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Digoxin is a cardiac glycoside extracted from the foxglove plant, digitalis. It is widely used in the treatment of various heart conditions, namely atrial fibrillation, atrial flutter and congestive heart failure that cannot be controlled by other medication. more...

Dimethyl sulfoxide
Docusate sodium
Dornase alfa


The main effects of digoxin are on the heart, its extracardiac effects are responsible for most of the side effects, i.e. nausea, vomiting, diarrhea and confusion.

Its main cardiac effects are:

  • A decrease of conduction of electrical impulses through the AV node, making it a commonly used drug in controlling the heart rate during atrial fibrillation or atrial flutter.
  • An increase of force of contraction via inhibition of the Na+/K+ ATPase pump (see below).

Mechanism of action

Digoxin binds to a site on the extracellular aspect of the α-subunit of the Na+/K+ ATPase pump in the membranes of heart cells (myocytes). This causes an increase in the level of sodium ions in the myocytes, which then leads to a rise in the level of calcium ions. The proposed mechanism is the following: inhibition of the Na+/K+ pump leads to increased Na+ levels, which in turn slows down the extrusion of Ca2+ via the Na+/Ca2+ exchange pump. Increased amounts of Ca2+ are then stored in the sarcoplasmic reticulum and released by each action potential, which is unchanged by digoxin. This is a different mechanism from that of catecholamines.

Digoxin also increases vagal activity via its central action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node. This is important for its clinical use in different arrhythmias (see below).

Clinical use

Today, the most common indications for digoxin are probably atrial fibrillation and atrial flutter with rapid ventricular response. High ventricular rate leads to insufficient diastolic filling time. By slowing down the conduction in the AV node and increasing its refractory period, digoxin can reduce the ventricular rate. The arrhythmia itself is not affected, but the pumping function of the heart improves owing to improved filling.

The use of digoxin in congestive heart failure during sinus rhythm is controversial. In theory the increased force of contraction should lead to improved pumping function of the heart, but its effect on prognosis is disputable and digoxin is no longer the first choice for congestive heart failure. However, it can still be useful in patients who remain symptomatic despite proper diuretic and ACE inhibitor treatment.

Digoxin is usually given by mouth, but can also be given by IV injection in urgent situations (the IV injection should be slow, heart rhythm should be monitored). The half life is about 36 hours, digoxin is given once daily, usually in 125μg or 250μg dosing. In patients with decreased kidney function the half life is considerably longer, calling for a reduction in dosing or a switch to a different glycoside (digitoxin).


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Update on Digoxin Therapy in Congestive Heart Failure
From American Family Physician, 7/15/00 by Showkat A. Haji

Congestive heart failure is a progressive disease with significant morbidity and mortality. Despite advances in the prevention and treatment of cardiovascular diseases, the incidence and prevalence of congestive heart failure have increased in recent years. Contributing factors include increased survival in patients with coronary artery disease (especially myocardial infarction), an aging population and significant advances in the control of other potentially lethal diseases. New and existing agents, including angiotensin-converting enzyme inhibitors, beta blockers and, more recently, spironolactone, are being used increasingly to prolong life in patients with heart failure. Although digoxin has been used to treat heart failure for more than 200 years, its role in patients with congestive heart failure and sinus rhythm is still debatable. Over the past decade, digoxin has received renewed attention because of recognition of its neurohormonal effect and the successful use of lower dosages. In recent trials, digoxin has been shown to reduce morbidity associated with congestive heart failure but to have no demonstrable effect on survival. The goal of digoxin therapy in patients with congestive heart failure is to improve quality of life by reducing symptoms and preventing hospitalizations. (Am Fam Physician 2000;62:409-16.)

Congestive heart failure has been recognized as a syndrome of anatomic, functional and biologic alterations that interact together in a complex manner over a prolonged period. Initially, this syndrome was viewed predominantly as a problem of salt and water retention caused by abnormalities of renal blood flow. Over time, however, physicians began to recognize that congestive heart failure was associated with reduced cardiac output and excessive peripheral vasoconstriction.(1) Recognition of this association provided the rationale for the use of inotropic agents and intravenously administered vasodilators to improve cardiac output.

