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PubMed1996

Assessment of pharmacokinetic and pharmacodynamic drug interactions between nefazodone and digoxin in healthy male volunteers.

The effect of nefazodone on pharmacokinetic and pharmacodynamic parameters of digoxin were evaluated in an open, randomized, multiple-dose, three-way crossover study of 18 healthy male volunteers. The volunteers received nefazodone alone (200 mg twice daily), digoxin alone (0.2 mg daily), or nefazodone combined with digoxin during three 8-day treatment periods, with a single dose on the ninth day. There was a 10-day washout period between treatment periods. Coadministration of nefazodone with digoxin had no effect on the frequency and severity of adverse events compared with those observed with either drug alone. Steady-state area under the concentration-time curve (AUC) and peak (Cmax) and trough (Cmin) concentrations of digoxin were significantly higher (15%, 29%, and 27%, respectively) after coadministration of nefazodone/digoxin than after administration of digoxin. Despite these increases, no clinically significant changes in vital signs, heart rate, or PR, QRS, and QT intervals on the electrocardiogram occurred after coadministration from those measured after digoxin monotherapy. Coadministration did not affect the pharmacokinetics of nefazodone or its metabolites (hydroxynefazodone, m-chlorophenylpiperazine, triazole dione). Because digoxin has a narrow therapeutic index, monitoring of plasma digoxin levels and appropriate adjustment of dosage are recommended when nefazodone and digoxin are administered concurrently.

Adult↗
PubMed1997

Population-based investigation of relative clearance of digoxin in Japanese patients by multiple trough screen analysis: an update.

The steady-state concentrations of digoxin at trough levels were studied to reestablish the role of patient characteristics in estimating doses for digoxin using routine therapeutic drug-monitoring data. The data (n = 548) showing steady-state serum concentrations of digoxin after repetitive oral administration in 385 hospitalized patients were analyzed using NONMEM, a computer program designed to analyze pharmacokinetics in study populations by allowing pooling of data. Analysis of the pharmacokinetics of digoxin was accomplished with a simple steady-state pharmacokinetic model. The effect of a variety of developmental and demographic factors on the clearance of digoxin was investigated. Estimates generated by NONMEM indicated that clearance of digoxin was influenced by the demographic variables of age, total body weight, serum creatinine, estimated creatinine clearance, gender, the coadministration of spironolactone, the presence or absence of congestive heart failure, and the administration of a half-tablet. The interindividual variability in the clearance of digoxin was modeled with proportional error with an estimated coefficient of variation of approximately 22%; the residual variability was approximately 25.0%. An a priori method, based on the value for clearance of digoxin obtained by NONMEM analysis, was proposed as a useful adjunct for the prediction of the steady-state concentration of digoxin at trough level as a function of the maintenance dose of digoxin.

Adolescent↗
PubMed2005

Inhibitory effects of digoxin and ouabain on aldosterone synthesis in human adrenocortical NCI-H295 cells.

The present study was to investigate the effects and action mechanisms of digoxin and ouabain on steroidogenesis in human adrenocortical NCI-H295 cells. Administration of digoxin or ouabain for 24 h decreased the basal and angiotensin II (Ang II)-stimulated release of aldosterone by NCI-H295 cells. The conversions of corticosterone (substrate of cytochrome P450 aldosterone synthase, P450c11AS) to aldosterone or deoxycortisol (substrate of cytochrome P450 11beta-hydroxylase, P450c11beta) to cortisol were reduced by digoxin or ouabain. The basal and 22-hydroxy-cholesterol (a membrane-permeable cholesterol, substrate of cytochrome P450 side-chain cleavage enzyme, P450scc)-stimulated pregnenolone release in mitochondria was inhibited by digoxin or ouabain. Digoxin or ouabain suppressed the basal and Ang II-stimulated protein expression of steroidogenic acute regulatory (StAR) protein and P450scc. Incubation of digoxin or ouabain for 24 h reduced P450c11AS mRNA expression in NCI-H295 cells. Digoxin or ouabain (10(-6) M, 24 h)-treated cells showed a lower resting intracellular Ca2+ concentration ([Ca2+]i) and an attenuated response of [Ca2+]i to Ang II. Since no significant cytotoxicity was observed at 10(-6) M digoxin or ouabain, the digoxin- or ouabain-induced decrease of aldosterone or cortisol release was not associated with cytotoxicity. These results demonstrate that digoxin or ouabain inhibits the aldosterone or cortisol release via reduction of P450c11AS or P450c11beta and P450scc activities, inhibition of StAR and P450scc protein expression, suppression of P450c11AS mRNA expression, and attenuation of Ca2+ mobilization in NCI-H295 cells.

