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PubMed2006

Digoxin therapy for heart failure: an update.

Digoxin therapy has long been used to treat heart failure; however, its effectiveness was not completely known until recently. Results of the Digitalis Investigation Group trial showed that adding digoxin to standard heart failure therapy had no effect on mortality. However, adding digoxin decreased hospitalizations related to heart failure and improved symptoms in patients treated for heart failure. Reanalyses of the trial's findings have raised new questions about the role of digoxin in heart failure treatment. These new analyses showed that low serum digoxin concentrations used in patients with more severe disease offered the most benefit. Digoxin use in women was associated with increased mortality risk. This finding should be interpreted with caution, however, because it was based on retrospective data, and the cause of this phenomenon has not been fully elucidated. Prospective clinical trials are needed to determine the serum digoxin concentration that is associated with the most clinical benefit and to determine the role of digoxin therapy for women. Digoxin generally does not have a role in the treatment of diastolic heart failure and is not a first-line therapy for managing atrial fibrillation in patients with heart failure.

Algorithms↗
PubMed1991

Magnesium status and digoxin toxicity.

1. Eighty-one hospital patients receiving digoxin were separated into groups with and without digoxin toxicity using clinical criteria. Serum digoxin, sodium, potassium, calcium, creatinine, magnesium and monocyte magnesium concentrations were compared. 2. Subjects with digoxin toxicity had impaired colour vision (P less than 0.0001, Farnsworth-Munsell 100 hue test) and increased digoxin levels (1.89 (1.56-2.21) vs 1.34 (1.20-1.47) nmol l-1, P less than 0.01) (mean (95% confidence limits], though there was considerable overlap between two groups. 3. Subjects with digoxin toxicity had lower levels of serum magnesium (0.80 (0.76-0.84) vs 0.88 (0.85-0.91) mmol l-1, P less than 0.01) and monocyte magnesium (6.40 (5.65-7.16) vs 8.76 (7.81-9.71) mg g-1 DNA, P less than 0.01), but there were no significant differences in other biochemical parameters. A greater proportion of toxic subjects were receiving concomitant diuretic therapy (20/21 vs 37/60, P less than 0.05). 4. Magnesium deficiency was the most frequently identified significant electrolyte disturbance in relation to digoxin toxicity. In the presence of magnesium deficiency digoxin toxicity developed at relatively low serum digoxin concentrations.

Adult↗
PubMedDate not supplied

[Is there a correlation between changes in the electrocardiogram and high serum digoxin levels in the aged?].

In a group of 84 patients aged 65 to 89 years with the high serum digoxin levels, electrocardiograms, as well as serum creatinine and serum potassium levels were analysed. In an electrocardiogram, a rhythm and conduction disturbances, PR interval, PTQ index, corrected QT interval, both a corrected QT interval I using the second root from a heart frequency and a corrected QT interval II using the third root from a heart frequency were studied. A rhythm disturbances were seen in 37% and a conduction disturbances in 39% of the patients, but no changes were observed in 24% of the patients. There was no correlation between serum digoxin levels and the PR interval. There was a slight correlation between serum digoxin levels and the PTQ index, and no correlation could be demonstrated between serum digoxin levels and a corrected QT interval I as well as a corrected QT interval II. Also, no correlation was evident between serum digoxin levels and serum creatinine levels, although many of those patients suffered from chronic renal failure. In an analysis of the influence of digoxin on the heart, electrocardiographic changes together with serum digoxin levels and serum potassium levels have to be followed. Only one of these parameters is not enough for the analysis of the effect of digoxin on the heart. It is concluded that clinical examination is most important in the analysis of digoxin action.

Aged↗
PubMed1989

Digoxin toxicity: clinical and laboratory assessment.

A prospective study to correlate clinical digoxin toxicity with serum digoxin levels was carried out in 67 patients of whom 24 were clinically toxic and 43 were asymptomatic. The patients were clinically diagnosed to be toxic based on typical cardiac arrhythmias (n = 11) or non-cardiac symptoms (n = 13). Blood samples were collected at least six hours after the last digoxin dose and the sera assayed for digoxin using a radioimmunoassay method. The mean serum digoxin level in the toxic group (x1 = 2.09 +/- 1.28 ng/ml) was significantly higher than in the non-toxic group (x2 = 1.20 +/- 0.75 ng/ml), p less than 0.01. All the non-toxic patients had serum digoxin levels below 3 ng/ml. However, there was a considerable overlap of serum digoxin levels between the two groups of patients. Serum level cannot be the sole criterion in diagnosing digoxin toxicity. Nevertheless, raised serum digoxin levels especially above 3 ng/ml, in the presence of suggestive clinical features is strongly suggestive of toxicity.

