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PubMed1976

[Digoxin concentration in the blood during the treatment of cardiac insufficiency].

Blood concentrations of Digoxin were determined by radioimmuno-assay in 80 patients with different stages of circulatory insufficiency receiving maintenance therapy with Digoxin, 0.25-0.75 mg/day. The range of Digoxin concentration fluctuations is very wide--from 0.25 to 2.4 ng/ml. Some elevation of Digoxin concentration in blood was observed when the dose of the drug was increased, both in different groups of patients, and in the same patients when the maintenance dose was altered. Studies conducted during digitalis intoxication in 4 patients demonstrated different levels of Digoxin concentration in blood--from 0.8 to 2.6 ng/ml. The obtained results permitted to conclude that the concentration of Digoxin in blood has no significance in choosing the optimum therapeutic dose, unless the clinical data are taken into account.

Adult↗
PubMed1984

Audit of digoxin prescribing in ambulatory patients.

Digoxin prescribing for ambulatory patients with uncomplicated congestive heart failure in normal sinus rhythm (UCHF) was evaluated. The audit was conducted at a hospital primary care clinic and was performed retrospectively over a recent 2-year period. The audit focused on the discontinuance of digoxin prescribing and the attendant monitoring necessary. There was 34 patients prescribed digoxin during the study period who were classified as UCHF. Of these, 23 (68%) met our a priori criteria for digoxin discontinuance. However, only three of the 23 were discontinued and none met the criteria for proper follow-up. With regard to monitoring, the average patient was seen once every 2 months, but in fewer than half of the visits the patient was assessed on basic subjective and objective parameters of CHF status and digoxin toxicity. These results are being used in an educational program for the clinic physicians who before the audit had perceived their care of digoxin patients to be optimal.

Ambulatory Care↗
PubMed1999

Isolation and characterization of human monoclonal antibodies to digoxin.

Fab preparations of sheep polyclonal anti-digoxin Abs have proven useful for reversal of the toxic effects of digoxin overdoses in patients. Unfortunately, the use of foreign species proteins in humans is limited because of the potential for immunological responses that include hypersensitivity reactions and acute anaphylaxis. Immunization of recently developed transgenic mice, whose endogenous micro heavy and kappa light chain Ig genes are inactivated and which carry human Ig gene segments, with a digoxin-protein conjugate has enabled us to generate and isolate eight hybridoma cell lines secreting human sequence anti-digoxin mAbs. Six of the mAbs have been partially characterized and shown to have high specificity and low nanomolar affinities for digoxin. In addition, detailed competition binding studies performed with three of these mAbs have shown them to have distinct differences in their digoxin binding, and that all three structural moieties of the drug, the primary digitoxose sugar, steroid, and five-member unsaturated lactone ring, contribute to Ab recognition.

Animals↗
PubMed1979

Immunogenicity and kinetics of distribution and elimination of sheep digoxin-specific IgG and Fab fragments in the rabbit and baboon.

To evaluate the relative merits of purified IgG and Fab preparations of defined specificity for potential clinical use, immunogenicity studies were carried out in baboon and rabbit experimental models. Distribution and elimination kinetics of purified sheep digoxin-specific IgG and Fab fragments were also studied following intravenous administration to baboons. Serial plasma and urine Fab concentrations were determined from trichloroacetic acid-precipitable 125I counts from pre-labelled preparations and also by measurement of the antibody's functional 3H-digoxin binding capacity. Results were compared with data obtained from IgG by 3H-digoxin binding. Kinetic data analysed by computer-fitted functions demonstrated that plasma Fab disappearance was best described by a tri-exponential function, whereas a bi-exponential function best described the IgG data. Initial distribution half-life (t 1/2) of Fab (0.28-0.32 hr) was considerably shorter than that of IgG (4.0 hr) and contributed a greater proportion of the total fall in plasma level over 24 hr. Fab elimination t 1/2 (9-13 hr) was also shorter than IgG (61 hr), but appreciably longer than earlier estimates in rabbits, guinea-pigs, rats and mice. The total volume of distribution of Fab was 8.7 times greater than that of IgG measured by the same method. Over the first 24 hr after administration 30-45% of administered Fab was recoverable in active form in urine, while 93% of total administered 125I counts from 125I-Fab preparations (bound and free) could be recovered. Less than 1% of administered IgG binding activity was recovered in urine during the initial 24 hr. The relative immunogenicities of sheep digoxin-specific IgG and Fab fragments were studied in six baboons. Both IgG and Fab elicited prompt immune responses when injected intramuscularly with Freund's complete adjuvant. Intravenous injection of soluble sheep IgG resulted in a prompt immune response in one baboon while repeated injections caused only a late, weak response in a second animal. Soluble sheep Fab fragments elicited only delayed and weak responses in the two baboons thus challenged. Further immunogenicity studies in ninteen rabbits showed significantly earlier and greater antibody responses to intravenously administered sheep IgG antigen than to Fab fragments derived from the same IgG population. These studies demonstrate that digoxin-specific Fab fragments undergo more rapid and extensive distribution to the extra vascular compartment and also more rapid renal excretion than IgG. Furthermore, Fab fragments are significantly less immunogenic than the parent IgG population. These data indicate potentially important therapeutic advantages for digoxin-specific Fab compared with IgG when administered for the reversal of life-threatening digitlis toxicity.