Adrenal Cortex Neoplasms↗
PubMed1977

Physiologically based pharmacokinetic model for digoxin disposition in dogs and its preliminary application to humans.

A physiologically based pharmacokinetic model for digoxin disposition developed in the rat was modified to account for the interspecies differences in tissue-to-plasma digoxin concentration ratios and applied to the dog. The model provided a quantitative assessment of the time course of digoxin concentrations in dog plasma, various tissues, and urine. It also predicted the effect of renal failure on digoxin pharmacokinetics in the dog. An attempt to scale the dog model to humans by simply considering differences in organ volumes, organ flow rates, and digoxin clearances was partially successful. Good predictions of plasma digoxin concentration and urinary digoxin excretion after a single dose and of steady-state plasma, heart, and skeletal muscle digoxin concentrations were obtained. However, the model predicted considerably higher kidney digoxin concentrations than are actually found. Although the model adequately characterized the time course of digoxin concentrations in patients with moderate renal impairment, it provided a relatively poor fit to that observed in anuric patients.

Animals↗
PubMed1992

Effect of salbutamol on digoxin pharmacokinetics.

A single dose of the beta 2-adrenoceptor agonist salbutamol has previously been shown to decrease serum digoxin concentration in healthy volunteers. A possible explanation of the phenomenon is a beta 2-adrenoceptor-mediated increase in the specific binding of digoxin to skeletal muscle. The present study was undertaken to further elucidate the effect of salbutamol on the pharmacokinetics of digoxin in man. Nine volunteers were studied on two occasions during salbutamol or placebo treatment. On test days salbutamol, 4 micrograms.kg-1.h-1 or saline was infused for 10 h, preceded and followed by four and three days, respectively, of oral administration. A single i.v. injection of digoxin 15 micrograms.kg-1, was given 20 min after starting the infusion. At the end of the infusion a muscle biopsy was taken from the vastus lateralis. Blood samples for the analysis of serum digoxin and potassium were repeatedly taken over 72 h. Urine was collected over a period of 24 h for determination of the renal excretion of digoxin and potassium. The serum digoxin concentration, expressed as the AUC 0-6 h was 15% lower during salbutamol infusion than during saline infusion. Salbutamol caused significantly faster elimination of digoxin from the central volume of distribution to deeper compartments. Salbutamol had no effect on the renal clearance of digoxin. The skeletal muscle digoxin concentration tended to be higher (48%) during salbutamol compared to placebo treatment. The serum potassium concentration was significantly lower after salbutamol compared to placebo, as was the rate of renal excretion of potassium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Interaction of ORG 10172, a low molecular weight heparinoid, and digoxin in healthy volunteers.

Potential pharmacokinetic and pharmacodynamic interactions between a new low molecular weight heparinoid Org 10172 (bolus injection of 3250 anti-Xa units) and digoxin (0.25 mg once daily for 8 days) were studied in 6 healthy male volunteers using an open, randomised three-way cross-over design. Digoxin produced a slight increase in clearance of anti-Xa activity from 4.3 to 4.8 ml.min-1, while plasma antithrombin and thrombin generation inhibiting (TG1) activity remained unchanged. Digoxin did not affect the actions of Org 10172 on the clotting tests. In the presence of Org 10172 there was a reduction in the AUC of digoxin during one dosing interval after the seventh digoxin tablet from 20 to 17 ng.ml-1.h, and a significant reduction in the average serum digoxin concentration. Since renal digoxin clearance was not significantly changed this probably might be due to a change in the non-renal clearance of digoxin. Atrio-ventricular node conduction, as measured by PR-time intervals, remained unchanged during all three treatments. In conclusion, although the pharmacokinetics of Org 10172 and digoxin were slightly changed by the combination, it is probably safe to administer Org 10172 and digoxin simultaneously. The clinical relevance of the slight decrease in plasma anti-Xa activity levels cannot yet be defined.

Administration, Oral↗
PubMed1979

Absorption of digoxin in severe right heart failure.