Adolescent↗
PubMed1977

Serum digoxin levels in neonates, infants and children with heart disease.

Serum digoxin levels were measured in 53 neonates and infants receiving 18-22 microgram/kg/day (high dose) oral maintenance digoxin, and 44 neonates, infants and children receiving less than 18 microgram/kg/day (low dose) oral maintenance digoxin. In both groups, patients under four months of age had significantly higher serum digoxin levels than older patients, in the high dose group 2.6 ng/ml compared with 1.4 ng/ml and in the low dose group 2.2 ng/ml compared with 1.0 ng/ml. Correlation between digoxin dosage and serum level was weak and unaffected by blood urea level. Only two patients in the entire series showed toxic manifestations. Sixteen patients had serum digoxin levels measured before and after corrective cardiac surgery while receiving comparable dosages of digoxin. Despite lower serum digoxin levels postoperatively pulse rates fell significantly, illustrating the influence of changing haemodynamic status on the inter-relationships of digoxin dosage, serum levels and clinical response. Recommended dosage regimens are outlined.

Adolescent↗
PubMed1987

[Pharmacokinetics and pharmacodynamic effects of digoxin in dilated cardiomyopathies. Influence of nicardipine].

Numerous studies have been devoted to the effect of slow calcium channel inhibitors on plasma digoxin concentrations. The principal drugs tested, verapamil and nifedipine, were found to increase significantly plasma digoxin levels mainly by reducing digoxin total clearance. Very few studies on the nicardipine-digoxin interaction have been reported. The dual purpose of the present study was to evaluate the influence of orally administered nicardipine on plasma digoxin concentrations over 24 hours and to measure possible variations in the pharmacodynamic effects of digoxin in 9 patients with chronic congestive heart failure. The pharmacodynamic assessment involved simple and cross-sectional echocardiography, systolic time interval measurements and cardiac catheterization. In these patients under chronic digoxin treatment, oral nicardipine had little effect on plasma digoxin concentrations which increased but not significantly; no sign of digitalis toxicity was observed. Nicardipine improved left ventricular function and myocardial contractility by reducing after-load, the nicardipine-induced peripheral vasodilatation tending to counteract the digoxin-induced vasoconstriction.

Aged↗
PubMed1988

Effects of quinidine on the renal tubular and biliary transport of digoxin: in vivo and in vitro studies in the dog.

Quinidine is known to inhibit the renal clearance of digoxin without affecting glomerular filtration rate. The renal interaction between these drugs was investigated by a combination of in vivo and in vitro methods. The uptake of digoxin by brush border membrane vesicles was not affected by quinidine. Similarly, digoxin did not inhibit the uptake of the cation N-methylnicotinamide by these vesicles and did not alter the binding kinetics of digoxin to the Na+, K+-adenosine triphosphatase by the antiluminal membrane vesicles. By using the in vivo multiple indicator dilution technique transtubular transport of digoxin was documented; renal-artery infusion of quinidine did not affect the recovery of digoxin in the renal vein or urine. Clearance studies documented that the decrease in the renal clearance of digoxin is paralleled by a significant fall in renal blood flow evidenced by a decrease in p-aminohippuric acid clearance. It is concluded that quinidine inhibits the renal excretion of digoxin not by competition at the tubular cell membrane level, but rather by decreasing renal blood flow. A parallel decrease in biliary clearance of digoxin is documented and may suggest a similar mechanism.

Animals↗
PubMed1986

Cellular mechanisms of digoxin transport and toxic interactions in the kidney.