Animals↗
PubMed2002

Digoxin assays: frequent, substantial, and potentially dangerous interference by spironolactone, canrenone, and other steroids.

BACKGROUND: A case of digoxin toxicity resulted from falsely low values with the MEIA II assay for digoxin (AxSYM; Abbott). The low results were caused by negative interference from canrenone and spironolactone, the latter of which has recently been advocated for the treatment of severe heart failure. Analytical interference from spironolactone has been reported, but little information is available for this effect with newer digoxin assays. METHODS: We examined nine assays (AxSYM, IMx, TDx, Emit, Dimension, aca, TinaQuant, Elecsys, and Vitros for interference by spironolactone, canrenone, and three metabolites. Additionally, all routine digoxin measurements (AxSYM) over a period of 16.5 months (n = 3089) were monitored for interference. RESULTS: Suppression of the expected values by canrenone (3125 microg/L) was observed for the AxSYM (42% of expected value), IMx (51%), and Dimension (78%) assays. A positive bias was observed for the aca (0.7 microg/L), the TDx (0.62 microg/L), and the Elecsys (>0.58 microg/L). Twenty-five of 669 routinely monitored patients had falsely low results. Nineteen of these had potentially toxic concentrations of digoxin (Emit; >2.0 microg/L), although the AxSYM assay indicated therapeutic or less severe toxic concentrations (Delta(max) = 7.1 microg/L). Except for two unresolved cases, this was attributable to spironolactone, canrenone, hydrocortisone, or prednisolone. Standard doses of spironolactone (up to 50 mg/day) in patients with heart failure displayed inhibition <11%. CONCLUSIONS: The frequency and magnitude of the false-negative results particularly compromise the use of both microparticle enzyme immunoassays. Not only may toxic concentrations remain unidentified, but intoxication could occur should dosage be increased because of falsely low results. With 11 million digoxin tests/year ordered in the US, conceivably many patients could be adversely affected.

Anti-Arrhythmia Agents↗
PubMed2001

Hypothalamic digoxin mediated model for oncogenesis.

This study assessed the changes in the isoprenoid pathway and its metabolites digoxin, dolichol and ubiquinone in neoplasms (CNS astrocytomas - glioblastoma multiforme and high grade non - Hodgkin's lymphoma). The following parameters were assessed-isoprenoid pathway metabolites, tyrosine and tryptophan catabolites, glycoconjugate metabolism, RBC membrane composition and free radical metabolism. There was an elevation in plasma HMG CoA reductase activity, serum digoxin and dolichol and a reduction in RBC membrane Na+-K+ ATPase activity, serum ubiquinone and magnesium levels. Serum tryptophan, serotonin, nicotine and quinolinic acid were elevated while tyrosine, dopamine, noradrenaline and morphine were decreased. The total serum glycosaminoglycans and glycosaminoglycan fractions (except dermatan sulphate in the case of CNS astrocytomas), the activity of GAG degrading enzymes and glycohydrolases, carbohydrate residues of glycoproteins and serum glycolipids were elevated. HDL cholesterol showed a significant decrease and free fatty acids & triglycerides were increased. The RBC membrane glycosaminoglycans, hexose and fucose residues of glycoproteins and phospholipids were reduced. The activity of all free radical scavenging enzymes, concentration of glutathione, iron binding capacity and ceruloplasmin decreased significantly while the concentration of malondialdehyde (MDA), hydroperoxides, conjugated dienes and NO increased. The concentration of alpha tocopherol was unaltered. Membrane Na+-K+ ATPase inhibition due to elevated digoxin, altered membrane structure and digoxin related tyrosine / tryptophan transport defect leading to increased levels of depolarising tryptophan catabolites and decreased levels of hyperpolarising tyrosine catabolites can lead to alteration in intracellular calcium/magnesium ratios and oncogene activation. Intracellular magnesium deficiency can produce defective microtubule related spindle fibre dysfunction and chromosomal non-dysjunction contributing to neoplastic cellular polyploidy and aneuploidy. Digoxin induced tryptophan/tyrosine transport defect can alter neurotransmitter patterns with increased serotonin, quinolinic acid, nicotine & glutamatergic transmission and reduced dopamine, morphine and noradrenaline levels leading to oncogenesis. Glycoconjugate metabolism is altered by elevated dolichol levels and magnesium depletion consequent to Na+-K+ ATPase inhibition. There is a qualitative alteration in proteoglycans and glycoproteins, defective membrane formation and structure and reduced lysosomal stability leading to disordered contact inhibition and tumour antigen presentation contributing to oncogenesis. Digoxin induced alteration in intracellular calcium/magnesium ratios and low ubiquinone levels can lead to a mitochondrial dysfunction resulting in increased free radical generation and reduced scavenging & caspase-3 activation producing a P21 defect contributing to oncogenesis.

