. We found no changes in the digoxin levels in serum and skeletal muscle in spite of an increased uptake of glucose in the muscle. Thus, glucose uptake in skeletal muscle is probably not an important regulatory factor for the change in muscle digoxin binding induced by exercise.

Adult↗
PubMed1977

Transient changes in plasma digoxin concentration and the development of cardiotoxicity.

1. Eight dogs were given two infusions of digoxin 0.1 mg/kg, one over 9 min and the other one over 90 min in a randomized sequence, allowing at least 12 days between each experiment. 2. Digoxin plasma profiles reflected the rate of digoxin infusion, the peak concentration of drug attained at the end of each infusion being considerably higher but more transient after the 9 min than after the 90 min transfusion. 3. Digoxin reduced the amount of acetylstrophanthidin required to produce electrocardiographic evidence of cardiotoxicity. This increase in cardiac sensitivity at 150 and at 360 min after the start of the digoxin infusion was independent of rate of infusion. 4. These results suggest that the development of cardiotoxicity is dependent upon the quantity of digoxin delivered into the systemic circulation regardless of the plasma concentration. 5. By inference, cardiotoxicity is related solely to the amount and not the rate of absorption from a given dose of digoxin.

Animals↗
PubMed1995

Effect of R56865 on cardiac sarcoplasmic reticulum function and its role as an antagonist of digoxin at the sarcoplasmic reticulum calcium release channel.

1. The effect of R56865 (N-[1-[4-(4-fluorophenoxy)-butyl]-4-piperidinyl]-N-methyl-2- benzothiazolamine) on cardiac sarcoplasmic reticulum (SR) Ca(2+)-release channel function was investigated. The effect of R56865 on [3H]-ryanodine and [3H]-digoxin binding to SR vesicles and its effect on the ATP-stimulated 45Ca2+ uptake into SR vesicles was also studied. 2. R56865 (0.5-50 microM) had no effect on single-channel open probability (Po) when added to native cardiac SR Ca(2+)-release channels, incorporated into planar phospholipid bilayers, that had previously been activated by 10 microM Ca2+. The single-channel conductance (93 pS) and the Ca2+/Tris+ permeability ratio (12.5) were also unaffected by R56865. 3. R56865 failed to affect the rapid Ca(2+)-induced efflux of 45Ca2+ from cardiac SR vesicles. The initial efflux rate at an extravesicular [Ca2+] of 0.1 microM was 176 +/- 33 nmol 45Ca2+ mg-1 protein s-1 (n = 5). Addition of 0.5-50 microM R56865 to the efflux solution did not affect the initial efflux rate or the total amount of 45Ca2+ released from the vesicles. 4. The specific binding of [3H]-ryanodine to SR vesicles can be viewed as a marker for SR Ca(2+)-release channel activation. R56865 (0.05-50 microM) did not change the amount of specific [3H]-ryanodine bound at 10 microM activating Ca2+. Taken together these data (points 2, 3 and 4) suggest that R56865 does not affect the Ca2+ activation of the cardiac SR Ca(2+)-release channel. 5. R56865 (0.5-50 microM) decreased the ATP-stimulated uptake of 45Ca2+ into cardiac SR vesicles. The total amount of 45Ca2+ taken up into the vesicles was decreased by 26-37% and the initial rate of uptake was also reduced.6. R56865 decreased the binding of [3H]-digoxin to cardiac SR vesicles. It inhibited binding of[3H]-digoxin to both sites on SR membranes. However, it acted as a mixed type of non-competitive antagonist, as it increased the Kd and reduced the Bmax for [3H]-digoxin. Additionally, when SRCa2+-release channels incorporated into bilayers were activated by 1 nM digoxin at 10 micro M Ca2+, 5 microMR56865 decreased single-channel Po to that seen prior to activation by digoxin, confirming that R56865is an antagonist at the cardiac glycoside receptor site on the cardiac SR Ca2+-release channel.7. The results presented here show that R56865 decreases 45Ca2+ uptake into SR vesicles and also non-competitively decreases the binding of cardiac glycosides to their activation sites on the SRCa2+-release channel. Since this compound fails to affect other aspects of the functioning of the SR, we conclude that inhibition of Ca2+-uptake into the SR and/or antagonism of digoxin binding to its high affinity sites on the cardiac SR Ca2+-release channel may contribute to the protection against glycoside induced toxicity seen with R56865. Indeed the reduction of Ca2+ uptake into the SR during Ca2+overload may contribute to the protective action of R56865 against arrhythmias induced by veratridine or by ischaemia. Notwithstanding this, it is possible that the multitude of other actions on specific ion translocation processes, as well as the possible non-specific membrane effects of R56865, may be as responsible for the protection against arrhythmias as the effects on SR function we have documented here. However, the simultaneous interference with more than one of these processes by R56865 may be required for its anti-arrhythmic action.

