LETTER TO THE EDITOR
Controlling the effectiveness of digoxin
Bernard G. Krohn, MD, FACC*
* 16250 Woodruff Avenue, Bellflower, California 90706, USA
bernard.krohn{at}verizon.net
In a recent issue of the Journal, Adams, et al. (1) correctly stated that: "Patients taking digoxin did significantly better than those not taking the drug, but the serum concentration did not correlate with outcome." Nevertheless, they concluded: "These results support the possibility that a lower therapeutic goal for serum digoxin concentration is warranted in patients with heart failure."
This conclusion is flawed because in individual patients the concentration of digoxin in the serum does not accurately represent the amount of digoxin in the tissues where it works. The digoxin in the serum is only a tiny fraction of the total amount of digoxin in the body. The total amount of digoxin in the body is easy to calculate from the doses administered, and it does correlate with outcome (2–4). Guiding dosage this way allowed high doses of digoxin (15 to 19 µg/kg of lean body weight) to be given to patients after cardiac operations, and the patients recovered rapidly (5,6).
Because serum digoxin concentrations poorly guide dosage and results, contradictions between serum levels and results have been seen by many doctors. Low serum concentrations of digoxin appeared in patients who received therapeutic benefits. In contrast, high serum concentrations of 2.5 ng/ml have been seen in patients who had no signs or symptoms of toxicity.
Dr. Jelliffe published a method for calculating the milligrams of digoxin needed to produce a specific peak total body load of digoxin and to engender a desired therapeutic result (2–4). A safe, effective amount of peak total body digoxin to treat heart failure is 8 to 10 µg/kg of lean body weight. This program is used at the University of Southern California/Los Angeles County Medical Center and at several other hospitals.
Studying the effects of digoxin requires knowing the total amount of digoxin in the body, which controls the amount of digoxin in the tissues where digoxin works.
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References
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1. Adams KF Jr, Gheorghiade M, Uretsky BF, Patterson JH, Schwartz TA, Young JB. Clinical benefits of low serum digoxin concentrations in heart failure. J Am Coll Cardiol. 2002;39:946–953[Abstract/Free Full Text]
2. Jelliffe RW. An improved method of digoxin therapy. Ann Intern Med. 1968;69:703–717[Abstract/Free Full Text]
3. Jelliffe RW. Digitalis therapy: simple formulas to plan and adjust dosage regimens. MD Comput. 1984;2:36–43
4. Jelliffe RW, Buell J, Kalaba R. Reduction of digitalis toxicity by computer-assisted glycoside dosage regimes. Ann Intern Med. 1972;77:891–906[Abstract/Free Full Text]
5. Krohn BG, Saenz JM, Eto KK. The critical dose of digoxin for treating supraventricular tachycardias after heart surgery. Chest. 1989;95:729–734[Abstract/Free Full Text]
6. Krohn BG, Kay JH, Mendez MA, Zubiate P, Kay GL. Rapid sustained recovery after cardiac operations. J Thorac Cardiovasc Surg. 1990;100:194–197[Abstract]
This article has been cited by other articles:
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S. S. Rathore, J. P. Curtis, Y. Wang, M. R. Bristow, and H. M. Krumholz
Association of Serum Digoxin Concentration and Outcomes in Patients With Heart Failure
JAMA,
February 19, 2003;
289(7):
871 - 878.
[Abstract]
[Full Text]
[PDF]
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