Renal tubular secretion of digoxin appears to be one of the main ports of elimination of the glycoside from the body. Because of its narrow therapeutic window and severe toxicity, the mechanisms of tubular handling of digoxin are important. Moreover, several drugs which are commonly administered with digoxin, including quinidine, spironolactone, verapamil and amiodarone have been shown to decrease renal clearance of digoxin without affecting GFR. We studied the handling of digoxin using in vitro and in vivo approaches. The handling of the glycoside by the brush border suggests passive reabsorption which is not enhanced by commonly coadministered drugs. Digoxin binding to the antiluminal (basal) membrane suggests that the secretion of the glycoside may not involve the pharmacologic receptor, the Na+, K+, ATPase. Using the multiple indicator dilution technique, we could directly show the two steps of secretion of digoxin: Its sequestration from the postglomerular circulation, and its appearance in the urine after transtubular transport. Digoxin transport is not inhibited by a cationic or anionic molecule (PAH and tolazoline). It is possible that digoxin is secreted by a yet unidentified transport mechanism.

Animals↗
PubMed1985

Prediction of digoxin treatment failure in infants with supraventricular tachycardia: role of transesophageal pacing.

Transesophageal atrial pacing was used to initiate and terminate tachycardia in 24 infants (seven female and 17 male, aged 1 to 34 days) with ECG documentation of supraventricular tachycardia. Six infants received no chronic treatment, and chronic oral digoxin prophylaxis was administered to 18 infants in an effort to prevent recurrences of tachycardia. In these 18 infants, the effectiveness of digoxin therapy in preventing the initiation of tachycardia by transesophageal pacing was compared with its ability to prevent spontaneous recurrences of supraventricular tachycardia. While receiving chronic oral digoxin therapy, tachycardia could be reinitiated in 15/18 (83%) infants. In these infants, the cycle length of tachycardia and the atrioventricular interval were the same before and during chronic digoxin treatment. Three infants in whom tachycardia could not be initiated during chronic digoxin therapy had no spontaneous recurrences during 6 months of follow-up, whereas 10/15 (67%) infants in whom tachycardia could be reinitiated had clinically significant recurrences in spite of chronic digoxin therapy. Six infants who received no chronic drug treatment had no documented recurrences during 6 months of follow-up. This study demonstrates that digoxin was effective in preventing significant spontaneous recurrences of supraventricular tachycardia in only 8/18 (44%) infants treated with digoxin. The ability to initiate supraventricular tachycardia with transesophageal pacing may be useful in determining which digoxin-treated infants are at risk for recurrence. Finally, not all infants with supraventricular tachycardia require chronic prophylaxis; six of the untreated infants had no documented recurrences.

Atrioventricular Node↗
PubMed1985

Combined liquid chromatography/radioimmunoassay with improved specificity for serum digoxin.

This method for assaying digoxin in serum with improved specificity combines small-column extraction of serum, "high-performance" liquid chromatography, and RIA of the eluted fractions. Analytical recoveries of 1.0, 0.5, and 0.1 microgram/L standards were 95%, 93%, and 84%, respectively. The CVs for duplicates and replicates of sera with values of 0.5 to 1 microgram/L were 4 to 6%. Fifty-nine sera from 50 patients receiving digoxin were so studied. All digoxin metabolites appear to cross react with antibody to digoxin to various degrees. The most polar metabolites were quantitatively the most important, their average cross reactivity being 33%. For eight patients the value for digoxin by the present method was less than 60% of the RIA value. Sera from nine patients not taking digoxin but with falsely high digoxin values were also studied by the present method. The digoxin peak was well resolved from those for (a) digoxin metabolites (except dihydrodigoxin), (b) digitalis-like factors in neonates and in patients with renal failure or combined hepatic and renal failure, and (c) two cross reacting drugs and their metabolites.

Adult↗
PubMed1985

Effect of assay conditions on cross reactivity of digoxin-like immunoreactive substance(s) with radioimmunoassay kits.

One or more digoxin-like immunoreactive substances (DLIS), most frequently present in serum of premature and full-term neonates. cross react to various extents with different digoxin immunoassay kit reagents. Mostly, this variation is attributed to the relative cross reactivity of DLIS with the antiserum in each kit. However, modification of standard assay procedures for digoxin can also greatly alter the relative cross reactivity of DLIS. Using sequential RIA kit methods for digoxin by 20 to 60% relative to the standard equilibrium RIA mode. Cross reactivity was decreased still more if the concentrations of antiserum (binding-site concentration) and tracer (125 l-labeled digoxin) were decreased, and conversely. Serum samples containing only digoxin, analyzed by the modified method, consistently yielded results well comparable with those obtained with the manufacturers' recommended procedures. We describe use of the different responses to digoxin and DLIS of standard and sequential radioimmunoassays and use of simultaneous equation to calculate the concentration of DLIS (in digoxin equivalents) in digoxin-containing samples.