Adenosine Triphosphate↗
PubMed1986

Clinical digoxin toxicity in the aged in association with co-administered verapamil. A report of two cases and review of the literature.

Digoxin toxicity occurs more commonly in aged than younger individuals. Cardioactive drugs such as quinidine effect digoxin pharmacokinetics so as to increase the potential for digoxin toxicity. The calcium-channel antagonists have become extensively used for cardiac disorders and are often co-administered with digoxin. Despite documented calcium-channel antagonist interactions with digoxin, clinically significant digoxin toxicity associated with their concurrent use is apparently unusual. Two elderly patients receiving digoxin and verapamil simultaneously are presented to demonstrate the clinical importance and potential danger of the concomitant use of these drugs.

Aged↗
PubMed1997

Use of digoxin, diuretics, beta blockers, angiotensin-converting enzyme inhibitors, and calcium channel blockers in older patients in an academic hospital-based geriatrics practice.

OBJECTIVE: To investigate the prevalence of and indications for digoxin use and the prevalence of beta blocker and calcium channel blocker use in older patients with previous myocardial infarction or coronary artery disease (CAD), and the prevalence of use of diuretics, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium channel blockers in older patients with hypertension in an academic hospital-based geriatrics practice. DESIGN: A retrospective analysis of charts from 528 unselected older patients, seen from June 1995 through July 1996 at an academic hospital-based geriatrics practice, was performed to investigate the prevalence of digoxin use and indications for digoxin use, the prevalence of beta blocker and calcium channel blocker use in older patients with previous myocardial infarction or coronary artery disease (CAD), and the prevalence of use of diuretics, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium channel blockers in older patients with hypertension. SETTING: An academic hospital-based, primary care geriatrics practice staffed by fellows in a geriatrics training program and full-time faculty geriatricians. PATIENTS: A total of 416 women and 112 men, mean age 81 +/- 8 years (range 58 to 101), were included in the study. MEASUREMENTS AND MAIN RESULTS: Ninety-two of the 528 patients (17%) were taking digoxin. Recorded indications for digoxin were atrial fibrillation with or without congestive heart failure (CHF) in 39% of patients, CHF with sinus rhythm and abnormal left ventricular ejection fraction (LVEF) in 18% of patients, a clinical assessment of CHF with sinus rhythm and no recorded measurement of LVEF in 20% of patients, paroxysmal atrial fibrillation in 14% of patients, and coronary artery disease (CAD) in 9% of patients. Of 121 patients with previous myocardial infarction, 23 (19%) were prescribed beta blockers, and 54 (45%) were taking calcium channel blockers. Of 173 patients with CAD, 41 (24%) were treated with beta blockers, and 79 (46%) were taking calcium channel blockers. LVEF was not recorded in the charts of 90 of 121 patients (74%) with prior myocardial infarction and of 125 of 173 patients (72%) with CAD. Of 480 older patients with hypertension, 154 (37%) were treated with diuretics, 55 (13%) were treated with beta blockers, 160 (38%) were treated with ACE inhibitors, and 197 (47%) were treated with calcium channel blockers. CONCLUSIONS: In 528 older patients seen in an academic hospital-based geriatrics practice, the prevalence of digoxin use was 19%. Appropriate indications for digoxin were documented clearly in the charts of 53 of 92 patients (57%). Calcium channel blockers were used more often than beta blockers in patients with previous myocardial infarction or CAD. Calcium channel blockers were the most frequently used antihypertensive drugs.

Academic Medical Centers↗
PubMed1977

Passage of digoxin into cerebrospinal fluid in man.

