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PubMed1998

The short-term effects of digoxin in patients with right ventricular dysfunction from pulmonary hypertension.

OBJECTIVE: Studies on the effects of digoxin in patients with right ventricular failure and normal left ventricular function have not been performed. We evaluated the short-term effects of digoxin administration in patients with primary pulmonary hypertension on hemodynamics, neurohormones, and baroreceptor responsiveness. DESIGN: This was a prospective study with patients serving as their own controls. SETTING: University Hospital Intensive Care Unit with central monitoring. PATIENTS: Seventeen patients with primary pulmonary hypertension and symptomatic heart failure were enrolled. INTERVENTIONS: Following baseline hemodynamics, neurohormonal samples were drawn and the heart rate response to change in blood pressure following a challenge of phenylephrine and nitroprusside were recorded. One mg of intravenous digoxin was given and the measurements repeated after 2 hours. RESULTS: Following digoxin there was a significant increase in cardiac output (3.49+/-1.2 to 3.81+/-1.2 L/min., p=0.028), a significant fall in norepinephrine (680+/-89 to 580+/-85 pg/ml, p=.013), and a significant increase in atrial natriuretic peptide (311+/-44 to 421+/-9 pg/ml, p=0.01). All of the patients had changes in heart rate and blood pressure following phenylephrine and nitroprusside challenge, but there was no significant difference in the change in heart rate response to change in blood pressure when rechallenged after digoxin treatment. CONCLUSION: Digoxin produces a modest increase in cardiac output in patients with pulmonary hypertension and right ventricular failure, as well as a significant reduction in circulating norepinephrine. No detectable effects of digoxin on baroreceptor responsiveness were apparent. The use of digoxin in pulmonary hypertension is warranted.

Adult↗
PubMed1992

Effect of digoxin on the in vitro secretion of renin and angiotensin II/III immunoreactivity by the human adrenal gland.

Cardiac glycosides in man inhibit renin secretion, probably through a direct effect at the renal level (i.e. inhibition of juxtaglomerular cell Na/K ATPase). Since there is evidence that the human adrenal possesses an intrinsic renin-angiotensin system, we investigated the effect of digoxin on the in vitro generation of renin and angiotensin II/III, as well as of aldosterone, by the human adrenal gland. Minced normal adrenal tissues were studied in a superfusion system, measuring in the 15-min superfusate fractions active renin by immunoradiometric assay and angiotensin II/III and aldosterone by radioimmunoassay, respectively. In a first set of four experiments using different concentrations of digoxin in sequence for 45 min periods, digoxin 10(-5), but not 10(-8) and 10(-6) mol/l, significantly reduced renin and angiotensin II/III output from adrenals, while no change in aldosterone was observed. In a second set of three experiments, the addition of digoxin 10(-5) mol/l for 120 min caused a sustained reduction of renin and angiotensin II/III, but not of aldosterone. In the final experiment, the decrease of renin and angiotensin II/III during superfusion with digoxin 10(-5) mol/l was significantly greater than that observed during superfusion with digoxin in the presence of antidigoxin antibodies. Our data indicate that digoxin at high doses reduces renin and angiotensin II/III but not aldosterone secretion by the human adrenal gland. This suggests two different effects of digoxin, probably both mediated by inhibition of the Na/K ATPase activity, on the adrenal renin-angiotensin- and aldosterone-secreting cells.

Adrenal Glands↗
PubMed1985

Hemodynamic effects of digoxin on congestive heart failure in old myocardial infarction, dilated cardiomyopathy, acute myocardial infarction and mitral stenosis.

The hemodynamic effects of digoxin (0.01 mg/Kg) on congestive heart failure were compared in 32 patients with old myocardial infarction (OMI) (n = 9), dilated cardiomyopathy (DCM) (n = 10), acute myocardial infarction (AMI) (n = 5) and mitral stenosis (MS) (n = 8). The responses of heart rate (HR) and pulmonary capillary pressure (PCP) to digoxin in OMI, DCM and MS were marked but different in each of these groups and no significant changes were found in patients with AMI. The responses of cardiac index (CI) to digoxin in patients with OMI and DCM in whom left ventricular myocardial contractile force was impaired were divided into 2 groups (Group 1: CI increased more than 15% and Group 2: less than 15%). In Group 1, both CI and percent fractional shortening (%FS) before digoxin administration were lower than in Group 2, i.e., 1.97 +/- 0.27 vs 2.80 +/- 0.48 L/min/m2 (p less than 0.001) and 10.9 +/- 8.0 vs 19.5 +/- 11.9% (p less than 0.05), respectively. In MS, CI increased after digoxin administration only in the 2 patients with low CI and rapid HR in the control state. These results indicate that the mode of hemodynamic response to digoxin is considerably different in various diseases. They further suggest that digoxin should not be used in the early phase of AMI, although digoxin was of great clinical benefit in patients with OMI and DCM through such mechanisms as its positive inotropic and negative chronotropic effects and lowering of PCP.

