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Digoxin

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...

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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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Lower serum digoxin levels may improve mortality - Tips from Other Journals - Author Abstract
From American Family Physician, 8/1/03 by Caroline Wellbery

Little is known about the efficacy and risk of different serum digoxin concentrations (SDC). The Digitalis Investigation Group (DIG) trial, a randomized, placebo-controlled study, has concluded that digoxin therapy had no effect on mortality, but that it modestly reduced hospitalizations caused by worsening heart failure. Rathore and colleagues conducted a post-hoc evaluation of this trial to determine the relationship between SDC, mortality risk, and risk of hospitalization in patients with heart failure and left ventricular dysfunction.

Study subjects in the DIG trial included patients with stable heart failure and a left ventricular ejection fraction of 45 percent or less. Rathore and colleagues restricted their analysis to men who were randomly assigned to digoxin or placebo and who had a valid SDC level measured at least six hours after their previous digoxin dose. The study sample consisted of 2,611 subjects assigned to placebo and 1,171 assigned to digoxin (N = 3,782). Patients in the digoxin group were divided further into three groups: 0.5 to 0.8 ng per mL, 0.9 to 1.1 ng per mL, and 1.2 ng per mL and higher.

The authors used the DIG trial's primary end point of all-cause mortality, and secondary outcomes of death caused by cardiovascular causes and heart failure, and all-cause hospitalization and hospitalization for suspected digoxin toxicity. Of the 1,171 men with SDC levels assessed at one month, 572 (49 percent) had an SDC of 0.5 to 0.8 ng per mL, 322 (27 percent) had an SDC of 0.9 to 1.1 ng per mL, and 277 (24 percent) had an SDC of 1.2 ng per mL and higher. There was no difference in all-cause mortality between placebo patients and patients taking digoxin. However, higher SDC levels were associated with higher crude all-cause and cardiovascular mortality, but not mortality caused by heart failure. Patients with the lowest SDC levels had lower rates of mortality in all categories: 6.3 percent lower for all-cause mortality, 3.7 percent for cardiovascular mortality, and 4.7 percent for mortality caused by worsening heart failure. Patients with the highest SDC levels had higher rates of mortality except with worsening heart failure. Multivariate adjustment did not change the association of lower SDC levels with lower mortality but did attenuate the association between higher SDC levels and mortality. Higher SDC levels were also associated with higher rates of hospitalization, including hospitalization for digoxin toxicity.

The authors conclude that the effectiveness of digoxin varies with SDC, with higher SDC levels associated with higher rates of mortality and hospitalization. The optimal SDC appears to be between 0.5 and 0.8 ng per mL for men with stable heart failure and left ventricular dysfunction. The authors attribute the mechanism of these findings to the neurohormonal benefits of digoxin at lower concentrations, as opposed to the harmful inotropic effects that occur at higher dosages. The authors' analysis was insufficiently powered to determine whether these effects hold for women.

Rathore SS, et al. Association of serum digoxin concentration and outcomes in patients with heart failure. JAMA February 19, 2003;289:871-8.

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