Cross Reactions↗
PubMed1981

Study of the sensitivity of neonates to digoxin: contribution of erythrocyte 86rubidium uptake test.

In general, there is little agreement how digoxin should be used in newborn, and the results of studies in this field seem contradictory. This study attempts a quantitative assessment of the number and the sensitivity of cellular receptors for digoxin in the organism, by the in vitro measurement of erythrocyte 86Rubidium uptake in neonates compared with adults and old people. Red blood cells are first incubated with differing concentrations of digoxin, and then incubated with 86Rb. The initial level of 86Rb uptake (Rbi) is that observed in the absence of digoxin. The 50% index of captation (IC50) is the digoxin concentration in nanograms per ml at which 86Rb uptake is half Rbi. Three groups of patients were studied: Group I: 12 neonates, less than 5 days old; Group II: 11 adults (26 to 57 years old); Group III: 9 elderly people (71 to 82 years old). Rbi was significantly lower in neonates (Mean +/- SD: 25.8% +/- 3.5, P less than 0.001) and in the elderly (29.9% +/- 3.1) than in adults (36.8% +/- 4.6). IC50 was significantly lower in the elderly (12.1 ng/ml +/- 2.4) than in the adult patients (20.5 ng/ml +/- 5.5, P less than 0.001). In the newborns, values of IC50 were widely scattered (16.2 ng/ml +/- 7.2). The authors suggest that since Rbi reflects Na+, K+-ATPase activity, this activity is diminished in newborn and old people, and indicates that they have fewer cellular receptors for digoxin than adults. In the elderly, the low IC50 would imply increased sensitivity to digoxin. In neonates, the wide range of values for IC50 suggests considerable individual variation in sensitivity to digoxin. The results are consistent with the recently recommended lower dosages of digoxin in neonates.

Adult↗
PubMed1984

Role of sympathetic nervous system in ischemia-induced reduction of digoxin tolerance in anesthetized cats.

Acute myocardial ischemia reduces tolerance of the heart to arrhythmogenic actions of digitalis glycosides. Because both ischemia and the glycoside produce profound changes in activity of the autonomic nervous system and because sympathetic discharge or catecholamines enhance toxic actions of the cardiac glycosides, the possibility that alterations in digitalis sensitivity of ischemic heart involve changes in sympathetic nerve activity was examined using alpha-chloralose-anesthetized cats. Left anterior descending coronary artery (LAD) was completely occluded by ligation and, 40 min later, a slow i.v. infusion of digoxin was started at a rate of 1 microgram/kg/min. LAD ligation alone did not produce arrhythmias in that condition, but shortened the time to onset of digoxin-induced arrhythmias and thereby reduced the amount of digoxin required to produce the toxic manifestation. Concomitantly, digoxin concentration in plasma and nonischemic areas of the heart were lower in LAD-ligated cats at the onset of arrhythmias than those in sham-operated cats. Myocardial digoxin content in the ischemic area of the LAD-occluded heart was lower than that in nonischemic areas of the same heart. At the onset of digoxin-induced arrhythmias, Na,K-adenosine triphosphatase activity of ischemic myocardium was significantly higher than that in the nonischemic area, reflecting a lower digoxin occupancy of the glycoside binding sites on the sodium pump. Spinal cord (C1) transection or propranolol treatment prolonged the time to arrhythmias in both control and LAD-ligated cats, but failed to abolish the effect of LAD ligation to augment digoxin toxicity. Bilateral vagotomy also did not alter the enhancement of digoxin toxicity caused by ligation of LAD.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1993

Heavy chain position 50 is a determinant of affinity and specificity for the anti-digoxin antibody 26-10.

