TY - JOUR
T1 - The hemodynamic effects of sotalol and quinidine
T2 - Analysis by use of rest and exercise gated radionuclide angiography
AU - Mahmarian, John J.
AU - Verani, M. S.
AU - Hohmann, T.
AU - Hill, R.
AU - Thornton, B. C.
AU - Bolli, R.
AU - Young, J. B.
AU - Roberts, R.
AU - Pratt, Craig
PY - 1987
Y1 - 1987
N2 - This placebo-controlled, double-blind trial compared the hemodynamic effects of sotalol and quinidine with the use of rest and exercise gated radionuclide angiography. Patients had frequent ventricular premature depolarizations (≥ 30 VPDs/hour) and depressed cardiac function (mean ejection fraction 43 ± 15%). Resting left ventricular ejection fraction and stroke volume index increased (p < .002, p < .001, respectively) during sotalol therapy, associated with a concomitant fall in heart rate (p < .001). Quinidine also increased mean left ventricular ejection fraction, but less so than did sotalol (p < .05). Quinidine significantly decreased left ventricular end-diastolic (p < .05) and end-systolic (p < .002) volumes, but had no effect on stroke volume index or heart rate. Neither drug affected cardiac index. Quinidine resulted in no symptomatic deterioration in left ventricular function or serious arrhythmia aggravation. In contrast, five patients on sotalol developed either decompensated congestive heart failure (two patients), arrhythmia aggravation (two patients), or hypotension associated with bradyarrhythmia (one patient). These patients had a unique hemodynamic profile that can be used to identify patients likely to have a poor outcome on sotalol. This profile reflected a lack of cardiac reserve, characterized by an inability to increase stroke volume and cardiac output with supine bicycle exercise.
AB - This placebo-controlled, double-blind trial compared the hemodynamic effects of sotalol and quinidine with the use of rest and exercise gated radionuclide angiography. Patients had frequent ventricular premature depolarizations (≥ 30 VPDs/hour) and depressed cardiac function (mean ejection fraction 43 ± 15%). Resting left ventricular ejection fraction and stroke volume index increased (p < .002, p < .001, respectively) during sotalol therapy, associated with a concomitant fall in heart rate (p < .001). Quinidine also increased mean left ventricular ejection fraction, but less so than did sotalol (p < .05). Quinidine significantly decreased left ventricular end-diastolic (p < .05) and end-systolic (p < .002) volumes, but had no effect on stroke volume index or heart rate. Neither drug affected cardiac index. Quinidine resulted in no symptomatic deterioration in left ventricular function or serious arrhythmia aggravation. In contrast, five patients on sotalol developed either decompensated congestive heart failure (two patients), arrhythmia aggravation (two patients), or hypotension associated with bradyarrhythmia (one patient). These patients had a unique hemodynamic profile that can be used to identify patients likely to have a poor outcome on sotalol. This profile reflected a lack of cardiac reserve, characterized by an inability to increase stroke volume and cardiac output with supine bicycle exercise.
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U2 - 10.1161/01.CIR.76.2.324
DO - 10.1161/01.CIR.76.2.324
M3 - Article
C2 - 3301053
AN - SCOPUS:0023219915
SN - 0009-7322
VL - 76
SP - 324
EP - 331
JO - Circulation
JF - Circulation
IS - 2
ER -