Why the study?
Does intravenous tocainide alter acute hemodynamics in patients undergoing cardiac catheterization?
Does intravenous tocainide alter acute hemodynamics in patients undergoing cardiac catheterization?
Intravenous tocainide causes mild, subclinical depression of left ventricular function without significantly compromising overall cardiac output.
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IV tocainide linked to mild LV depression without output compromise; leaves open safety in reduced-EF patients pending RCTs.
To characterize the acute hemodynamic effects of tocainide hydrochloride, a new antiarrhythmic agent, 11 patients undergoing diagnostic cardiac catheterization were given intravenous infusions of the drug for 15 minutes at rates of 0.50 (six patients) or 0.75 (five patients) mg/kg/min. The hemodynamic status of these subjects was determined before, during, and for 15 minutes after treatment, and blood levels of tocainide were followed during and after treatment. Tocainide blood levels at the end of the infusions were 14.9 +/- 1.6 microgram/ml (S.E.) and 15 minutes later were 6.0 +/- 0.7 microgram/ml. In these subjects treatment was not associated with significant changes in Ao or PCW, but it was associated with a statistically significant but small decrease in LV dp/dt. At the same time, LVED was not significantly elevated. Treatment was also accompanied by small increases in PA diastolic and mean pressures, but RA and RV were unchanged. Significant changes were not seen in HR, CO, CI, SV, SVR, or PVR. Thus, the intravenous infusion of 0.50 and 0.75 mg/kg/min of tocainide for 15 minutes produced small but statistically significant depression of left ventricular function without producing changes in CO or clinical evidence of congestive heart failure.
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Schwartz et al. (1979) studied this question.
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