When was digoxin approved by the fda

Ouabain-the insulin of the heart. Rahimtoola, S. The use of digitalis in heart failure. Kang, Y. Disaster Med. Public Health Prep. Zou, X. Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to nCoV infection.

Akhmerov, A. COVID and the heart. Cao, X. COVID immunopathology and its implications for therapy. Ong, E. Cell Host Microbe 27 , 1—4. Qin, C. Shi, Y. Immunopathological characteristics of coronavirus disease cases in Guangzhou, China. Xu, Z. Lancet Resp. Harcourt, J. Backer, J. Incubation period of novel coronavirus nCoV infections among travellers from Wuhan, China, 20—28 January Eurosurveillance 25 , Zheng, Y.

COVID and the cardiovascular system. Digitoxin inhibits the growth of cancer cell lines at concentrations commonly found in cardiac patients. Goldberger, Z. Therapeutic ranges of serum digoxin concentrations in patients with heart failure.

Prescribing Information Lanoxin Digoxin. Burkard, C. ATP1A1-mediated Src signaling inhibits coronavirus entry into host cells. Pollard, H. Kim, J. Osong Public Health Res. Download references. Division of Infectious Disease, Seoul St. You can also search for this author in PubMed Google Scholar. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Reprints and Permissions. Cho, J. Sci Rep 10, Download citation. Received : 10 June Accepted : 08 September Published : 01 October Anyone you share the following link with will be able to read this content:. May decrease serum digoxin concentration, especially in patients with renal dysfunction, by increasing the non-renal clearance of digoxin.

Thyroid administration to a digitalized, hypothyroid patient may increase the dose requirement of digoxin. Concomitant use of digoxin and sympathomimetics increases the risk of cardiac arrhythmias.

Succinylcholine may cause a sudden extrusion of potassium from muscle cells, and may thereby cause arrhythmias in digitalized patients. Use with digoxin may be useful in combination to control atrial fibrillation, their additive effects on AV node conduction can result in advanced or complete heart block.

Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia. Therefore, increased monitoring of digoxin is recommended when initiating, adjusting, or discontinuing carvedilol.

Spironolactone and DLIS are much more extensively protein-bound than digoxin. It is also not known whether digoxin can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. Digoxin should be given to a pregnant woman only if clearly needed. However, the estimated exposure of a nursing infant to digoxin via breastfeeding will be far below the usual infant maintenance dose. Therefore, this amount should have no pharmacologic effect upon the infant.

Nevertheless, caution should be exercised when digoxin is administered to a nursing woman. Newborn infants display considerable variability in their tolerance to digoxin. Premature and immature infants are particularly sensitive to the effects of digoxin, and the dosage of the drug must not only be reduced but must be individualized according to their degree of maturity.

Digitalis glycosides can cause poisoning in children due to accidental ingestion. The majority of clinical experience gained with digoxin has been in the elderly population. This experience has not identified differences in response or adverse effects between the elderly and younger patients. However, this drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, which should be based on renal function, and it may be useful to monitor renal function.

This difference is not likely to be clinically important. The impact of race differences on digoxin pharmacokinetics have not been formally studied. Because digoxin is primarily eliminated as unchanged drug via the kidney and because there are no important differences in creatinine clearance among races, pharmacokinetic differences due to race are not expected.

Since the clearance of digoxin correlates with creatinine clearance , patients with renal impairment generally demonstrate prolonged digoxin elimination half-lives and greater exposures to digoxin. Therefore, titrate carefully in these patients based on clinical response and based on monitoring of serum digoxin concentrations, as appropriate. In a small study, plasma digoxin concentration profiles in patients with acute hepatitis generally fell within the range of profiles in a group of healthy subjects.

No dosage adjustments are recommended for patients with hepatic impairment; however, serum digoxin concentrations should be used, as appropriate, to help guide dosing in these patients. Use digoxin solution to obtain the appropriate dose in infants, young pediatric patients, or patients with very low body weight. When switching from intravenous to oral digoxin formulations, make allowances for differences in bioavailability when calculating maintenance dosages. Monitor for signs and symptoms of digoxin toxicity and clinical response.

Adjust dose based on toxicity, efficacy, and blood levels. Serum digoxin levels less than 0. Interpret the serum digoxin concentration in the overall clinical context, and do not use an isolated measurement of serum digoxin concentration as the basis for increasing or decreasing the digoxin dose.

Serum digoxin concentrations may be falsely elevated by endogenous digoxin-like substances [see Drug Interactions 7. If the assay is sensitive to these substances, consider obtaining a baseline digoxin level before starting digoxin and correct post-treatment values by the reported baseline level.

Obtain serum digoxin concentrations just before the next scheduled digoxin dose or at least 6 hours after the last dose. However, there will be only minor differences in digoxin concentrations using twice daily dosing whether sampling is done at 8 or 12 hours after a dose. The cardiologic consequences of these direct and indirect effects are an increase in the force and velocity of myocardial systolic contraction positive inotropic action , a slowing of the heart rate negative chronotropic effect , decreased conduction velocity through the AV node, and a decrease in the degree of activation of the sympathetic nervous system and renin-angiotensin system neurohormonal deactivating effect.

Digoxin is one of the cardiac or digitalis glycosides , a closely related group of drugs having in common specific effects on the myocardium. These drugs are found in a number of plants. Digoxin is extracted from the leaves of Digitalis lanata.