Adult↗
PubMed1985

Determination of the onset of beta-methyl-digoxin action by potentiation of the adenosine response in guinea pigs.

The onset of beta-methyl-digoxin action was investigated by the potentiation of the adenosine response in guinea pigs and rats, and compared with that of digoxin and dipyridamole. A number of i.v. infusions of adenosine were given to determine the mean control adenosine response and its 95% confidence limits. After oral administration of the drugs, successive infusions of adenosine were continued until a drug-induced potentiation of the adenosine response was observed. The time of appearance of the potentiated adenosine response was marked as the onset of action of the drugs. The onset of action in guinea pigs was 9 to 12 min for 0.2 to 0.4 mg/kg of beta-methyl-digoxin, 90 to 100 min for 0.2 mg/kg of digoxin and 25 min for 5 mg/kg of dipyridamole. The maximal potentiation was 48.8 to 53.8% at 18 to 21 min for beta-methyl-digoxin, 74.5% at 130 min for digoxin and 74.8% at 80 min for dipyridamole. Adenosine infused i.v. into rats produced heart block, as in guinea pigs. However, in rats, the adenosine response was not potentiated by beta-methyl-digoxin and digoxin. Dipyridamole at a dose as high as 200 mg/kg produced 25.8% potentiation at 36 min after oral administration to rats.

Adenosine↗
PubMed1999

Inappropriate use of digoxin in the elderly: how widespread is the problem and how can it be solved?

Cardiovascular disease is ubiquitous within the elderly population and requires treatment with multiple types of medications. As with any cardiovascular pharmaceutical regimen, the risk versus the benefit of each medication must be strongly considered. This is particularly true where, for various reasons, adverse effects are more often prevalent and pronounced. Over the years, it has been documented that digoxin is a frequently prescribed medication in elderly populations. Although this drug can be beneficial when used in the appropriate setting, recent data would suggest that inappropriate administration of digoxin is common and not without potentially serious consequences. Currently, the use of digoxin can be advocated to control heart failure in atrial fibrillation and when added to ACE inhibitors and diuretics in those patients with symptomatic heart failure related to systolic left ventricular dysfunction. It is likely that the excessive use of digoxin in elderly populations as discussed in this review is perhaps based on the prevalence of diastolic heart failure in the elderly as well as other co-morbid conditions that may mimic heart failure signs and symptoms. Since the elderly appear to be at high risk for digoxin toxicity, the inappropriate use of this medication to treat these conditions could result in significant and unnecessary morbidity. It is proposed that echocardiography should be performed in most elderly patients when congestive heart failure is suspected. This simple diagnostic tool, along with a careful history and medical examination, would hopefully prevent the misinterpretation of confusing clinical findings and would help to identify the patients with normal systolic function or valvular disease such as critical aortic stenosis, where digoxin treatment would not be warranted. If it is necessary to administer digoxin, then the likelihood of significant toxicity can be greatly reduced by using an algorithm to calculate the appropriate dosage, which takes into consideration the patient's gender, bodyweight and creatinine clearance. Although it is probable that the indications for digoxin use to treat congestive heart failure will continue to evolve, at the present time most would recommend using this agent in symptomatic heart failure related to a reduction in left ventricular systolic function or when associated with atrial fibrillation.

Aged↗
PubMedDate not supplied

Interpretation of the serum digoxin concentration.