Antibody produced by a variant of the murine antidigoxin hybridoma 26-10 has reduced affinity for digoxin but enhanced recognition of the digoxin 12-hydroxyl due to a Tyr to His substitution at heavy chain position 50 (Schildbach, J. F., Panka, D. J., Parks, D. R., Jager, G. C., Novotny, J., Herzenberg, L. A., Mudgett-Hunter, M., Bruccoleri, R. E., Haber, E., and Margolies, M. N. (1991) J. Biol. Chem. 266, 4640-4647). Consistent with these data, the 26-10 Fab-digoxin x-ray crystal structure (Jeffrey, P. D., Strong, R. K., Sieker, L. C., Chang, C. Y., Campbell, R. L., Petsko, G. A., Haber, E., Margolies, M. N., and Sheriff, S. (1993) Proc. Natl. Acad. Sci. U. S. A., in press) reveals that Tyr-50 contacts a region of digoxin that includes the hapten-12 carbon. To determine the effects of other heavy chain position 50 substitutions, mutant antibodies were engineered, and their affinities for digoxin and digoxin analogues were measured. The affinity of the mutant antibodies for digoxin roughly correlates with the size of the position 50 side chain. Substitutions of Trp or Phe have no effect on affinity, whereas substitutions of Asn, His, Leu, Ala, Gly, and Asp confer progressively lower affinities. Although Trp and Phe mutants exhibit wild-type specificity, Asn and Asp mutants have improved affinity for digoxin relative to digitoxin (12-deshydroxydigoxin). Leu, Ala, and Gly mutants have improved affinity for 12-acetyldigoxin relative to digoxin as compared with 26-10. These results indicate that position 50 is a determinant of both antibody affinity and fine specificity for antibody 26-10 and that single-amino acid substitutions can alter antibody fine specificity. Models of the mutants were computationally constructed, and haptens were docked into the modeled binding sites. The results suggest that 12-acetyldigoxigenin occupies different orientations in the 26-10 and in the Ala mutant binding sites, resulting in altered binding.

Amino Acids↗
PubMedDate not supplied

Clinical decision analysis modeling: short-term control of ventricular response rate in atrial fibrillation or atrial flutter-digoxin versus diltiazem.

OBJECTIVE: To develop a clinical decision model to compare the outcome of therapy with digoxin versus diltiazem for short-term control of ventricular response rate (VRR) in patients with atrial fibrillation or atrial flutter. DESIGN: Review of data from two studies that examined the percentages of response and frequency of adverse reactions in patients treated with intravenous digoxin or diltiazem to control VRR in atrial fibrillation or flutter. We constructed a clinical decision model and performed sensitivity analysis to determine if the model's predictions could be altered. SETTING: Large teaching, university hospitals. PARTICIPANTS: Adults age 18 years or older treated with intravenous digoxin or intravenous diltiazem for atrial fibrillation or flutter (VRR > or = 120 beats/min). Patients with severe heart failure New York Heart Association class III or IV, a surgical procedure prior to the exacerbation, or an acute myocardial infarction were excluded. MEASUREMENTS AND MAIN RESULTS: We measured VRR control after 1 and 24 hours of therapy (VRR < 100 beats/min or decrease of > or = 20%) and assessed the likelihood that a patient would suffer an adverse drug reaction. Initial assumptions were that the probability digoxin would achieve VRR control was 0.10 (95% confidence interval 0.04-0.20) at 1 hour and 0.70 (95% CI 0.56-0.80) at 24 hours; the probability that diltiazem would achieve VRR control was 0.94 (95% CI 0.82-0.99) at 1 hour and 0.83 (95% CI 0.68-0.94) at 24 hours; and the probability of no serious adverse drug reaction would be 0.90 (95% CI 0.80-0.96) for digoxin and 0.96 (95% CI 0.86-0.98) for diltiazem. RESULTS: Diltiazem was superior to digoxin with respect to the composite end point score at 1 hour (91.20 vs 17.29) and 24 hours (81.65 vs 66.43). Digoxin was superior to diltiazem at 24 hours only if the VRR was assumed to be at the highest 95% CI limit for digoxin and simultaneously at the lowest 95% CI for diltiazem (74.62 vs 68.63). CONCLUSIONS: Clinical decision analysis suggests that intravenous diltiazem is superior to intravenous digoxin in controlling VRR in patients with atrial fibrillation or flutter.

Adolescent↗
PubMed1993

Role of P-glycoprotein in renal tubular secretion of digoxin in the isolated perfused rat kidney.