Adult↗
PubMed1975

[Proceedings: Studies on the digoxin resorption in patients with decompensated right cardiac insufficiency].

Digoxin absorption was investigated in 7 patients suffering from severe right cardiac failure. After successful treatment and disappearance of the symptoms of right cardiac failure, the study was repeated in the same patients. Tritium-labelled digoxin in a dose of 0.1 mg as a solution, and non-labelled digoxin as a 0.25 mg tablet, were given to the patients in the fasting state. Blood samples were taken at specified time intervals up to 120 h and the urine was collected during the same period. The concentrations of digoxin in plasma and urine were measured in a liquid scintillation counter. The unlabelled digoxin was estimated by radioimmunoassay. The concentrations obtained in the plasma and urine were used to compute pharmacokinetic parameters. There was no significant difference in the plasma concentration curves in severe right cardiac failure and after successful treatment, nor did the calculated pharmacokinetic parameters differ significantly. Inhibition of digoxin absorption in severe right cardiac failure therefore seems unlikely.

Digoxin↗
PubMed2002

Hypothalamic digoxin and regulation of body mass index.

The hypothalamus produces digoxin, an endogenous membrane Na+-K+ ATPase inhibitor and regulator of neurotransmission. Digoxin being a steroidal glycoside, is synthesised by the isoprenoid pathway. In view of the reports of elevated digoxin levels in metabolic syndrome X with high body mass index, the isoprenoid pathway mediated biochemical cascade was assessed in individuals with high and low body mass index. It was also assessed in individuals with differing hemispheric dominance to find out the relationship between digoxin status, body mass index and hemispheric dominance. The isoprenoid pathway metabolites, tryptophan / tyrosine catabolic patterns and membrane composition were assessed. In individuals with high body mass index an upregulated isoprenoid pathway with increased HMG CoA reductase activity, serum digoxin and dolichol levels and low ubiquinone levels were observed. The RBC membrane Na+-K+ ATPase activity and serum magnesium levels were decreased. The tyrosine catabolites (dopamine, morphine, epinephrine and norepinephrine) were reduced and the tryptophan catabolites (serotonin, quinolinic acid, strychnine and nicotine) were increased. There was an increase in membrane cholesterol : phospholipid ratio and a reduction in membrane glycoconjugates in individuals with high body mass index. The reverse patterns were seen in individuals with low body mass index. The patterns in individuals with high body mass index and low body mass index correlated with right hemispheric dominance and left hemispheric dominance respectively. Hemispheric dominance and digoxin status regulates the differential metabolic pattern observed in individuals with high and low body mass index.

Adult↗
PubMed2003

Interaction study between digoxin and a preparation of hawthorn (Crataegus oxyacantha).