Despite these therapeutic developments, it became apparent that at some point, congestive heart failure would progress independent of the patient's hemodynamic status. Thus, the neurohormonal model evolved.(1) According to this model, heart failure progresses as a result of overexpression of biologically active molecules that exert toxic effects on the heart and circulation.(2,3)


Following an initial index event that results in a decline of ventricular contractility, most patients remain asymptomatic or minimally symptomatic for some time. The initial event may be abrupt, such as a myocardial infarction, or it may have a gradual onset, as in the case of hypertension or volume overload. The index event may also be a hereditary condition such as a genetic cardiomyopathy.

Many compensatory mechanisms, including the sympathetic nervous system and salt- and water-retaining systems, become activated in the setting of a depressed cardiac output.(4,5) The compensatory systems can maintain left ventricular function for days to months. However, when patients become overtly symptomatic, they begin to experience a striking increase in morbidity and mortality. The transition to symptomatic heart failure is accompanied by further activation of the neurohormonal system, including the sympathetic nervous system and a series of adaptive changes in the myocardium, collectively referred to as "left ventricular remodeling."(6)

Epidemiology of Congestive Heart Failure and Evolution of Treatment

Congestive heart failure continues to be a major health problem. Despite significant advances in the prevention and treatment of cardiovascular diseases, the incidence and prevalence of congestive heart failure have been increasing in recent years. Contributing factors include increased survival in patients with coronary artery disease (especially myocardial infarction), an aging population and significant advances in the control of other potentially lethal diseases.

In the past two decades, the treatment of congestive heart failure has evolved and is now directed at the attenuation of neurohormonal activation using angiotensin-converting enzyme (ACE) inhibitors, beta blockers(7) and, more recently, spironolactone (Aldactone).(8) Because neurohormonal antagonists have been shown to prolong survival in patients with congestive heart failure,(8-11) the role of digoxin (Lanoxin) has become less certain.

Controversy over an Old Drug

In 1785, Withering published an account of digitalis (dried leaves of the purple foxglove) and some of its medical uses.(12) Although digoxin continues to be viewed as beneficial in patients with heart failure and atrial fibrillation, its role in patients with heart failure and sinus rhythm has been increasingly challenged. Mackenzie and Christian, two eminent clinicians and coeditors of Oxford Medicine, debated this issue in 1922. Mackenzie advocated the use of digitalis only in heart failure with associated atrial arrhythmias, whereas Christian argued that digitalis was effective irrespective of an irregular pulse. In 1938, Cattell and Gold first showed a direct inotropic effect of digitalis on cardiac muscle.

For many more years, digitalis continued to be an important part of heart failure management. The detrimental aspects of digoxin therapy were not considered important until excess mortality was reported in survivors of myocardial infarction who received digitalis.(13,14) Uncontrolled observations that the withdrawal of digoxin produced no ill effects also raised concerns about the efficacy of the drug.(15,16)

Trials of Digoxin in Heart Failure

The role of digitalis in the treatment of heart failure has continued to be controversial and has been studied in clinical trials over the years. This role was recently addressed by the Digitalis Investigation Group (DIG)(17) in a large multicenter trial sponsored by the National Heart, Lung, and Blood Institute and the Department of Veterans Affairs. The trial involved patients in 302 centers in the United States and Canada.

Over the past decade, randomized double-blind, placebo-controlled trials and other new findings, such as the successful use of lower dosages, have revived interest in the use of digoxin in the treatment of heart failure. One study(18) demonstrated that compared with placebo, digoxin improved signs and lessened symptoms in patients with heart failure who had normal sinus rhythm and were receiving maintenance diuretic therapy. The benefits of digoxin were greatest in patients with more severe heart failure, a third heart sound gallop, left ventricular enlargement and a depressed left ventricular ejection fraction.

In 1993, trials conducted in the Prospective Randomized Study of Ventricular Failure and Efficacy of Digoxin (PROVED)(19) and the Randomized Assessment of Digoxin on Inhibitors of Angiotensin-Converting-Enzyme (RADIANCE)(20) study examined the effects of withdrawal of digoxin in patients with stable, mild to moderate heart failure (New York Heart Association [NYHA] functional classes II and III) and left ventricular systolic dysfunction (left ventricular ejection fraction of 35 percent or less). Both trials showed that digoxin prevented clinical deterioration and hospitalizations, and improved exercise tolerance and left ventricular function in patients, but had no survival benefit in patients who had congestive heart failure (Table 1).(19,20)

In the DIG trial,(17) patients with heart failure and sinus rhythm were randomized to receive digoxin (N = 3,397) or placebo (N = 3,403). The investigators were strongly encouraged to also give ACE inhibitors to patients in the trial. No difference was found in all-cause mortality between patients who were treated with digoxin and those who were given placebo. However, the patients who received digoxin had significantly fewer hospital admissions when the drug was given in addition to diuretics and ACE inhibitors (Table 2).(17) Compared with the placebo group, the digoxin-treated group had 270 fewer patients who required hospital admission for worsening heart failure (P [less than] 0.001). Furthermore, there were 626 fewer hospital admissions in patients with worsening heart failure as the primary diagnosis (1,927 in the digoxin group versus 2,553 in the placebo group). The trial showed little evidence of risks related to digoxin therapy.