The passage of digoxin into the cerebrospinal fluid (CSF) was studied in 8 infants on maintenance therapy with digoxin, 11 adult patients on long-term digoxin therapy, and 15 patients, previously non-digitalized, who were given 0.5 mg digoxin orally 1 hr to 12 hrs prior to lumbar puncture. Digoxin in the serum and CSF was determined by radioimmunoassay. In the infants a mean serum concentration of 1.5 ng/ml (range 0.7-2.3 ng/ml) was found, and a simultaneous mean CSF concentration of 0.5 ng/ml (range 0.3-1.1 ng/ml). In the adults on long-term therapy, the corresponding figures were 1.1 ng/ml (range 0.5-2.2 ng/ml) and 0.3 ng/ml (range 0-0.6 ng/ml). Among the 15 patients given a single oral dose of digoxin, detectable CSF concentrations (0.2-0.3 ng/ml) were found in five, 1-12 hrs after the administration of the drug. In three paediatric patients with hydrocephalus (3 months-5 years) digoxin therapy was started as an attempt to decrease CSF production. In these patients, the production of CSF was reduced by 17, 25 and 30%, respectively.

Aged↗
PubMed1979

Effects of digoxin on islated human mesenteric vessels.

Digoxin had contractant effects on isolated, human mesenteric arteries and veins. Veins were more sensitive to this action of the glycoside than arteries. The contractions were not affected by phentolamine or by washing with a digoxin-free solution. However, they were abolished by the calcium antagonist nifedipine, and by washing with a calcium-free medium. In the presence of digoxin, the maximum response to noradrenaline (1.8 x 10(-5) M) increased markedly in both arteries and veins, and the concentration-response curve for the amine was displaced to the left. Immersion of vein preparations in calcium-free solution for 30 min. abolished the digoxin contracture; an increase in extracellular calcium restored the response. Changes in extracellular potassium concentration caused changes in tension in tension of the mesenteric veins similar to those previously demonstrated in peripheral veins--both in the presence and in the absence of digoxin. It is concluded that digoxin contracts mesenteric vessels by a direct action on the muscle cells, and potentiates the contractant effects of noradrenaline. These effects are dependent on the availability of extracellular calcium. Mesenteric vascular reactions caused by changes in extracellular potassium are influenced by digoxin.

Aged↗
PubMed1979

Effects of digoxin in isolated human pulmonary vessels.

In isoalted human pulmonary arteries and veins the contractile response to noradrenaline (1.8 X 10(-5)M) was 33 +/- 7.4% and 20 +/- 4.5% (Mean +/- S.E.M.) of that induced by potassium (127 mM). A variable degree of spontaneous contractile activity was recorded in the vein preparations. This activity was abolished by nifedipine (2.9 X 10(-6)M). Digoxin (10(-6)M) induced contractions in pulmonary vessels. In the arteries, the digoxin contraction developed slowly and reached a maximum amplitude of 90 +/- 4% (Mean +/- S.E.M.) of the potassium evoked contraction. In the veins, the amplitude of the digoxin contraction was 32 +/- 5% of that induced by potassium. Digoxin (10(-6)M) also increased the maximum response to noradrenaline and potassium in both arteries and veins. In the arteries, the noradrenaline and potassium contractions increased to 211 +/- 6.8% and 145 +/- 8.9 of control, and in the veins to 169 +/- 13.5% and 163 +/- 9.9%, respectively. Nifedipine in concentrations which completely relaxes arterial and venous preparations contracted by potassium, had only a slight relaxing effect on digoxin induced contraction. It is concluded that digoxin increases the tension in pulmonary arteries and veins, and increases the maximum response to noradrenaline and potassium in both types of vessels. The digoxin induced contraction is highly resistant to blockade of extracellular calcium influx.

Adult↗
PubMed1983

Digoxin therapy and left ventricular performance in premature infants with patent ductus arteriosus.

Left ventricular systolic time intervals were assessed in 16 preterm infants with symptomatic left-to-right ductal shunts, before, during and after digoxin therapy. An intravenous loading dose of digoxin, 20 micrograms/kg, resulted in a serum digoxin concentration of 1.94 +/- 0.44 nmol/l (mean +/- 1 SD) but in no significant change in heart rate or systolic time intervals. Digoxin maintenance, 2.5 micrograms/kg/12 h, led 3-7 days later to serum concentrations of 2.57 +/- 1.06 nmol/l with an associated shortening of left ventricular ejection time (p less than 0.05) which probably reflected a reduced ductal shunt. Digoxin therapy was withdrawn after ductal closure. The terminal serum half-life was 87 +/- 17 h. Decreasing digoxin concentrations were associated with prolongation of left ventricular ejection time (p less than 0.01). Digoxin therapy did not seem to influence left ventricular systolic time intervals while ductal patency persisted. This may be attributed to limitations of the method or the left ventricle already working at its maximum.

Digoxin↗