The mechanism for renal tubular secretion of digoxin as well as its interaction with quinidine or verapamil were investigated using the isolated perfused rat kidney. [3H]Digoxin was instantaneously administered into the renal artery together with [14C]inulin and Evans blue-albumin, and renal venous and urinary outflow curves were measured. The ratio of fractional excretion to filtration fraction for digoxin was 2.40 +/- 0.40, indicating involvement of tubular secretion. Quinidine and verapamil decreased the ratio of fractional excretion to filtration fraction in a concentration-dependent manner, and this inhibition was indicated to occur at transport from cells to lumen across luminal membranes. Neither tetraethylammonium nor p-aminohippurate affected the renal handling of digoxin. Because ouabain and digitoxose showed no influence on the value of fractional excretion to filtration fractions, Na+,K(+)-ATPase is not involved in the tubular secretion of digoxin. A metabolic inhibitor, 2,4-dinitrophenol, markedly inhibited digoxin secretion. Agents that bind to P-glycoprotein, such as vinblastine, daunorubicin and reserpine, markedly inhibited the secretion of digoxin. Recently, we have found that digoxin is a substrate transported by P-glycoprotein. The findings obtained here support the hypothesis that digoxin is secreted by P-glycoprotein located on the luminal membrane of renal tubular epithelial cells, and that clinically important interactions with quinidine and verapamil are caused by the inhibition of P-glycoprotein.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1993

Captopril versus digoxin in patients with coronary artery disease and mild heart failure. A prospective, double-blind, placebo-controlled multicenter study. The CADS Study Group.

We conducted a prospective, double-blind, placebo-controlled multicenter trial in order to evaluate the long-term effects of captopril (50 mg/day), digoxin (0.25 mg/day) and placebo on quality of life, cardiovascular events, clinical symptoms and exercise tolerance in patients with documented myocardial infarction, resulting in regional wall motion abnormalities, and with mild heart failure (NYHA class II to III without treatment) and exercise not limited by angina. 222 patients were studied, 63 were randomized to captopril, 66 to digoxin, 67 to placebo. Follow-up was conducted for two years. Base line characteristics in the three treatment groups were similar. After one year of therapy, digoxin had significantly improved general well-being (p < 0.01 vs captopril), symptom score (p < 0.05 vs captopril and placebo), and vitality (p < 0.05 vs captopril). Digoxin improved NYHA class in 45% as compared to placebo (28%, p < 0.05). Worsening of angina was more frequent with captopril as compared to digoxin (p < 0.05). However, cardiovascular events during follow-up were lower in the captopril group as compared to placebo and digoxin (p < 0.01 captopril vs placebo). No differences between groups were observed in baseline and follow-up exercise tolerance between the three groups. Dizziness during upright tilt and cough were more frequent with captopril as compared to digoxin or placebo. After two years of follow-up (captopril n = 32, digoxin n = 29, placebo n = 27) general well-being was improved with both digoxin and captopril (p < 0.004 and p < 0.03 vs placebo).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Coronary vasoconstriction induced by digoxin in normal subjects and in patients with coronary atherosclerosis].

This study evaluated the effects of digoxin infusion (0.014 mg/kg in 10 min i.v.) on large coronary arteries measured by quantitative digital angiography. Twenty-two patients (aged 47 +/- 12), divided in 3 groups were studied. The effects of digoxin infusion (after 10 and 20 min) and sublingual administration of isosorbide dinitrate were investigated in Group I (patients with angiographically normal coronary arteries, n = 9) and in Group II (patients with atherosclerotic coronary arteries, n = 8). In Group III (n = 5) to determine whether or not the effects of digoxin were mediated by activation of alpha-adrenergic receptors, coronary angiographies were performed after alpha-adrenoceptor blockade (phentolamine 0.11 mg/kg, i.v.). In Group I, 10 min after the end of digoxin infusion, cross-sectional area decreased from 7.7 +/- 4.1 mm2 to 6.0 +/- 2.2 mm2, and after 20 min to 5.6 +/- 2.6 mm2 (p < 0.05). Isosorbide dinitrate reverted digoxin-induced vasoconstriction as cross-sectional area increased to 8.5 +/- 3.4 mm2 (NS versus baseline). By 20 min after digoxin infusion heart rate was significantly reduced from 79 +/- 16 to 74 +/- 13 b/min (p < 0.01). Peripheral vascular resistances increased significantly 10 min after digoxin infusion (from 1396 +/- 693 to 1693 +/- 984 dyne*s*cm-5, p < 0.05), whereas cardiac output did not change. In Group II, minimal stenosis diameter decreased significantly 20 min after digoxin infusion from 1.6 +/- 0.5 mm to 1.4 +/- 0.5 mm (p < 0.05). Again, isosorbide dinitrate reverted digoxin-induced vasoconstriction as minimal stenosis diameter increased (NS versus control).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