Digoxin for atrial fibrillation: a drug whose time has gone?

Article Abstract:

Atrial fibrillation is an irregular heart rhythm that originates in the atria, or upper chambers of the heart. In some patients, this rhythm becomes chronic; in others, it occurs only episodically. For over 200 years, digitalis, and now its successor, digoxin, have been used to treat atrial fibrillation, but only in recent years have studies been done to document the true usefulness of digoxin therapy. In a resting patient, digoxin acts to increase the effect of the vagus nerve on the heart, and since the action of the vagus nerve is to slow the heart rate, the rate of chronic atrial fibrillation is slowed at rest. However, during exercise, the vagus nerve's activity is diminished, and digoxin may no longer slow the rate of the atrial fibrillation. One longstanding belief is that digoxin can restore normal, or sinus rhythm in new-onset atrial fibrillation. If the patient also has congestive heart failure, digoxin (which has proven benefits in heart failure) may improve the heart's function sufficiently such that a spontaneous return to a normal rhythm occurs. In the absence of heart failure, digoxin is no better than a placebo in permitting this reversion to normal sinus rhythm. Traditionally, patients who suffer only paroxysmal atrial fibrillation have been placed on maintenance digoxin therapy to keep them in normal sinus rhythm after an episode, but the existing data suggest that digoxin is ineffective preventing a recurrence of the abnormal rhythm. Evidence exists that a certain subgroup of patients may have a greater predisposition to recurrence while on digoxin. Thus, the current role that digoxin should play in treating patients with atrial fibrillation is unclear. A stable patient with rapid atrial fibrillation should still receive digoxin to slow his rate, but if the episode was triggered by certain precipitants, such as fever or blood loss, then digoxin alone is unlikely to control his rate. Thus, the predominant role digoxin has played thus far in the control of atrial fibrillation should probably be reduced. (Consumer Summary produced by Reliance Medical Information, Inc.)

Drug therapy, Atrial fibrillation

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Influence of gastric acidity on the bioavailability of digoxin

Article Abstract:

Digoxin is a drug used in heart failure to improve the pumping action of the heart, and in certain abnormal heart rhythms to slow them. Digoxin levels in the blood are measured as a means of monitoring for toxicity, but some people are known to have toxic reactions even when their blood levels suggest that the digoxin is at therapeutic levels. The blood test for digoxin is unable to distinguish between digoxin itself and its metabolic byproducts. A study was done to determine how much digoxin is absorbed into the bloodstream after oral ingestion, and if administering certain other drugs at the same time might affect the blood level of digoxin. Doses of digoxin were administered to a group of healthy volunteers along with either omeprazole, a new anti-ulcer drug that dramatically reduces stomach acid, pentagastrin, which stimulates the stomach to produce more acid, or placebo. The amounts of digoxin recovered in the urine were then measured. When more unmetabolized digoxin is recovered in the urine, more of the drug is available (or bioavailable) to the digestive tract for absorption into the bloodstream. Thus, under conditions that produce high levels of unmetabolized digoxin in the urine, higher blood levels, and thus greater toxicity, might be expected. When digoxin was given with placebo, 34 percent was recovered in the urine. When digoxin was given with omeprazole, 48 percent was recovered unmetabolized in the urine. When the digoxin was given with pentagastrin, only 21 percent was recovered in the urine. Thus, conditions that produce decreased levels of stomach acid can greatly increase the bioavailability of digoxin, and predispose patients to digoxin toxicity. Achlorhydria, a condition of diminished stomach acid, is common in the elderly, thus suggesting that they might be more prone to digoxin toxicity. Drugs such as omeprazole can produce the same condition, and should be given with caution to persons who are also taking digoxin. (Consumer Summary produced by Reliance Medical Information, Inc.)

Complications and side effects, Bioavailability, Gastric acid, Achlorhydria

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Influence of digoxin immune Fab therapy and renal dysfunction on the disposition of total and free digoxin

Article Abstract:

Removal of digoxin from the body may be prolonged in patients with end stage kidney disease after treatment with digoxin Fab antibodies. Digoxin Fab antibodies are used to treat patients with digoxin intoxication. Among 14 patients with digoxin intoxication who were treated with digoxin Fab antibodies, four had end-stage kidney disease, one had acute kidney failure and nine had different degrees of kidney dysfunction. Removal of digoxin from the body was a two-phase process. Blood levels of free digoxin decreased rapidly after treatment with digoxin Fab antibodies. They rebounded to a maximum concentration an average of three days after treatment. The time for this rebound to occur was longer for patients with end-stage kidney disease than for the other patients.

Kidney diseases, Immunotherapy

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