Its molecular formula is C41H64O14, its molecular weight is Digoxin injection USP is a sterile solution of digoxin for intravenous or intramuscular injection. Each mL contains: digoxin 0. Dilution is not required. The times to onset of pharmacologic effect and to peak effect of preparations of digoxin are shown in the table below. Hemodynamic Effects: Short- and long-term therapy with the drug increases cardiac output and lowers pulmonary artery pressure, pulmonary capillary wedge pressure , and systemic vascular resistance in patients with heart failure.

These hemodynamic effects are accompanied by an increase in the left ventricular ejection fraction and a decrease in end-systolic and end-diastolic dimensions. ECG Changes: The use of therapeutic doses of digoxin may cause prolongation of the PR interval and depression of the ST segment on the electrocardiogram. Digoxin may produce false positive ST-T changes on the electrocardiogram during exercise testing. These electrophysiologic effects are not indicative of toxicity. Digoxin does not significantly reduce heart rate during exercise.

Distribution: Following drug administration, a 6 to 8 hour tissue distribution phase is observed. This is followed by a much more gradual decline in the serum concentration of the drug, which is dependent on the elimination of digoxin from the body.

Other side effects include gynecomastia, thrombocytopenia, and a maculopapular rash. Fortunately these side effects are infrequent but do occur more often when the digoxin levels rise, particularly over 2. Many of these side effects improve simply by stopping or reducing the dose of digoxin. The speed with which they dissipate relates to renal function and serum concentration of the drug. Life-threatening complications of digoxin can occur with massive overdoses or extremely high levels, particularly in the setting of acute renal failure.

Ventricular fibrillation or tachycardia can be dramatic, producing bizarre looking QRS complexes and electrocardiogram. Hyperkalemia can be seen and is a result of the drug effects on the sodium-potassium cell wall pump described above. Patients with massive digoxin ingestion suicide attempt as an example should receive large doses of activated charcoal to prevent absorption. When hemodynamic compromise is evident, usually in the setting of problematic ventricular or supraventricular arrhythmias, and remembering that digoxin is not dialyzable, administration of Digibindshould be considered.

Digoxin immune Fab binds to digoxin, making the molecule incapable of activating receptor sites on the myocyte cell wall. The drug-immune complex accumulates in the blood stream and is excreted by the kidney. Watching the rapid resolution of the malignant arrhythmias induced by digoxin toxicity during Digibind infusion can be an amazing experience. It also is a way to quickly confirm that a problematic arrhythmia is caused by digoxin. Drug interactions with digoxin are important to understand.

Nonpotassium sparring diuretics can cause hypokalemia and hypomagnesemia, which with digoxin increases arrhythmia risk. Intravenous calcium administration can also increase arrhythmia risk. Reducing digoxin clearance and decreasing the volume of distribution, which will increase serum digoxin levels, is amiodarone, quinidine, verapamil, propafenone, itraconazole, alprazolam, and spironolactone.

Erythromycin, clarithromycin, and tetracycline increase digoxin absorption by inactivating intestinal bacterial metabolism. Antacids, bran, cholestyramine, kaolin-pectin, and metaclopromide decrease digoxin absorbtion. Rifampin increases renal excretion of digoxin. Sympathomimetics increase myocyte automaticity and increase the risk of arrhythmias with digoxin. Beta adrenergic blockers, nondihydropyridine calcium channel blockers, flecainide, disopyramide, and bepridil decrease sinoatrial or AV nodal conduction and with digoxin increase the risk of sinoatrial and AV block.

ACE inhibitors, angiotensin receptor blockers, and nonsteroidal antiinflammatory agents can decrease renal function, which could diminish renal clearance and increase digoxin levels. Classics of Cardiology. This remarkable "case series" is fun to read. It was written by a master clinician and botanist in the late 18th century.

It is a "case series" filled with anecdote and insight. Required reading for anyone interested in cardiovascular therapeutics and digoxin in particular. Int J Cardiol. A very nice contribution lamenting the fact that digoxin use has diminished dramatically over the last decade, whereas publications about this drug were common a decade ago, few studies of the agent, clinical trials, or use descriptions are currently available.

This is the most recent one, with few appearing in the last 5 to 7 years, and thoughtful. An older but excellent review of digoxin. Nothing has changed since Written by master cardiovascular clinicians. Young, JB. J Am Coll Cardiol. An editorial written in response to a reanalysis of the DIG trial database, which demonstrated that digoxin was safe and quite effective at lower serum concentrations.

Packer, M. N Engl J Med. A very well written and curmudgeonly editorial in response to the DIG trial conclusion and publication. Classic, large scale, multicenter randomized clinical trial demonstrating the important contribution digoxin makes to heart failure patients in normal sinus rhythm. The database has been plumbed repeatedly over the last decade and, generally, no matter the technique of analysis or question asked, digoxin comes out in a positive light.

First of the digoxin clinical trial troika that led to FDA approval of digoxin for heart failure [though it had been on the "market" for decades]. It is considered adjunctive therapy, rather than first-line therapy. Withering W. Birmingham, England: M.

Swinney; Pharmacotherapy of congestive heart failure. Digoxin: clinical highlights: a review of digoxin and its use in contemporary medicine. Crit Pathw Cardiol. The short-term effects of digoxin in patients with right ventricular dysfunction from pulmonary hypertension.

A controlled trial of digoxin in congestive heart failure. Am J Cardiol. Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med. Double-blind placebo-controlled trial of digoxin in symptomatic paroxysmal atrial fibrillation. J Am Coll Cardiol.

Recommendations on the management of pulmonary hypertension in clinical practice. Updated evidence-based treatment algorithm in pulmonary arterial hypertension. Treatment of pulmonary arterial hypertension. Incidence of digoxin toxicity in outpatients. West J Med. Featured Issue Featured Supplements.

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