Digoxin-Induced Neurohormonal Modulation

In the past, digoxin was considered to be solely a positive inotropic agent. In patients with heart failure, digoxin exerts its positive inotropic effect by inhibiting sodium-potassium adenosine triphosphatase (ATPase). Inhibition of this enzyme in cardiac cells results in an increase in the contractile state of the heart. In recent years, it has been shown that digoxin exerts a positive inotropic effect at higher dosages (0.25 mg or more per day); however, at lower dosages (less than 0.25 mg per day), this drug exerts a mainly neurohormonal effect and has little inotropic activity.(21)

The neurohormonal effect of digoxin was first demonstrated in a small study in 1987.(22) The study findings showed that digoxin reduced plasma norepinephrine levels; these results were validated in other studies.(23,24) The explanation for this effect was that digoxin improves impaired baroreceptor reflexes in heart failure.(25) Digoxin may also lower plasma renin levels,(24) either because of a direct renal effect or secondary to inhibition of sympathetic activity. By inhibiting sodium-potassium ATPase in the kidney, digoxin decreases renal tubular reabsorption of sodium, thereby increasing delivery of sodium to the distal tubules and suppressing renin secretion.

Digoxin in Patients with Mild to Moderate Heart Failure

In the DIG trial,(17) digoxin therapy was most beneficial in patients with ejection fractions of 25 percent or lower, patients with enlarged hearts (cardiothoracic ratio of greater than 0.55) and patients in NYHA functional class III or IV. The findings of the DIG trial also indicated that digoxin was clinically beneficial in subgroups of patients with less severe forms of heart failure.

Using direct clinical measures of heart failure, the PROVED(19) and the RADIANCE(20) trials showed definite clinical improvement in patients who were treated with digoxin, even patients with mild heart failure.

Based on the study findings, digoxin therapy may be effective in patients with mild or moderate heart failure,(26) although the magnitude of the effect may be quite modest.

Digoxin in Patients with Preserved Left Ventricular Systolic Function

Much has been learned about the effective treatment of patients who have congestive heart failure associated with left ventricular systolic dysfunction. In contrast, little is known about how best to treat patients with preserved left ventricular systolic function.

As many as 30 percent of patients with congestive heart failure have a normal or nearly normal left ventricular ejection fraction. In these patients, congestive heart failure is often described as "left ventricular diastolic dysfunction." Left ventricular diastolic dysfunction is considered to be a diagnosis of exclusion (or assumption) in patients with congestive heart failure and preserved left ventricular systolic function.

Diagnostic tools such as radionuclide angiography and Doppler echocardiography have made it possible to identify patients who have normal or nearly normal left ventricular systolic function but abnormal left ventricular filling parameters. The majority of patients with congestive heart failure who have only diastolic dysfunction have no identified diagnosis. Most of these patients are elderly or have a history of hypertension. Some patients have coronary artery disease without extensive scar tissue. Such patients also commonly have diabetes mellitus.


In patients with diastolic dysfunction, appropriate measures include the diagnosis and treatment of myocardial ischemia (if present) and the aggressive treatment of hypertension (if needed). Digitalis therapy has been considered inappropriate in these patients. In some patients, treatment with diuretics and nitrates could reduce pulmonary congestion.

In the DIG trial,(17) a subgroup of nearly 1,000 patients with a left ventricular ejection fraction of 45 percent or greater experienced a reduction in congestive heart failure end points similar to patients with a left ventricular ejection fraction of 25 to 45 percent. One group of investigators(27) suggested that this effect may be the result of digoxin's ability to reduce neurohormonal activities. However, they concluded that information about the effect of digoxin in patients with congestive heart failure and preserved left ventricular systolic function is limited and does not warrant routine use of the drug in this setting until the results of more studies are available.