Hawthorn, an herbal supplement, is currently being evaluated for the treatment of heart failure. The flavonoid components of hawthorn may be responsible for hawthorn's beneficial effects in the treatment of heart failure. However, these components may also affect P-glycoprotein function and cause interactions with drugs that are P-glycoprotein substrates, such as digoxin, which is also used to treat heart failure. Therefore, the purpose of this study was to determine the effect of hawthorn on digoxin pharmacokinetic parameters. A randomized, crossover trial with 8 healthy volunteers was performed evaluating digoxin 0.25 mg alone (D) for 10 days and digoxin 0.25 mg with Crataegus special extract WS 1442 (hawthorn leaves with flowers; Dr. Willmar Schwabe Pharmaceuticals) 450 mg twice daily (D + H) for 21 days. Pharmacokinetic studies were performed for 72 hours. There were no statistically significant differences in any measured pharmacokinetic parameters. The AUC0-infinity, Cmax-Cmin, Cmin, and renal clearance for the D group were 79 +/- 26 mcg.h/L, 1.4 +/- 0.7 mcg/L, 0.84 +/- 0.2 mcg/L, and 74 +/- 10 mL/min versus 73 +/- 20 mcg.h/L, 1.1 +/- 0.1 mcg/L, 0.65 +/- 0.2 mcg/L, and 81 +/- 22 mL/min for the D + H group, respectively (p > 0.05). Following 3 weeks of concomitant therapy, hawthorn did not significantly alter the pharmacokinetic parameters for digoxin. This suggests that both hawthorn and digoxin, in the doses and dosage form studied, may be coadministered safely.

Adult↗
PubMed1992

A correlation between digoxin plasma concentrations and systolic time intervals in hospitalized congestive heart failure patients.

Plasma digoxin level is at best an indirect measure of pharmacological response to digoxin in patients being treated for congestive heart failure. Systolic time interval (STI) measurement reflecting left ventricular function at the physiological site of action of digoxin, is both more direct and non-invasive. With a portable instrument to measure systolic time intervals, the measurement can also be convenient for hospital staff. A portable electrocardiogram (ECG) machine was modified to mimic the capabilities of a large, multichannel model. Upon satisfactory evaluation, it was employed in the collection of systolic time interval data from five hospitalized patients undergoing digoxin treatment. An attempt was made to show a relationship between STI indices and digoxin plasma concentrations. Additionally, a statistical comparison was made of change in STI (delta STI) and plasma digoxin concentration both before and after drug administrations. The change in pre-ejection period (delta PEP) values show a significant difference over the changes in total electromechanical systole (delta QS2) and the changes in left ventricular ejection time (delta LVET). In three congestive heart failure patients, the time course of the change in plasma concentration showed good correspondence with delta PEP.

Adolescent↗
PubMed2003

[Confirmed and suspected digoxin intoxications].

AIMS: To quantify and analyze suspected and actual digoxin intoxications. METHOD: A drug-use study has been carried out of digoxinaemia requests and results in patients treated chronically with digoxin. RESULTS: Digoxin intoxication (presence of symptoms and typical signs) was suspected in 31.3% of the patients. The percentage analytically confirmed intoxications (digoxinaemia >2 ng/mL) was 16.6%. Sex, age, and dosage had no significant effect in the suspicion or confirmation of digoxin intoxication. Hospitalization and the association of hypokalaemic drugs or those increasing digoxinaemia had no effect in the suspicion of digoxin intoxication. In analytically confirmed intoxications, no significant differences were found between suspected and non-suspected cases. CONCLUSIONS: The suspicion of this intoxications is not usually related with digoxin serum levels, and thus, the toxic limit is imprecise.

Aged↗
PubMed1992

[The use of digoxin in primary care].

OBJECTIVE: A study aimed at a population attended at the Primary Health level was designed, in order to reach a greater understanding of the use of Digoxin by doctors and patients. DESIGN: A crossover observational study, carried out wholly at the Primary Care level. PATIENTS: 205 patients under long-term Digoxin treatment were studied. 94 (46%) were men and 111 (54%) women. The average age (SD) was 67 (13). MEASUREMENTS AND MAIN RESULTS: The indication was considered adequate in 62.9% of patients. The average dose (AD) of Digoxin was 0.163 mg a day (0.04): the age of the patients is not taken into account on working out the dose of Digoxin. 52 patients (25.4%) recognised they had not properly carried out the prescription. In this group the view that Digoxin was unnecessary was more common (X = 10.63; p = 0.001). The average Digoxinemia (AD) was 0.85 (0.46) ng/ml. 57% of patients had plasmatic levels below a therapeutic level. The variables related to plasmatic level were: daily dosage (r = 0.4, p = 0.001); age (r = 0.2, p = 0.001; plasmatic creatinine (r = 0.3, p = 0.001); clearing of creatinine (r = -0.4, p = 0.001) and compliance (t = 2.42, p = 0.01). The same independent variables were identified as significant in the multivariant analysis. The week-end break from dosage supposed a fall in the plasmatic levels of 67.7%. CONCLUSIONS: In spite of being a widely-used drug, the dosage of Digoxin is not adequately worked out and compliance is a long way from the optimum. Digoxinemia correlates to the dosage, renal function and compliance with the prescription.