The absorption of digoxin has been investigated in 8 patients before and after successful treatment of severe right heart failure. 3H-digoxin 0.1 mg as a solution, and un-labelled digoxin 0.25 mg as a tablet, were given to fasted patients. Blood samples were taken at various time intervals up to 120 hours and urine was collected over the same period. The concentrations of labelled digoxin in plasma and urine were measured in a liquid scintillation counter, unlabelled digoxin was estimated by radioimmunoassay, and various pharmacokinetic parameters were calculated. There was no significant difference in the plasma concentration curves in severe right heart failure and after its successful treatment, nor did any of the calculated pharmacokinetic parameters change significantly. Therefore, inhibition of the absorption of digoxin appears unlikely. In an additional study to estimate absolute bioavailability two different groups of patients in severe right heart failure were given 3H-digoxin 0.1 mg or unlabelled digoxin 0.25 mg i.v. and the pharmacokinetic parameters were compared with those from the previous study. The bioavailability of the 3H-digoxin solution and of the digoxin tablet were in the same range as values previously published for healthy volunteers, and patients both with and without cardiac failure.

Biological Availability↗
PubMed1986

Effect of two different doses of nitrendipine on steady-state plasma digoxin level and systolic time intervals.

The effect of two different doses of nitrendipine on plasma digoxin levels, urinary recovery and systolic time intervals was investigated in 8 healthy volunteers. Following a loading dose, digoxin 0.25 mg b.d.p.o. was given alone for 2 weeks. Then 0.25 mg digoxin b.d. was administered for two 1-week periods combined with nitrendipine 10 mg or 20 mg once daily. The study was completed with another digoxin monotherapy phase lasting 7 days. Nitrendipine 20 mg daily led to a significant increase in plasma digoxin levels and in its area under the plasma concentration-time curve AUC (0-12) was 9.7 ng ml-1h when digoxin alone was given and 11.2 ng ml-1h on co-administration of the calcium antagonist. Urinary recovery and renal clearance of digoxin were slightly but not significantly increased by nitrendipine. Nitrendipine 10 mg once daily caused a small, insignificant tendency to elevate the plasma digoxin level. Nitrendipine co-administration (10 and 20 mg once daily) did not significantly alter systolic time intervals, as non-invasively measured haemodynamic parameters, compared to digoxin treatment alone. Thus, nitrendipine 20 mg daily caused a significant increase in plasma digoxin concentrations and in its AUC, which would rarely be of clinical relevance.

Adult↗
PubMed1977

[Intestinal absorption of digoxin in systemic sclerosis (author's transl)].

Gastro-intestinal absorption of digoxin was evaluated in 18 patients with progressive systemic sclerosis. In 8 patients a single-dose crossover study was performed after oral and intravenous administration of 0.5 mg digoxin by comparing the aera under the eight-hour plasma concentration curve. The fraction of the dose absorbed was diminished in 4 patients to less than 55%. There was a significant positive correlation between the extent of digoxin absorption and xylose renal excretion. In addition, steady state digoxin plasma levels and 24-h urinary excretion of digoxin were determined during maintenance therapy in 12 patients. In 6 patients renal excretion of digoxin was clearly less than in normal subjects during chronic dosing of the same digoxin preparation. This finding corresponded well with digoxin plasma levels below the usual therapeutic range in most of the patients. The impaired absorption of digoxin failed to correlate with the extent of the skin manifestation or the time course of the disease while there was massive oesophageal dysfunction in most of these patients. The results suggest that an inadequate therapeutic response to cardiac glycosides in patients suffering from progressive systemic sclerosis is at least partially due to impaired digoxin absorption. Similar problems could occur in therapy of the disease itself due to insufficient enteral absorption of drugs used in treatment of systemic sclerosis.

Administration, Oral↗
PubMed1992

Measurement of digitalis-glycoside levels in ocular tissues: a way to improve postmortem diagnosis of lethal digitalis-glycoside poisoning? I. Digoxin.

Prompted by animal studies reporting the accumulation of digitalis-glycosides in ocular tissues, we investigated whether measurement of digoxin levels in human ocular tissues can improve the postmortem diagnosis of lethal digoxin intoxication. Digoxin was measured in the vitreous humor and choroid-retina of patients who had received in-patient treatment with digoxin prior to death (therapeutic group) and in a single case of suicidal intoxication. The results were compared with the digoxin levels in the femoral vein blood, myocardium, kidney and liver, and evaluated in light of the medical history of each patient. In the therapeutic group the mean digoxin level was higher in the choroid-retina than in other tissues and body fluids. The range of variation in levels in the choroid-retina following therapeutic doses was comparable to that in the other tissues. An extremely high level of digoxin was present in the choroid-retina in the case of suicidal intoxication. In all cases, levels in the vitreous humor were very low compared to those in the choroid-retina. Hence, it is unlikely that significant distortion of choroid-retinal levels occurs due to postmortem diffusion of digoxin into the vitreous body. Our results indicate that measurement of digoxin levels in the choroid-retina can aid the postmortem diagnosis of lethal digoxin intoxication.