At present, the consensus is that digoxin therapy is probably inappropriate in patients with preserved left ventricular systolic function. In addition, digoxin therapy may not be useful in patients with congestive heart failure and a high cardiac output syndrome such as anemia or thyrotoxicosis.

Adverse Effects of Digoxin

Adverse reactions to digoxin are usually dose dependent and occur at dosages higher than those needed to achieve a therapeutic effect. The actual incidence of digoxin toxicity may be lower than is historically reported.(28) Adverse reactions are less common when digoxin is used in the recommended dosage range and careful attention is given to concurrent medications (Table 3) and medical conditions.

The principal manifestations of digoxin toxicity include cardiac arrhythmias (ectopic and reentrant cardiac rhythms and heart block), gastrointestinal tract symptoms (anorexia, nausea, vomiting and diarrhea) and neurologic symptoms (visual disturbances, headache, weakness, dizziness and confusion). Most adult patients with clinical toxicity have serum digoxin levels greater than 2 ng per mL (2.6 nmol per L). Conditions such as hypokalemia, hypomagnesemia or hypothyroidism may predispose patients to have adverse reactions even at lower serum digoxin concentrations.(29)

Dosages of Digoxin

Although some investigators advocate the use of serum levels to guide digoxin dosing, little evidence supports this approach.(30) The serum level of digoxin may be used to assist in evaluating a patient for toxicity, but not to determine the efficacy of the drug.

When digoxin was considered to be mainly an inotrope, higher dosages (greater than 0.25 mg per day) were generally used, and the incidence of toxicity was much higher. In the PROVED and RADIANCE trials, the mean digoxin dosage was 0.375 mg per day. However, a study of a subset of patients in the RADIANCE trial(31) showed that increasing the digoxin dosage from a mean of 0.2 mg per day to 0.39 mg per day did not significantly improve heart failure symptoms, exercise time or serum norepinephrine levels.

When lower dosages are used, the side effects of digoxin, especially ventricular arrhythmias, decrease. Use of lower dosages is particularly important in the elderly, because digitalis toxicity may be difficult to recognize in this patient population.(32) It is generally agreed that digoxin should be given in a dosage of 0.125 to 0.25 mg per day. Dosages higher than 0.25 mg per day are probably unwarranted.

Renal function plays a major role in the pharmacokinetics of digoxin and is an important factor in determining the dosage. Medications such as quinidine, amiodarone (Cordarone) and verapamil (Calan) can increase the serum digoxin concentration. Thus, safe and effective dosing requires recognition of concomitant disease states and medications that could change digoxin pharmacokinetics, along with a recognition of digoxin toxicity.(33)

Digoxin in Acute Myocardial Infarction

Digoxin has been reported to have detrimental effects following myocardial infarction.(13,14,34) The drug may increase myocardial oxygen consumption(35) by augmenting contractility and inducing peripheral or coronary vasoconstriction.(36) It may also provoke ventricular arrhythmias and increase infarct size.(37)

Because myocardial stunning may be present for weeks after an infarction, digoxin therapy should be avoided in the acute phase after myocardial infarction, unless its use is strongly indicated. For example, digoxin may be indicated to control the ventricular rate in patients with atrial fibrillation when rate control cannot be achieved with beta blockers or calcium channel blockers, or when the use of these medications is contraindicated.

Digoxin and Other Medications for Congestive Heart Failure

ACE inhibitors, beta blockers and spironolactone have been shown to improve survival in patients with heart failure. Consequently, the role of digoxin in the treatment of heart failure remains secondary (Table 4), despite renewed interest in its use. Digoxin has been shown to reduce the morbidity associated with congestive heart failure but to have no demonstrable effect on survival.

In the absence of a survival benefit, the goal of digoxin therapy is to improve quality of life by reducing symptoms and preventing hospitalizations. Digoxin should be used routinely, in conjunction with diuretics, ACE inhibitors, beta blockers and spironolactone, in all patients with severe congestive heart failure and reduced systolic function. It also should be added to the therapy of patients with mild to moderate congestive heart failure if they have not responded adequately to an ACE inhibitor or a beta blocker.(30,38) If digoxin acts primarily by reducing neurohormonal activation, its value is in question in patients with heart failure who are already being treated with beta blockers.


(1.) Packer M. How should physicians view heart failure? The philosophical and physiological evolution of three conceptual models of the disease. Am J Cardiol 1993;71:3C-11C.

(2.) Bristow MR. The adrenergic nervous system in heart failure. [Editorial] N Engl J Med 1984;311:850-1.