Adult↗
PubMed1990

Serum digoxin concentration: increase after rest in different body positions.

If outpatients are allowed to rest in the supine position before their blood is sampled, serum digoxin increases. In a recent study, the serum digoxin concentration after 2-h standardized supine rest correlated better with the clinical status of patients than the value before rest. In the present study, 21 outpatients were studied on 2 consecutive days, approximately 24 h after the latest dose of digoxin. Blood samples for the assay of serum digoxin were taken on arrival at the department and after 1.5- and 2-h rest either supine or sitting (random order). The increases after 1.5-h rest were 12% (0-25%; p less than 0.001) and 12% (-3-47%; p less than 0.001), supine and sitting, respectively. The respective increases after 2-h rest were 14% (-11-32%; p less than 0.001) and 16% (0-74%; p less than 0.001). There were no statistically significant differences between the increases in serum digoxin concentration after supine and sitting rest. These results make it possible to recommend standardized rest in the sitting position (1.5-2 h) for outpatients before blood samples are collected when reliable serum digoxin analyses are of importance.

Aged↗
PubMed1990

A V kappa-J kappa junctional change in an antidigoxin recombinant antibody destroys digoxin-binding activity.

A set of high affinity antidigoxin antibodies were previously identified with high homologous V kappa 1A L chain sequences but were associated with two entirely different VH regions and two dramatically different specificities for digoxin analogs. Antibodies 40-20, 40-60, 40-90, and 40-100 displayed similar binding specificities but differed from that of antibody 26-10. In a previous study using somatic cell fusion for Ig chain recombination we demonstrated that a recombinant antibody consisting of the H chain of antibody 26-10 and the L chain of antibody 40-20 retained digoxin binding and the 26-10 Id, but displayed a binding specificity pattern dominated by the 26-10 H chain donor. In the present study we produced three additional chain recombinant antibodies that contain the 26-10 H chain recombined with each of the L chains of antibodies 40-60, 40-90, and 40-100. All four recombinants expressed the 26-10 Id indistinguishably from the 26-10 antibody. Two of the recombinants (using the 40-60 and 40-90 L chains) bind digoxin; however, the recombinant using the 40-100 L chain failed to bind digoxin. Complete sequence analyses of the 40-20, 40-60, 40-90, and 40-100 VH and VL regions were performed. Antibodies 40-90 and 40-100 have identical VH region sequences but differed only in their L chains at position 96 (proline/leucine). This single difference at the VK-JK junction abolished digoxin binding in the context of one H chain (26-10), but does not cause a significant change in binding in association with the "normal" parental chains 40-90 and 40-100. Thus, structurally closely related VL regions can recombine with different VH regions to form digoxin binding sites of different specificity; in one binding site the identity of a L chain junctional residue is critical whereas in the second binding site that residue is unimportant. Molecular modeling studies revealed major differences between calculated binding site structures for 26-10 when leucine is substituted for proline at position 96 in the 26-10 VL region.

Amino Acid Sequence↗
PubMed1990

[False results of measuring digoxin levels in patients with renal failure. Comparison of the RIA--FPIA methods].

During last few years were reports concerning a new endogenous digoxin -like immunologic factor (DLIF) in patients not receiving digitalis. DLIF was stated in pregnant women's blood umbilical and neonatal blood as well as in patients with renal failure or hepatopathy. This phenomenon could be related to hormones changes (pregnancy) as well as alterations of cholesterol, triglycerides, free fatty acids, albumins or total protein level (nephropathy, hepatopathy). DLIF overstated determination of serum digoxin concentration, which in the case of exceptional narrow digoxin therapeutic spectrum as well as its concentration-dependent toxicity became a significant clinical problem. Effect extent of DLIF on serum digoxin level could be also related to applied analytic technics. The aim of the study was to compare two routinely applying analytic methods: polarized immunofluorescence (FPIA-TDx Abbott) with radioimmunological assay (RIA). The study was performed in patients with renal failure to estimate DLIF effect on real serum digoxin concentration as well as on extent and DLIF elimination velocity during dialysis. DLIF occurrence in patients with renal failure not receiving digitalis was experimentally stated using both RIA and FPIA methods. However, RIA revealed DLIF in all cases: before and after dialysis as well as in not dialyzed patients with a concentration above 0.3 ng/ml, when FPIA values were respectively: 0.087; 0.043; 0.078 ng/ml, which was less than 10% of digoxine therapeutic range (0.9-2.0 ng/ml). DLIF lowered in a course of dialysis to FPIA advantage, which was proved by FPIA/RIA ratio decrease nearly of a half of its predialysis value. Pre- and postdialysis values of FPIA/RIA ratio were 0,204 and 0,134 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnostic Errors↗
PubMed1990

Efficacy of digoxin for treatment of cats with dilated cardiomyopathy.