Significant problems exist in the interpretation of serum digoxin concentration data. Failure to distinguish between results that do not require precise clinical correlation (proof of absorption, presence of drug, etc) and those which depend upon clinical correlation for their meaning ('toxicity' or 'effectiveness') can result in interpretive errors. Problems relating to the source of the serum digoxin concentration can also confound interpretation. Such difficulty may be controllable (obtaining the sample at the proper time, haemolysis, etc) or related to the laboratory technique (cross-reactivity with digoxin metabolites or other medications, technical errors, or lack of precision). Variation within the same patient over time or between patients related to disease (alterations in electrolytes, adrenergic or parasympathomimetic tone, or other medications) may prevent the direct attribution of an observed phenomenon to a particular digoxin concentration. Techniques for determining the effect of digoxin do exist and can be used to gather data for clinical correlations. Ways of improving the interpretaion of serum digoxin concentrations also exist and should be used to improve their value in patient management. The serum digoxin concentration seems to have an important future role. However, we need to know how better to interpret and exploit serum digoxin concentration data.

Adenosine Triphosphatases↗
PubMed1995

Assessment of the pharmacokinetic interaction between zileuton and digoxin in humans.

The effects of coadministration of zileuton on the pharmacokinetic profile of digoxin were investigated in a double-blind placebo-controlled crossover study in 12 healthy male volunteers. During each study phase, the subjects received zileuton 600mg every 6 hours (regimen A) or placebo (regimen B) for 13 days. In addition, all subjects received concomitant digoxin 0.25 mg/day on study days 1 to 11 during both study phases. The study results provide no evidence of any significant overall effect of zileuton on digoxin plasma concentration-time profiles. Although the mean time to reach the maximum plasma concentration for digoxin was significantly shorter after concomitant administration of digoxin and zileuton than after concomitant administration of digoxin and placebo (0.95 vs 1.43 hours), there were no significant differences between the 2 regimens in the values for maximum plasma concentration, area under the plasma concentration-time curve from 0 to 24 hours, elimination half-life, oral clearance, and apparent volume of distribution associated with the terminal phase. Therefore, it is concluded that digoxin and zileuton may be coadministered without risk of clinically relevant effects on the pharmacokinetic profile of digoxin.

Administration, Oral↗
PubMed2006

Mechanisms, manifestations, and management of digoxin toxicity in the modern era.

Because of the common use of digoxin and because of its narrow therapeutic index, digoxin toxicity has been prevalent historically and, therefore, most clinicians are well aware of the classical dose/concentration-related signs and symptoms of toxicity. Yet, in the modern era the incidence of digoxin toxicity has been declining for a variety of reasons, including a new (lower) therapeutic range, the development of more effective drug therapies for heart failure, and more accurate dosing methods. In addition, digoxin toxicity, once commonly fatal, can now be quickly and effectively treated by the emergency administration of antidigoxin Fab fragments. Indeed, it may be possible to expand the use of Fab fragments to select patients with non-life-threatening digoxin toxicity, in order to save costs and improve patient comfort. Most cases of digoxin toxicity are caused by inappropriately high dosages, which are usually prescribed in the setting of renal dysfunction, while other cases can be attributed to system errors such as multiple prescriptions, poor patient counseling, or errors in transcribing. With modern computerized prescribing systems, such as direct physician order entry and prompts that alert the clinician to the potential for error, it is possible to decrease the incidence of digoxin toxicity even further. A realistic goal is to nearly eradicate once commonplace digoxin toxicity or at least make its occurrence a rare event.

Adverse Drug Reaction Reporting Systems↗
PubMed1995

Digoxin does not accelerate progression of diabetic retinopathy.

OBJECTIVE: To test the hypothesis that digoxin, an inhibitor of Na(+)-K(+)-ATPase activity, accelerates the progression of diabetic retinopathy. RESEARCH DESIGN AND METHODS: We compared the incidence and risk of retinopathy in 120 digoxin-taking vs. 867 non-digoxin-taking diabetic participants in the Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR) and in 117 digoxin-taking vs. 1,883 non-digoxin-taking diabetic subjects in the Early Treatment Diabetic Retinopathy Study (ETDRS). In both studies, retinopathy was detected by grading stereoscopic color photographs using the modified Airlie House classification scheme, and a two-step difference in baseline retinopathy grade was considered significant. RESULTS: After controlling for other risk factors, we found no statistically significant association with either 4-year incidence of retinopathy (WESDR) or progression of retinopathy (WESDR and ETDRS) in patients taking digoxin at baseline compared with those not taking digoxin. CONCLUSIONS: These data suggest that digoxin therapy does not adversely affect the course of diabetic retinopathy.