(3.) Tan LB, Jalil JE, Pick R, Janicki JS, Weber KT. Cardiac myocyte necrosis induced by angiotensin II. Circ Res 1991;69:1185-95.

(4.) Eisenhofer G, Friberg P, Rundqvist B, Quyyumi AA, Lambert G, Kaye DM, et al. Cardiac sympathetic nerve function in congestive heart failure. Circulation 1996;93:1667-76.

(5.) Eichhorn EJ, Bristow MR. Medical therapy can improve the biological properties of the chronically failing heart. A new era in the treatment of heart failure. Circulation 1997;94:2285-96.

(6.) Mann DL. Mechanisms and models in heart failure. A combinatorial approach. Circulation 1999;100:999-1008.

(7.) Rich MW, Brooks K, Luther P. Temporal trends in pharmacotherapy for congestive heart failure at an academic medical center. Am Heart J 1998;135:367-72.

(8.) Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999;341:709-17.

(9.) Effects of enalapril on mortality in severe congestive heart failure. Results of the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). The CONSENSUS Trial Study Group. N Engl J Med 1987;316:1429-35.

(10.) Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. The SOLVD Investigators. N Engl J Med 1991;325:293-302.

(11.) Packer M, Bristow MR, Cohn JN, Colucci WS, Fowler MB, Gilbert EM, et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart Failure Study Group. N Engl J Med 1996;334:1349-55.

(12.) Withering W. An account of the foxglove and some of its medical uses, with practical remarks on dropsy and other diseases. In: Willius FA, Keys TE, eds. Classics of cardiology: a collection of classic works on the heart and circulation with comprehensive biographic accounts of the authors. Malabar, Fla.: Krieger, 1983.

(13.) Ryan TJ, Bailey KR, McCabe CH, Luk S, Fisher LD, Mock MB, et al. The effects of digitalis on survival in high-risk patients with coronary artery disease. The Coronary Artery Surgery Study (CASS). Circulation 1983;67:735-42.

(14.) Bigger JT, Fleiss JL, Rolnitzky LM, Merab JP, Ferrick KJ. Effect of digitalis treatment on survival after acute myocardial infarction. Am J Cardiol 1985;55: 623-30.

(15.) Dall JL. Maintenance digoxin in elderly patients. Br Med J 1970;2:705-6.

(16.) Hull SM, Mackintosh A. Discontinuation of maintenance digoxin therapy in general practice. Lancet 1977;2(8047):1054-5.

(17.) The effect of digoxin on mortality and morbidity in patients with heart failure. The Digitalis Investigation Group. N Engl J Med 1997;336:525-33.

(18.) Lee DC, Johnson RA, Bingham GB, Leahy M, Dinsmore RE, Goroll AH, et al. Heart failure in outpatients: a randomized trial of digoxin versus placebo. N Engl J Med 1982;306:699-705.

(19.) Uretsky BF, Young JB, Shahidi FE, Yellen LG, Harrison MC, Jolly MK. Randomized study assessing the effect of digoxin withdrawal in patients with mild to moderate chronic congestive heart failure: results of the PROVED trial. PROVED Investigative Group. J Am Coll Cardiol 1993;22:955-62.

(20.) Packer M, Gheorghiade M, Young JB, Costantini PJ, Adams KF, Cody RJ, et al. Withdrawal of digoxin from patients with chronic heart failure treated with angiotensin-converting-enzyme inhibitors. RADIANCE Study. N Engl J Med 1993;329:1-7.

(21.) Packer M. The development of positive inotropic agents for chronic heart failure: how have we gone astray? J Am Coll Cardiol 1993;22:119A-26A.

(22.) Alicandri C, Fariello R, Boni E, Zaninelli A, Castellano M, Beschi M, et al. Captopril versus digoxin in mild-moderate chronic heart failure: a crossover study. J Cardiovasc Pharmacol 1987;9(suppl 2):S61-7.

(23.) Gheorghiade M, Hall V, Lakier JB, Goldstein S. Comparative hemodynamic and neurohormonal effects of intravenous captopril and digoxin and their combinations in patients with severe heart failure. J Am Coll Cardiol 1989;13:134-42.

(24.) van Veldhuisen DJ, Man in't Veld AJ, Dunselman PH, Lok DJ, Dohmen HJ, Poortermans JC, et al. Double-blind placebo-controlled study of ibopamine and digoxin in patients with mild to moderate heart failure: results of the Dutch Ibopamine Multicenter Trial (DIMT). J Am Coll Cardiol 1993; 22:1564-73.

