Key result
Intravenous digoxin uptake transiently increases in hypertrophied canine RVs before normalizing at one hour.
Why the study?
Does right ventricular hypertrophy alter myocardial digoxin uptake in a canine model?
Does right ventricular hypertrophy alter myocardial digoxin uptake in a canine model?
Right ventricular hypertrophy increases initial myocardial digoxin uptake but does not alter binding affinity per unit mass in a canine model.
Answers are grounded in this paper and cite their sources.
Does not support altered digoxin dosing in RV hypertrophy; leaves open translation from canine model to patients.
The hypertrophied right ventricle of the dog with pulmonary stenosis exhibited a greater than normal uptake of digoxin 5 min after intravenous administration. After 1 hr the digoxin concentration had fallen and was not different from the normal, this latter result suggesting that hypertrophy per se did not change the ventricle's binding affinity for digoxin per unit mass. Greater initial binding of digoxin by the hypertrophied ventricle was probably associated with some function of the mechanical activity of the stressed ventricle and/or with greater tissue delivery of digoxin in greater myocardial blood flow.
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Hopkins et al. (1974) studied Pressure overload right ventricular hypertrophy. Intravenous digoxin vs. Normal dogs was evaluated on Myocardial digoxin uptake. Intravenous digoxin uptake was greater than normal in the hypertrophied right ventricle of dogs with pulmonary stenosis at 5 minutes, but not different from normal at 1 hour.
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