Serial serum digoxin concentrations and quantitative electrocardiographic changes

Joubert, P. H.; Kroening, Bruce; Weintraub, Michael

doi:10.1002/cpt1975186757

Cited by 18 publications

(7 citation statements)

References 2 publications

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“…Adequate serum concentrations of digoxin and digitoxin within the therapeutic ranges (digoxin, 1·3 Ϯ 0·5 ng mL -1 ; digitoxin, 21·8 Ϯ 4·5 ng mL -1 ) and significant reduction in the T-wave amplitude (placebo, 0·63 Ϯ 0·34 and 0·65 Ϯ 0·24 mV; digoxin, 0·42 Ϯ 0·29 mV; digitoxin, 0·39 Ϯ 0·14; P Ͻ 0·05) confirmed clinically relevant glycoside effects [5,6]. Figures 1 and 2 illustrate the 24-h blood-pressure profile at day 10 for the digoxin study and the digitoxin study respectively.…”

Section: Effect Of Cardiac Glycosides On Blood Pressure In Normal Submentioning

confidence: 71%

Effects of cardiac glycosides on 24-h ambulatory blood pressure in healthy volunteers and patients with heart failure

Großmann

2001

Eur J Clin Invest

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Blood pressure effects of cardiac glycosides in humans have been infrequently reported. Although direct infusion of ouabain or digoxin causes vasoconstriction, indirect effects of cardiac glycosides may have the opposite effect, owing to changes in sympatho-vagal balance. This paper summarises three studies on the effects of cardiac glycosides on circadian blood pressure, utilizing automatic 24-h ambulatory blood pressure measurement (ABPM). In healthy volunteers, 10 days of oral digoxin or digitoxin caused decreases in diastolic blood pressure and heart rate during overnight sleep. No effect was detectable during daytime activities. In patients with heart failure (NYHA stage II), 7 days of oral digoxin also caused a decrease in diastolic blood pressure but only a small increase in systolic pressure during overnight sleep. Again, no effect was detectable during the day. Cardiac glycosides have significant effects on blood pressure, which only appear during overnight sleep, i.e. a phase when sympathetic background activity is lowest. Regular daytime activities may 'overwrite' these effects. Effects of cardiac glycosides on blood pressure may have therapeutic impact, depending on the stage of heart failure and concomitant diseases.

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Section: Effect Of Cardiac Glycosides On Blood Pressure In Normal Submentioning

confidence: 71%

Effects of cardiac glycosides on 24-h ambulatory blood pressure in healthy volunteers and patients with heart failure

Großmann

2001

Eur J Clin Invest

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“…ECG recordings at days 4 and 10 of digoxin and digitoxin treatment showed T-wave reduction as a typical sign of cardiac glycoside effect [14,15]. ECG recordings at days 4 and 10 of digoxin and digitoxin treatment showed T-wave reduction as a typical sign of cardiac glycoside effect [14,15].…”

Section: Discussionmentioning

confidence: 96%

Effects of digoxin and digitoxin on circadian blood pressure profile in healthy volunteers

Großmann

Jamieson

Kirch

1998

Eur J Clin Investigation

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“…They assumed that a small fraction of the body content of digoxin is closely bound to receptors mediating chronotropic and toxic effects. Contrary to this, Taubert and Shapiro (I975) demonstrated a slowing of heart rate at the time of the highest serum digoxin level after ingestion of the 8 relation with serum digoxin concentrations during maintenance therapy (Joubert et al, 1975).…”

Section: Chronotropic Effectsmentioning

confidence: 96%

Clinical Pharmacokinetics of Digoxin

Iisalo

1977

Clinical Pharmacokinetics

213

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About 70 to 80% of an oral dose of digoxin is absorbed, mainly in the proximal part of the small intestine. The degree of binding to serum albumin is 20 to 30%. Digoxin is extensively distributed in the tissues, as reflected by the large volume of distribution. High concentrations are found in the heart and kidneys, but the skeletal muscles form the largest digoxin storage. The half-life of elimination in healthy persons varies between 26 and 45 hours. The main route of elimination is renal excretion of digoxin, which is closely correlated with the glomerular filtration rate. In addition, some tubular secretion and perhaps tubular reabsorption occurs. Nearly all of the digoxin in the urine is excreted unchanged, with a small part as active metabolites. The clinical significance of dihydrodigoxin as a metabolite remains to be resolved. About 25 to 28% of digoxin is eliminated by nonrenal routes. Biliary excretion may rise up to 30% of a given dose, but the enterohepatic cycle seems to be of minor importance. The pharmacodynamic effects of digoxin, including toxic symptoms, are correlated with the uptake of digoxin in the heart after a single dose and with the steady state serum digoxin concentration during maintenance therapy. Impaired kidney function is the most important condition with an influence on the pharmacokinetics of digoxin. In addition to the renal clearance of creatinine, the biovailability of the digoxin formulation used, the volume of distribution, the amount of extrarenal clearance, body weight and serum albumin concentration, are other factors which may modify the serum level of digoxin. Certain drug interactions may also occur during the absorptive phase. Exact prediction of serum digoxin concentrations by various dosage calculations has not succeeded. Since many factors may influence the sensitivity of the myocardium to digoxin, measurement of serum digoxin levels in only one, but a useful criterion, when making clinical decisions about adjustment of digoxin dosage.

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Serial serum digoxin concentrations and quantitative electrocardiographic changes

Cited by 18 publications

References 2 publications

Effects of cardiac glycosides on 24-h ambulatory blood pressure in healthy volunteers and patients with heart failure

Effects of cardiac glycosides on 24-h ambulatory blood pressure in healthy volunteers and patients with heart failure

Effects of digoxin and digitoxin on circadian blood pressure profile in healthy volunteers

Clinical Pharmacokinetics of Digoxin

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