TY - JOUR
T1 - Effect of oral sotalol on systemic hemodynamics and programmed electrical stimulation in patients with ventricular arrhythmias and structural heart disease
AU - Winters, Stephen L.
AU - Kukin, Marrick
AU - Pe, Elena
AU - Stewart, Debra
AU - Deitchman, David
AU - Gomes, J. Anthony
PY - 1993/8/12
Y1 - 1993/8/12
N2 - We explored the central hemodynamic responses to oral sotalol during dose titration in patients with ventricular arrhythmias who underwent programmed ventricular stimulation. Twelve patients were included in the study, 9 with a history of sustained ventricular tachyarrhythmias (6 postmyocardial infarction and 3 with cardiomyopathy) and 3 with a history of nonsustained ventricular tachycardia postmyocardial infarction. Left ventricular ejection fractions were <45% in 10 patients, and <35% in 5; the mean ejection fraction was 37% (range 20-51%). Sotalol prevented the induction of ventricular tachycardia in each of 3 patients wtth nonsustained ventricular tachycardia and in 6 of 9 wtth sustained ventricular tachycardia at baseline study. At peak action (2 hours) after sotalol loading (mean dose, 167 mg orally twice daily), the hemodynamic effects included bradycardia, decreased cardiac index, increased left ventricular filling pressure and systemic vascular resistance, and no change in stroke volume or stroke work index. One patient was not continued on sotalol, owing to an excessive increase in the pulmonary capillary wedge pressure, despite the lack of symptomatic heart failure. Congestive heart failure in association with marked bradycardia developed in another patient, who had suppression of inducible ventricular tachycardia after sotalol loading; this patient was managed wtth a reduction in the dose of sotalol and a regimen of digoxin and furosemide, and has been well compensated and without a recurrence of sustained ventricular tachycardia for more than 4 years. Ventricular tachycardia has been controlled wtth sotalol, without hemodynamic deterioration, in 6 of these patients. The evidence supports the idea that, despite its β-adrenergic blocking effects, sotalol can be used, albeit with some caution, even in patients with compromised left ventricular systolic function.
AB - We explored the central hemodynamic responses to oral sotalol during dose titration in patients with ventricular arrhythmias who underwent programmed ventricular stimulation. Twelve patients were included in the study, 9 with a history of sustained ventricular tachyarrhythmias (6 postmyocardial infarction and 3 with cardiomyopathy) and 3 with a history of nonsustained ventricular tachycardia postmyocardial infarction. Left ventricular ejection fractions were <45% in 10 patients, and <35% in 5; the mean ejection fraction was 37% (range 20-51%). Sotalol prevented the induction of ventricular tachycardia in each of 3 patients wtth nonsustained ventricular tachycardia and in 6 of 9 wtth sustained ventricular tachycardia at baseline study. At peak action (2 hours) after sotalol loading (mean dose, 167 mg orally twice daily), the hemodynamic effects included bradycardia, decreased cardiac index, increased left ventricular filling pressure and systemic vascular resistance, and no change in stroke volume or stroke work index. One patient was not continued on sotalol, owing to an excessive increase in the pulmonary capillary wedge pressure, despite the lack of symptomatic heart failure. Congestive heart failure in association with marked bradycardia developed in another patient, who had suppression of inducible ventricular tachycardia after sotalol loading; this patient was managed wtth a reduction in the dose of sotalol and a regimen of digoxin and furosemide, and has been well compensated and without a recurrence of sustained ventricular tachycardia for more than 4 years. Ventricular tachycardia has been controlled wtth sotalol, without hemodynamic deterioration, in 6 of these patients. The evidence supports the idea that, despite its β-adrenergic blocking effects, sotalol can be used, albeit with some caution, even in patients with compromised left ventricular systolic function.
UR - http://www.scopus.com/inward/record.url?scp=0027201697&partnerID=8YFLogxK
U2 - 10.1016/0002-9149(93)90023-6
DO - 10.1016/0002-9149(93)90023-6
M3 - Article
C2 - 8346725
AN - SCOPUS:0027201697
SN - 0002-9149
VL - 72
SP - A38-A43
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 4
ER -