Aged↗
PubMed1987

Pharmacokinetic drug interactions between digoxin and antiarrhythmic agents and calcium channel blocking agents: an appraisal of study methodology.

While preliminary screening for interactions between new cardiovascular pharmacotherapeutic agents and digoxin can be efficiently and safely conducted in normal healthy volunteers, it is particularly important to detect and quantify drug interactions in patients with varying degrees of cardiac, hepatic and/or renal dysfunction. Much of the previously published literature provides only minimal data to guide clinical practice because of limitations of study design including sample size and measurement techniques. Important factors that determine the ability of a particular study design to detect a drug interaction with digoxin include the accuracy and precision of the assay method for serum digoxin concentrations, intrasubject and intersubject variability in serum digoxin concentration, and sample size. The format of the trial (chronic versus single digoxin dosing in cardiac patients; chronic versus single digoxin dosing in normal subjects) and the method of assessment of alterations in digoxin handling (formal determination of digoxin clearance, comparison of multiple or single digoxin measurements during various phases of trial) also impact greatly on the clinical relevance of such investigations. Guidelines for future studies of drug interactions with digoxin in cardiac patients are proposed with particular emphasis on laboratory methods; measurement techniques during baseline, placebo, and active drug phases; calculation of the statistical power of the study; time course of the trial; and assessment of the clinical significance of the findings.

Anti-Arrhythmia Agents↗
PubMed1999

The local effects of systemic digoxin on the cutaneous microcirculation.

OBJECTIVE: The present study was designed to explore whether digoxin modifies cutaneous vascular responses to an endothelium-dependent vasodilator (acetylcholine) or to the vasoconstrictor norepinephrine. METHODS: In a double-blind cross-over study 12 healthy subjects received digoxin 0.25 mg twice daily (after adequate loading doses) or placebo for a total of 11 days. Dose-response curves to iontophoresis of acetylcholine or norepinephrine were constructed at day 11. Laser Doppler flux (LDF) was measured at the same sites. Mean arterial pressure (MAP) was measured non-invasively and cutaneous vascular conductance (CVC) was calculated (CVC = LDF/MAP). RESULTS: Serum concentrations of digoxin were within the therapeutic range [1.3 (0.5) ng x ml(-1); mean with (SD)]. Blood pressure and heart rate were significantly lower during supine rest under digoxin treatment [mean with (SD); minute 10 to 70 of supine rest; systolic blood pressure: 121 (11) mmHg (placebo) vs 116 (11) mmHg (digoxin); P = 0.001; diastolic blood pressure: 63 (6) mmHg vs 58 (8) mmHg; P = 0.007; heart rate: 60 (10) beats x min(-1) vs 54 (8) beats x min(-1); P = 0.001]. Digoxin also caused significantly higher baseline CVC [169 (25) Perfusion Units (PU) x mmHg(-1) (digoxin) vs 109 (14) PU x mmHg(-1)(placebo); P = 0.013] and significantly increased the vasoconstriction to norepinephrine iontophoresis. Acetylcholine iontophoresis was unaltered by digoxin treatment. CONCLUSIONS: Digoxin does not modify the cutaneous vascular response to an administered endothelium-dependent vasodilator. It reduces resting heart rate, blood pressure and baseline cutaneous blood flow and augments the vasoconstrictive effect of exogenous norepinephrine. The findings do not support the hypothesis that digoxin lowers diastolic blood pressure through a direct action on blood vessels.

Acetylcholine↗
PubMed1975

Effects of ischemia and coronary reperfusion on myocardial digoxin uptake.