Adult↗
PubMed1999

[An 88-year-old woman with symptoms of intoxication due to a small dose of digoxin].

An 88-year-old woman was admitted to our hospital because of palpitations, dyspnea, orthopnea and appetite loss. On admission, small crackles were heard on her lower back, and her liver was swollen. Chest rentogenogram showed cardiomegaly (cardio-thoracic ratio 65.5%) and bilateral pleural effusion. Electrocardiograms showed atrial fibrillation with an average heart rate of 95 per minute. Echocardiography revealed mitral stenosis. Because the patient was considered to be suffered from heart failure due to mitral stenosis with atrial fibrillation, furosemide (20 mg per day) and digoxin (0.25 mg per day) was started. After digoxin had been raised to a dose of 0.50 mg per day because of sustained rapid ventricular response on the fourth hospital day, she complained of nausea and vomiting. Serum digoxin concentration was 2.55 ng/ml on the next day, and 1.08 ng/ml 96 hours after discontinuing digoxin. There was no complaint after digoxin was restarted with a dose of 0.05 mg per day. She complained of nausea again on the third day when the digoxin was raised to a dose of 0.083 mg in a blinded study. This observation indicates that digoxin intoxication could occur even in the smaller dose of digoxin than usual in the elderly.

Aged↗
PubMed2001

Albumin-dependent digoxin transfer in isolated perfused human placenta.

OBJECTIVE: To determine the effects of albumin (BSA) concentration in perfusion medium on digoxin transfer in isolated perfused human placental cotyledon. STUDY DESIGN: Isolated placental cotyledons from 13 normal human placentas were dually perfused after cannulating artery and vein of the chorionic plate and piercing 4 catheters through the corresponding basal plate with M199 medium enriched with BSA and glucose. Flow rates were 12 and 6 ml/min in the maternal and fetal circuits, respectively. Digoxin was added to the maternal reservoir at a final concentration of 5.51 +/- 1.00 ng/ml. BSA in maternal and fetal perfusate was kept at 3 concentrations: 1, 3 and 5 mg/ml (Groups I, II, III). Transplacental passage of digoxin was calculated from repeated fetal and maternal perfusate samples collected over 3 hours in the 3 groups. Digoxin levels were measured by FPIA (TDx, Abbott). RESULTS: There was no transfer of digoxin from the maternal to fetal compartment when the concentration of BSA was 1 mg/ml. Increasing the concentration of BSA led to a substantial increase in the transfer of digoxin to the fetal compartment. Steady state levels of digoxin in the fetal compartment were 0.61 +/- 0.19 ng/ml at 3 mg/ml of BSA. CONCLUSION: Maternal and fetal serum concentration of BSA affect digoxin transfer in isolated perfused human placentas. Three mg/ml are considered to be the optimal albumin concentration.

Analysis of Variance↗
PubMed1983

An endogenous digoxin-like substance in patients with renal impairment.

Digoxin concentrations were measured in serum samples from 102 patients with renal impairment who were receiving digoxin therapy. Many patients had values that differed widely on several currently available immunoassays, with differences as great as 2.9 ng/mL. In contrast, patients with normal renal function who were receiving digoxin had few discrepant results, with the largest difference being 0.5 ng/mL. We also assayed serum samples from 54 patients with renal impairment not on digoxin therapy and found that more than 60% of these digoxin-free patients had false-positive digoxin values on most assays. Our data suggest that a substance with digoxin-like immunoactivity is present in many patients with renal insufficiency. This substance may seriously compromise the accuracy and interpretation of digoxin concentration measurements.

Creatinine↗
PubMed2001

Effect of grapefruit juice on digoxin pharmacokinetics in humans.

