Key result
Continuing digoxin cuts worsening heart failure risk vs. withdrawal across all serum concentrations, including low levels.
Why the study?
The optimal serum digoxin concentration for clinical efficacy and acceptable toxicity in patients with symptomatic left ventricular dysfunction remains controversial.
Does continuation of digoxin at low serum concentrations prevent worsening heart failure in patients with symptomatic left ventricular dysfunction?
RCT
Double-blind
randomized
Does continuation of digoxin at low serum concentrations prevent worsening heart failure in patients with symptomatic left ventricular dysfunction?
p-value: p=<0.02
Low serum digoxin concentrations (0.5-0.9 ng/ml) provide similar clinical benefits in preventing worsening heart failure as higher concentrations, suggesting lower target levels may be effective.
OBJECTIVES: We sought to determine whether there was a relationship between serum digoxin concentration (SDC), including SDCs typically regarded as low, and clinical efficacy related to digoxin in patients with symptomatic left ventricular dysfunction. BACKGROUND: Digitalis glycosides have been used for 200 years in the treatment of heart failure (HF), but the SDC required for optimal clinical efficacy and acceptable toxicity remains controversial. METHODS: This relationship was investigated by utilizing data from two randomized, double-blinded, placebo-controlled, digoxin-withdrawal trials: the Prospective Randomized study Of Ventricular failure and Efficacy of Digoxin (PROVED) and the Randomized Assessment of Digoxin on Inhibitors of Angiotensin-Converting Enzyme (RADIANCE). Major end points were worsening HF, change in left ventricular ejection fraction and treadmill time after randomization. The primary analysis investigated the relationship between SDC at randomization and these end points. A secondary categorical analysis compared these end points in patients who discontinued digoxin versus patients who continued digoxin and had low (0.5 to 0.9 ng/ml), moderate (0.9 to 1.2 ng/ml) or high (>1.2 ng/ml) SDCs at randomization. RESULTS: Multiple regression analysis failed to find a relationship between randomization SDC, considered as a continuous variable, and any study end point (all p > 0.236). Multivariable Cox analysis found that the risk of worsening HF was significantly less (all p < 0.02) for patients in any category of SDC who continued digoxin, as compared with patients withdrawn from digoxin. Specifically, patients in the low SDC category were significantly less likely than placebo patients to experience worsening HF during follow-up (p = 0.018). CONCLUSIONS: The beneficial effects of digoxin on common clinical end points in patients with HF were similar, regardless of SDC.
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Adams et al. (2002) conducted an RCT in Symptomatic left ventricular dysfunction / heart failure. Digoxin continuation vs. Placebo (digoxin withdrawal) was evaluated on Worsening heart failure, change in left ventricular ejection fraction, and treadmill time (p=<0.02). Continuing digoxin significantly reduced the risk of worsening heart failure compared to placebo withdrawal across all serum digoxin concentrations, including low levels (0.5-0.9 ng/ml; p=0.018).
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