The effects of coronary reperfusion on the uptake of digoxin by ischemic myocardium were studied in 17 open chest dogs undergoing anterior wall infarction produced by snaring confluent branches of the left coronary arterial system. Epicardial electrograms delineated ischemic, border and nonischemic zones. The hearts were reperfused by snare release after 1, 2 and 6 hours of occlusion. After 15 minutes of reperfusion, 1.0 mg of tritiated digoxin (3H-digoxin) was given intravenously, and 2 hours later the hearts were excised and endocardial and epicardial samples from each zone were analyzed for 3H-digoxin concentration. In another group of eight dogs regional myocardial blood flow was assessed utilizing 15 mu of radio-labeled microspheres administered during occlusion and reperfusion. In five dogs with 1 hour of coronary occlusion and subsequent reperfusion, 3H-digoxin uptake was comparable in endocardial and epicardial layers of all three zones. In six dogs undergoing reperfusion after 2 hours of occlusion, mean 3H-digoxin concentration was significantly (P less than 0.001) reduced from the mean nonischemic concentration, by 54 percent in endocardial and 35 percent in epicardial layers of the ischemic zone. Border zone endocardial and epicardial 3H-digoxin uptake was reduced by 21 percent and 16 percent, respectively (P less than 0.05). In six dogs undergoing reperfusion after 6 hours of occlusion, 3H-digoxin uptake in the ischemic zone was significantly (P less than 0.001) reduced by 85 percent in endocardial and 60 percent in epicardial layers from the concentration in the nonischemic zone. Border zone uptake was decreased by 54 percent in endocardial and 36 percent in epicardial regions (P less than 0.01). These alterations of in vivo digoxin binding could not be explained by impaired reflow of blood to ischemic myocardium. We conclude that coronary reperfusion after 2 to 6 hours of occlusion is associated with a marked reduction in myocardial digoxin uptake, which is more pronounced in subendocardial than in subepicardial regions of ischemic tissue.

Animals↗
PubMed1985

Interpretation of excessive serum concentrations of digoxin in children.

Between January 1981 and April 1984, excessive serum concentrations of digoxin (5 ng/ml or higher) were recorded in 47 children, aged 2 days to 16 years. In 10 patients, the high concentrations were measured 9.25 to 48 hours after death and were significantly higher than antemortem levels in all cases (8.3 +/- 2.4 (+/- standard deviation) postmortem vs 3.3 +/- 1.5 antemortem, less than 0.0001). In 15 patients (40.5% of the living patients) serum concentrations of 5 ng/ml or higher reflected sampling errors; drug levels were monitored too closely to the administration of a dose. None of these children had toxic manifestations of digoxin. In 10 patients, the excessive concentrations were associated with renal failure and a prolonged elimination half-life (T1/2) of digoxin; in 3 of these patients, there were signs of digoxin toxicity. Six cases were caused by digoxin overdose (accidental ingestions, pharmacy error and a suicide attempt). In 6 additional cases, the existence of an endogenous digoxin-like substance (EDLS) was shown to contribute to the excessive levels of the drug. One case could be attributed to digoxin-amiodarone interaction. In 10 of 37 living patients, digoxin toxicity was diagnosed. After excluding the 15 sampling errors and 6 cases with EDLS, this represents 63% of the cases. There was a good correlation between digoxin elimination T1/2 and serum creatine concentrations (r = 0.71, p less than 0.01). The above observations suggest that excessive serum concentrations of digoxin may not necessarily reflect potentially toxic levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Clinical use of serum digoxin concentrations.

The development of the radioimmunoassay for digoxin by Smith and coworkers in 1969 was a landmark in digitalis therapy. Since then, the complex pharmacokinetics of digoxin have been defined. As a result, the incidence of digitalis toxicity has markedly decreased. To use the digoxin assay properly, however, the relation of this pharmacokinetic parameter to digoxin pharmacodynamics must be known and the limitations of the assay itself understood. Systolic time intervals (STI) are uniquely useful to quantitate the inotropic effect of digitalis preparations. This technique can demonstrate the onset and magnitude of the inotropic effect for both oral and intravenous digitalis administration. By defining the mathematical relation between STI and simultaneous serum digoxin concentrations following intravenous administration of 1 mg digoxin, computer simulations can be made of the effect of dosing changes on blood and tissue concentrations. The serum digoxin assay has technical problems relating to quality control, interference by metabolites, and cross-reactions with endogenous digitalis-like substances. Further, a standard time for measurement following dosing has not been established. Physical activity can significantly after the serum digoxin concentrations by increasing skeletal muscle binding. Numerous drugs can interfere with digoxin absorption or elimination. Using the serum digoxin assay is the only way to assess these interactions. Computer surveillance (ideally with physician or pharmacist interaction) has been used to monitor digitalis but has not yet gained widespread acceptance. This is clearly a method in need of further testing.