OBJECTIVES: Grapefruit juice is responsible for drug interactions mediated by intestinal cytochrome P4503A4 inhibition and possibly P-glycoprotein inhibition in enterocytes. Our main objective was to determine whether grapefruit juice alters the bioavailability of digoxin, a P-glycoprotein substrate. The secondary objective was to determine whether the magnitude of the pharmacokinetic interaction was influenced by P-glycoprotein genetic polymorphism. METHODS: Twelve healthy volunteers participated in this open randomized crossover study comparing the effect of grapefruit juice consumption (versus water) on the pharmacokinetics of a single oral dose of digoxin (0.5 mg). The P-glycoprotein genotype was determined according to MDR1 genetic polymorphism in exon 26 (C3435T). RESULTS: Grapefruit juice had no significant effect on the maximum plasma drug concentration (C(max)) of digoxin or the area under the plasma concentration-time curve (AUC) from time zero to 48 hours. However, there was a 9% increase in the digoxin AUC from time zero to 4 hours and from time zero to 24 hours (P =.01) during grapefruit juice administration. The digoxin renal clearance remained unchanged during both periods. No relationship between MDR1 C3435T genotype and early digoxin pharmacokinetic changes could be detected. CONCLUSION: The modest changes in digoxin pharmacokinetics observed during grapefruit juice ingestion do not support an important P-glycoprotein inhibition. Under our experimental conditions, grapefruit juice-mediated P-glycoprotein inhibition does not appear to play a relevant role in drug interactions, at least when assessed by use of digoxin disposition kinetics.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2001

Effects of ouabain and digoxin on gene expression of sodium pump alpha-subunit isoforms in rat myocardium.

OBJECTIVE: To compare the effects of ouabain and digoxin on the gene expression of sodium pump alpha-subunit isoforms in the myocardium of rats. METHODS: Normal Sprague-Dawley (SD) rats were injected with ouabain (20 micrograms.kg-1.d-1, i.p.), digoxin (32 micrograms.kg-1.d-1, i.p.) and normal saline (NS) once a day, respectively, and indirect systolic blood pressure was recorded once a week. Six weeks later, all of the rats were killed, and sodium pump alpha 1-, alpha 2-, and alpha 3-subunit mRNA levels in the myocardium were detected with the reverse transcription polymerase chain reaction (RT-PCR) method. RESULTS: The systolic blood pressure of the rats infused with ouabain increased significantly at the end of week 6 (132.6 +/- 9.0 mm Hg vs 115.7 +/- 8.2 mm Hg, P < 0.01), while no difference in blood pressure was found between the digoxin group and the NS group. The expression of sodium pump alpha-subunit isoforms in the ventricular myocardium was regulated by either ouabain or digoxin. Both ouabain and digoxin stimulated expression of the alpha 3-isoform, whereas alpha 2 was unchanged in those two groups. alpha 1-isoform expression decreased in the ouabain group and was unchanged in the digoxin group. CONCLUSIONS: These results suggest that both ouabain and digoxin could regulate sodium pump alpha-subunit isoform expression, which might be related to the physiological roles of endogenous ouabain and might be responsible for the difference in the pharmacological and toxicological effects of ouabain and digoxin, including their effects on blood pressure.

Animals↗
PubMed2001

[Differential regulation of sodium pump alpha-subunit isoform gene by ouabain and digoxin in myocardium of rats].

OBJECTIVE: To compare the effects of ouabain and digoxin on both the systolic blood pressure (SBP) and sodium pump alpha-subunit expression in myocardium of rats. METHODS: Normal Sprague-Dawley (SD) rats were injected with ouabain, digoxin or normal saline (NS) everyday and indirect SBP was recorded once a week. Six weeks later, all the rats were killed and sodium pump alpha1-, alpha2-, and alpha3-subunit were detected in the left ventricular myocardium with RT-PCR method and immunohistochemical assay at mRNA and protein levels. RESULTS: At the end of six weeks SBP of rats infused with ouabain increased significantly (132.6 +/- 9.0 vs 115.7 +/- 8.2 mm Hg, P < 0.01), while no difference of SBP was found between digoxin group and NS group. The effects of ouabain and digoxin on sodium pump alpha-subunit isoform expression in myocardium were also different: both ouabain and digoxin stimulated expression of alpha3-isoform whereas alpha2-isoform unchanged at both mRNA and protein levels. alpha1-isoform was decreased in ouabain group and alpha1-isoform unchanged in digoxin group at both mRNA and protein levels. CONCLUSION: It is suggested that both ouabain and digoxin could regulate sodium pump alpha-subunit isoform expression, which might be related to the physiological roles of endogenous ouabain and might be responsible for the difference between the pharmacological and toxicological effects of ouabain and digoxin, including their effects on blood pressure.

Animals↗
PubMed1975

Altered tissue digoxin uptake after a toxic dose.