The role of digoxin in treatment of cats with dilated cardiomyopathy and other forms of myocardial failure is unclear. We evaluated the chronotropic and inotropic effects of digoxin by comparing baseline, noninvasive indices of cardiac performance with those obtained after 9 +/- 1.3 (mean +/- SEM) days of digoxin treatment in 6 cats with heart failure attributable to dilated cardiomyopathy. Two-dimensionally directed, M-mode echocardiography and electrocardiography were used to determine left ventricular shortening fraction, preejection period (PEP), ejection time (LVET), PEP to LVET ratio, velocity of circumferential fiber shortening, electromechanical systole, heart rate, and PR interval. Treatment consisted of administration of furosemide (mean dosage, 2.4 mg/kg of body weight/day), digoxin in tablet form (approximately 0.01 mg/kg, q 48 h), aspirin (80 mg, q 48 h), and a commercial low-salt diet. In addition, 2 cats were administered short-term, low-dose fluids IV, and 2 were given taurine supplementation at rates of 500 and 1,000 mg/day. Other off-loading or inotropic agents were not administered. Therapeutic or toxic serum digoxin concentration was achieved in all cats. Significant (P less than 0.05) improvement was detected in mean values for shortening fraction, PEP, PEP to LVET ratio, and velocity of circumferential fiber shortening. Mean electromechanical systole and LVET did not change significantly. Improvement, as assessed by indices of cardiac function, was documented in 4 of the 6 cats treated with digoxin, including the 2 cats given taurine supplementation. In the cats given taurine, positive inotropic effect was observed prior to the time when taurine-induced improvement in ventricular function is detectable.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of intravenous digoxin on the heart at rest and during isometric exercise: a noninvasive study in normal and autonomically blocked volunteers.

Nine healthy volunteers were studied with echocardiography and systolic time intervals before and after administration of 1 mg digoxin intravenously at supine rest and during 3-min isometric handgrip exercise. Eight of them were also studied following autonomic blockade, atropine (0.04 mg/kg), and propranolol (0.2 mg/kg) administered intravenously, otherwise the study program was the same. At rest, intravenous digoxin decreased the heart rate from 61 +/- 3 to 50 +/- 2 beats/min (p less than 0.001). Blood pressure, preload [defined as left ventricular end-diastolic diameter (LVEDD)] or afterload [estimated as left ventricular midsystolic circumferential wall stress (WS)], did not change. Fractional shortening increased from 29 +/- 2 to 33 +/- 2% (p less than 0.05), and the electromechanic systole time index (QS2i) decreased from 522 +/- 7 to 500 +/- 5 ms (p less than 0.01). The results indicate improved contractility due to digoxin. During handgrip, the heart rate decreased from 73 +/- 5 to 65 +/- 5 beats/min (p less than 0.01) as a result of digoxin. The LVEDD, WS or ejection phase indices, and systolic time intervals, did not change, suggesting that digoxin does not affect inotropy during isometric exercise. There was no changes in heart rate, preload or afterload, as a result of intravenous digoxin during autonomic blockade. Fractional shortening rose from 25 +/- 1 to 29 +/- 2 (p less than 0.05) and QS2i fell from 561 +/- 3 to 533 +/- 4 ms (p less than 0.001). The results indicate increased inotropy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Use of digoxin in patients with paroxysmal supraventricular tachycardia].

The effectiveness and electrophysiologic mechanisms of antiarrhythmic effect of digoxin were examined in 27 patients with paroxysmal atrioventricular nodal reciprocal tachycardia (PAVNRT) and supraventricular tachycardia (SVT) due to latent complementary conductive pathways, i. e. latent Wolff-Parkinson-White (WPW) syndrome. To assess antiarrhythmic action of digoxin, transesophageal pacing and plasma digoxin radioimmonoassays were used. Preventive antiarrhythmic efficiency of digoxin was 53% in PAVNRT patients, and 25% in SVT patients with latent WPW syndrome. Antegrade atrioventricular conduction block seems to be the mechanism of oral digoxin preventive effect. There was no relationship between antiarrhythmic efficiency of digoxin and its plasma level.

Action Potentials↗