Digoxin↗
PubMed1983

Subcellular [3H]digoxin distribution after temporary myocardial ischemia in dogs.

Following a 90-min coronary occlusion and 2 h reperfusion in 11 dogs, total tissue and subcellular distributions of [3H]digoxin in non-ischemic and various ischemic tissues were measured. In the non-ischemic tissue, [3H]digoxin in the crude homogenate, sediments obtained from 1000 X g, 10000 X g and 100000 X g centrifugations, and final supernatant fraction were 0.70 +/- 0.05, 0.79 +/- 0.05, 0.64 +/- 0.04, 3.87 +/- 0.34 and 0.19 +/- 0.02 ng/mg protein, respectively. As in studies with total tissue [3H]digoxin uptake, a reciprocal correlation was observed in reduction of digoxin binding in the crude homogenates and the 1000 X g sediments with increasing severity of ischemic injury estimated from the loss of nitro-blue-tetrazolium (NBT) stain. A 20% and 80% loss of NBT stain was associated with a 13.3% and 63.5% decrease in digoxin binding, respectively. In contrast, digoxin binding in the 10000 X g sediments increased progressively with the severity of ischemia. No significant change was observed in the final supernatant fraction. Digoxin binding in the 100000 X g sediments, which generally represent specific binding and which are associated with the pharmacologic effects, was not altered in tissues with a loss of NBT stain up to 50%. In fact, a loss of 80% NBT was associated with only a 33.9% decrease in digoxin binding. Thus, it appears that measurement of total tissue digoxin uptake does not provide an accurate measure of the effects of acute ischemia on specific digoxin binding. The ability of the peri- and moderately ischemic tissues (with less than 50% loss of NBT stain) to specifically bind digitalis was not altered after temporary myocardial ischemia.

Animals↗
PubMed1985

Digoxin quinidine interaction: a pharmacokinetic study in the isolated perfused rat liver.

Digoxin-quinidine interaction was studied in the experimental model of isolated perfused rat liver. Neither digoxin nor quinidine were toxic to the isolated rat liver. The clearance of digoxin and quinidine by the liver was directly related to the rate of bile flow and the size of the initial dose of digoxin. In the presence of quinidine, after initial doses of digoxin of 0.5 and 1 micrograms, the concentration of digoxin in the perfusate was increased 2.5 and 3-fold. Its excretion in the bile was reduced by 45% and 20.5%, respectively (all comparisons, p less than 0.01). Digoxin concentration in the liver tissue was calculated and found to be appreciably elevated in the presence of quinidine. A reduction of about 30% (p less than 0.05) in the excretion of quinidine in the bile was observed in the presence of digoxin. Thus, a competition of digoxin and quinidine for biliary excretion was demonstrated as an underlying cause for digoxin-quinidine interaction in the isolated perfused rat liver.

Animals↗
PubMed1982

Effects of digoxin on left ventricular function in coronary artery disease patients.

To assess whether digitalis modifies or prevents the deterioration of the left ventricular ejection fraction and wall motion during acute ischemia, we performed gated blood pool radionuclide ventriculograms in 15 patients with angiographically documented coronary artery disease. All patients were studied in the resting state and during maximal supine bicycle exercise, both before and 1 hour after 1 mg intravenous digoxin. There was no significant difference, pre-digoxin vs post-digoxin, in exercise tolerance (415 +/- 84 vs 418 +/- 107 seconds), number of segments with abnormal resting wall motion (12 vs 11) or exercise wall motion (21 vs 19). Ten patients developed angina during the same exercise load, irrespective of digoxin administration. Twelve patients had subnormal left ventricular ejection fraction during exercise pre-digoxin, vs 13 patients post-digoxin (P = ns). In the resting state, the left ventricular ejection fraction was higher after digoxin (53 +/- 14% pre vs 58 +/- 14% post, P less than 0.05). During exercise, however, the left ventricular ejection fraction was not significantly improved after digoxin (50 +/- 16% pre vs 53 +/- 17% post, P = ns). These data indicate that although acute administration of digoxin improves the resting left ventricular function, it does not improve exercise tolerance to angina. Furthermore, intravenous digoxin does not appear to prevent the deterioration of left ventricular wall motion and ejection fraction during exercise induced ischemia.

Blood Pressure↗