(25.) Watanabe AM. Digitalis and the autonomic nervous system. J Am Coll Cardiol 1985;5:35A-42A.

(26.) Soler-Soler J, Permanyer-Miralda G. Should we still prescribe digoxin in mild-to-moderate heart failure? Is quality of life the issue rather than quantity? Eur Heart J 1998;19(suppl P):P26-31.

(27.) Massie BM, Abdalla I. Heart failure in patients with preserved left ventricular systolic function: do digitalis glycosides have a role? Prog Cardiovasc Dis 1998;40:357-69.

(28.) Williamson KM, Thrasher KA, Fulton KB, LaPointe NM, Dunham DG, Cooper AA, et al. Digoxin toxicity: an evaluation in current clinical practice. Arch Intern Med 1998;158:2444-9.

(29.) Steiner JF, Robbins LJ, Hammermeister KE, Roth SC, Hammond WS. Incidence of digoxin toxicity in outpatients. West J Med 1994;161:474-8.

(30.) Packer M, Cohn JN, on behalf of the Advisory Council to Improve Outcomes Nationwide in Heart Failure. Consensus recommendations for the management of heart failure. Am J Cardiol 1999;83: 1A-38A.

(31.) Gheorghiade M, Hall VB, Jacobsen G, Alam M, Rosman H, Goldstein S. Effects of increasing maintenance dose of digoxin on left ventricular function and neurohormones in patients with chronic heart failure treated with diuretics and angiotensin-converting enzyme inhibitors. Circulation 1995;92: 1801-7.

(32.) Warren JL, McBean AM, Hass SL, Babish JD. Hospitalizations with adverse events caused by digitalis therapy among elderly Medicare beneficiaries. Arch Intern Med 1994;154:1482-7.

(33.) Cauffield JS, Gums JG, Grauer K. The serum digoxin concentration: ten questions to ask. Am Fam Physician 1997;56:495-503,509-10.

(34.) Kober L, Torp-Pedersen C, Gadsboll N, Hildebrandt P, Hoilund-Carlsen PF. Is digoxin an independent risk factor for long-term mortality after acute myocardial infarction? Eur Heart J 1994; 15:382-8.

(35.) Covell JW, Braunwald E, Ross J, Sonnenblick EH. Studies on digitalis. XVI. Effects on myocardial oxygen consumption. J Clin Invest 1996;45:1535-42.

(36.) Gross GJ, Warltier DC, Hardman HF, Somani P. The effect of ouabain on nutritional circulation and regional myocardial blood flow. Am Heart J 1977;93:487-95.

(37.) Lynch JJ, Simpson PJ, Gallagher KP, McClanahan TB, Lee KA, Lucchesi BR. Increase in experimental infarct size with digoxin in a canine model of myocardial ischemia-reperfusion injury. Am Heart J 1988;115:1171-82.

(38.) Guidelines for the evaluation and management of heart failure. Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Evaluation and Management of Heart Failure). J Am Coll Cardiol 1995;26:1376-98.

This article is one in a series developed in collaboration with the American Heart Association. Guest editor of the series is Rodman D. Starke, M.D., Senior Vice President of Science and Medicine, American Heart Association, Dallas.

The Authors

SHOWKAT A. HAJI, M.D., is research associate in the cardiology section at East Carolina University School of Medicine, Greenville, N.C., and emergency department physician and hospitalist at Pungo District Hospital, Belhaven, N.C. Dr. Haji received his medical degree from Government Medical College, Kashmir, India, and completed a residency in internal medicine at Nassau County Medical Center, East Meadow, N.Y.

ASSAD MOVAHED, M.D., is director of nuclear cardiology and professor of medicine and radiology at East Carolina University School of Medicine. Dr. Movahed graduated from Jondi Shapour Medical School, Ahwaz, Iran, and completed a residency in internal medicine at Wayne State University School of Medicine, Detroit. Dr. Movahed also completed a fellowship in cardiology at Cleveland Metropolitan General Hospital and a fellowship in nuclear medicine at Johns Hopkins Medical Center, Baltimore.

Address correspondence to Assad Movahed, M.D., Section of Cardiology, Department of Medicine, East Carolina University School of Medicine, Greenville, NC 27858. Reprints are not available from the authors.

COPYRIGHT 2000 American Academy of Family Physicians
COPYRIGHT 2000 Gale Group

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