Tissue distribution and left ventricular (LV) effects of digoxin were studied after intravenous administration of low and high doses to dogs. LV dP/dt was increased by 0.03 mg/kg digoxin in nine, group A, and digoxin-induced arrhythmias or death occurred after 0.14 mg/kg in nine others, group B. Two hours after dosing during the slow excretion phase confirmed by serial serum sampling, the animals were killed. Serum and tissue extract digoxin determinations were performed by radioimmunoassay. Digoxin levels in group A were serum 3.9 ng/ml, kidney 428 ng/gm wet wt, liver 41, pancreas 39, diaphragn 21, apex, freewall, and septum LV 117-122, right ventricle (RV) 105, left atrium (LA) 51, right atrium (RA) 50, and the serum to apex LV ration was 1:32. The tissue contents and distribution were similar to previous [3H]digoxin data. The concentrations were higher in B; for all p less than 0.001. The toxic to therapeutic concentration ratios were serum 10, kidney 2.8, liver 5.5. pancreas 5,4, diaphragm 6.5, LV 4.3, RV 4.0, LA 3.5, RA 3.4. The serum to LV ratio was lower at 1:13, p less than 0.001. Myocardial toxicity was associated with marked but apparently limited increases in tissue digoxin content in this preparation. The disproportionately high serum level suggests paralysis or saturation of kidney and other tissue binding resulting in lower serum to tissue concentration ratios. Whenever serum to tissue ratios vary from expected values, serum digoxin levels may not be linearly related to tissue content or cardiac effects.

Animals↗
PubMed1992

Handling of digoxin and ouabain by renal tubular cells (LLC-PK1).

Digoxin is known to be secreted by renal tubular cells, but the mechanisms are still not fully understood. In this study, we examined renal tubular cell handling of digoxin and ouabain using LLC-PK1 cells, a model of proximal renal tubular cells. The cells were used in suspension for binding experiments and in monolayers on permeable filters for transport studies. The specific binding of digoxin to the cells, presumably to the ouabain binding site (i.e., membrane Na+,K(+)-ATPase), were characterized by Kd of 2.6 x 10(-7) M and Bmax (total number of specific binding sites) of 1.6 x 10(6)/cell. Kd and Bmax of ouabain binding were 1.3 x 10(-7) M and 1.9 x 10(6)/cell, respectively. In transport experiments, digoxin showed significantly higher flux than ouabain from the basolateral to the apical side across the cell monolayers. Importantly, this secretory transport was not inhibited by ouabain concentrations sufficient to block membrane Na+,K(+)-ATPase and to displace digoxin from the binding site on the enzyme (i.e., 10(-6) to 10(-4) M ouabain). However, the digoxin secretion was decreased by low temperature or excess digoxin in a concentration-dependent manner. These data suggest that digoxin undergoes unidirectional transport in favor of secretion, which does not involve its binding to the ouabain binding sites on membrane Na+,K(+)-ATPase.

Animals↗
PubMed1992

Lack of age-related differences in the clinical presentation of digoxin toxicity.

BACKGROUND: Digoxin toxicity occurs most commonly among the elderly. While the clinical syndrome of digoxin toxicity is well understood, how toxic manifestations change with age is not known. METHODS: We performed secondary analysis of data from a postmarketing surveillance study of patients with life-threatening digoxin toxicity treated with digoxin antibody therapy. Patients receiving long-term maintenance digoxin therapy and aged 55 years or older were divided into four age groups: 55 to 64, 65 to 74, 75 to 84, and 85 years and older (n = 45, 167, 183, and 83, respectively) and compared with regard to presenting manifestations, digoxin dosing, serum potassium and digoxin levels, and renal function. RESULTS: The prevalence of high-degree atrioventricular block showed an increasing but nonsignificant trend with age (40%, 40%, 42%, and 47%, respectively). Age-related trends in high-degree atrioventricular block were stronger among men than women and even stronger among men with underlying cardiac ischemia. The proportion of subjects with nausea/vomiting as a toxic manifestation did not consistently change with age (42%, 48%, 48%, and 46%, respectively). There were no age-related differences in degree of renal impairment or maintenance dose, but maintenance dose decreased with increasing renal impairment. CONCLUSIONS: Among patients with life-threatening digoxin toxicity, there is no age-related difference in clinical presentation.

Age Factors↗