Effect of oral sotalol on systemic hemodynamics and programmed electrical stimulation in patients with ventricular arrhythmias and structural heart disease

Stephen Winters, Marrick Kukin, Elena Pe, Debra Stewart, David Deitchman, J. Anthony Gomes

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
JournalThe American Journal of Cardiology
Volume72
Issue number4
DOIs
StatePublished - Aug 12 1993
Externally publishedYes

Fingerprint

Sotalol
Electric Stimulation
Cardiac Arrhythmias
Heart Diseases
Ventricular Tachycardia
Hemodynamics
Bradycardia
Stroke Volume
Infarction
Heart Failure
Pulmonary Wedge Pressure
Digoxin
Furosemide
Ventricular Pressure
Cardiomyopathies
Left Ventricular Function
Tachycardia
Vascular Resistance
Adrenergic Agents
Stroke

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Effect of oral sotalol on systemic hemodynamics and programmed electrical stimulation in patients with ventricular arrhythmias and structural heart disease",
abstract = "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.",
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Effect of oral sotalol on systemic hemodynamics and programmed electrical stimulation in patients with ventricular arrhythmias and structural heart disease. / Winters, Stephen; Kukin, Marrick; Pe, Elena; Stewart, Debra; Deitchman, David; Gomes, J. Anthony.

In: The American Journal of Cardiology, Vol. 72, No. 4, 12.08.1993.

Research output: Contribution to journalArticle

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T1 - Effect of oral sotalol on systemic hemodynamics and programmed electrical stimulation in patients with ventricular arrhythmias and structural heart disease

AU - Winters, Stephen

AU - Kukin, Marrick

AU - Pe, Elena

AU - Stewart, Debra

AU - Deitchman, David

AU - Gomes, J. Anthony

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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.

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