AIM: To find a rapid way of identifying non-responders to D, L-sotalol in patients with ventricular tachycardia. METHODS: Programmed ventricular stimulation and RR variability were studied in the control state and 10 days after treatment with 160 to 320 mg of D,L-sotalol in 36 consecutive patients with ventricular tachycardia. RESULTS: In 14 patients (group I) D,L-sotalol suppressed ventricular tachycardia inducibility. In 22 patients (group II) sustained ventricular tachycardia remained inducible during D,L-sotalol treatment. The ventricular tachycardia rate was slowed in eight patients and unchanged or accelerated in 14. At baseline, heart rate variability was similar in both groups. During treatment with D,L-sotalol, variables reflecting parasympathetic activity (pNN50, rMSSD, and high frequency amplitude (HF)) increased in both groups: HF increased from (mean (SD)) 75 (68) to 146 (134) in group I (p < 0.05) and from 60 (49) to 125 (79) in group II (p < 0.05). Other variables were unchanged in group I. In group II, the variables associated with sympathetic activity (coefficient of variance (CV), ratio of low frequency amplitude (LF) to HF) decreased significantly: CV decreased from 13 (4) to 9 (2) (p < 0. 001) and LF/HF from 4.74 (3.02) to 3.00 (2.02) (p < 0.05). CONCLUSIONS: The beta blocking effect of D,L-sotalol produced a significant improvement over control values in indices of parasympathetic tone in all treated patients. However, the heart rate variability indices related to sympathetic activity were decreased only in non-responders. This effect of D,L-sotalol on heart rate variability could help detect non-responders to the drug and avoid an electrophysiological study.
AIM: To find a rapid way of identifying non-responders to D, L-sotalol in patients with ventricular tachycardia. METHODS: Programmed ventricular stimulation and RR variability were studied in the control state and 10 days after treatment with 160 to 320 mg of D,L-sotalol in 36 consecutive patients with ventricular tachycardia. RESULTS: In 14 patients (group I) D,L-sotalol suppressed ventricular tachycardia inducibility. In 22 patients (group II) sustained ventricular tachycardia remained inducible during D,L-sotalol treatment. The ventricular tachycardia rate was slowed in eight patients and unchanged or accelerated in 14. At baseline, heart rate variability was similar in both groups. During treatment with D,L-sotalol, variables reflecting parasympathetic activity (pNN50, rMSSD, and high frequency amplitude (HF)) increased in both groups: HF increased from (mean (SD)) 75 (68) to 146 (134) in group I (p < 0.05) and from 60 (49) to 125 (79) in group II (p < 0.05). Other variables were unchanged in group I. In group II, the variables associated with sympathetic activity (coefficient of variance (CV), ratio of low frequency amplitude (LF) to HF) decreased significantly: CV decreased from 13 (4) to 9 (2) (p < 0. 001) and LF/HF from 4.74 (3.02) to 3.00 (2.02) (p < 0.05). CONCLUSIONS: The beta blocking effect of D,L-sotalol produced a significant improvement over control values in indices of parasympathetic tone in all treated patients. However, the heart rate variability indices related to sympathetic activity were decreased only in non-responders. This effect of D,L-sotalol on heart rate variability could help detect non-responders to the drug and avoid an electrophysiological study.
Authors: F Lombardi; D Torzillo; G Sandrone; L Dalla Vecchia; M L Finocchiaro; R Bernasconi; E Cappiello Journal: Am J Cardiol Date: 1992-10-15 Impact factor: 2.778