The potential for antiarrhythmic drugs to reduce mortality from sudden cardiac death

1991 ◽  
pp. 41-62
Author(s):  
J. Thomas Bigger
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Antiarrhythmic Drugs

Impact of Nontraditional Antiarrhythmic Drugs on Sudden Cardiac Death

2014 ◽  
pp. 1121-1128
Author(s):  
Leonard Ilkhanoff ◽  
Alan H. Kadish ◽  
Jeffrey J. Goldberger
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Antiarrhythmic Drugs

Impact of Nontraditional Antiarrhythmic Drugs on Sudden Cardiac Death

2004 ◽  
pp. 950-958 ◽  
Author(s):  
Jeffrey Goldberger ◽  
Kenneth M. Weinberg ◽  
Alan H. Kadish
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Antiarrhythmic Drugs

Impact of Nontraditional Antiarrhythmic Drugs on Sudden Cardiac Death

2018 ◽  
pp. 1084-1091 ◽  
Author(s):  
Raul D. Mitrani ◽  
Leonard Ilkhanoff ◽  
Jeffrey J. Goldberger
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Antiarrhythmic Drugs

scholarly journals The role of antiarrhythmic drugs in sudden cardiac death

1986 ◽  
Vol 8 (1) ◽  
pp. 104A-109A ◽  
Author(s):  
Brian F. Hoffman ◽  
Kenneth H. Dangman
Keyword(s):  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Antiarrhythmic Drugs

scholarly journals Targeted ablation of cardiac sympathetic neurons reduces the susceptibility to ischemia-induced sustained ventricular tachycardia in conscious rats

2010 ◽  
Vol 298 (5) ◽  
pp. H1330-H1339 ◽  
Author(s):  
Heidi L. Lujan ◽  
Gurunanthan Palani ◽  
Lijie Zhang ◽  
Stephen E. DiCarlo
Keyword(s):  
Ventricular Tachycardia ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Ventricular Arrhythmias ◽  
Antiarrhythmic Drugs ◽  
Sympathetic Neurons ◽  
Left Ventricular ◽  
Sustained Ventricular Tachycardia ◽  
Conscious Rats ◽  
Stellate Ganglia

The Cardiac Arrhythmia Suppression Trial demonstrated that antiarrhythmic drugs not only fail to prevent sudden cardiac death, but actually increase overall mortality. These findings have been confirmed in additional trials. The “proarrhythmic” effects of most currently available antiarrhythmic drugs makes it essential that we investigate novel strategies for the prevention of sudden cardiac death. Targeted ablation of cardiac sympathetic neurons may become a therapeutic option by reducing sympathetic activity. Thus cholera toxin B subunit (CTB) conjugated to saporin (a ribosomal inactivating protein that binds to and inactivates ribosomes; CTB-SAP) was injected into both stellate ganglia to test the hypothesis that targeted ablation of cardiac sympathetic neurons reduces the susceptibility to ischemia-induced, sustained ventricular tachycardia in conscious rats. Rats were randomly divided into three groups: 1) control (no injection); 2) bilateral stellate ganglia injection of CTB; and 3) bilateral stellate ganglia injection of CTB-SAP. CTB-SAP rats had a reduced susceptibility to ischemia-induced, sustained ventricular tachycardia. Associated with the reduced susceptibility to ventricular arrhythmias were a reduced number of stained neurons in the stellate ganglia and spinal cord (segments T1-T4), as well as a reduced left ventricular norepinephrine content and sympathetic innervation density. Thus CTB-SAP retrogradely transported from the stellate ganglia is effective at ablating cardiac sympathetic neurons and reducing the susceptibility to ventricular arrhythmias.

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