scholarly journals Prevention of sudden death after repair of tetralogy of fallot: Treatment of ventricular arrhythmias

1985 ◽  
Vol 6 (1) ◽  
pp. 221-227 ◽  
Author(s):  
Arthur Garson ◽  
David C. Randall ◽  
Paul C. GilletteD ◽  
Richard T. Smith ◽  
Jeffrey P. Moak ◽  
...  
Keyword(s):  
Sudden Death ◽  
Tetralogy Of Fallot ◽  
Ventricular Arrhythmias

Ventricular arrhythmias after repair of congenital heart disease: Who needs treatment?

1991 ◽  
Vol 1 (3) ◽  
pp. 177-181 ◽  
Author(s):  
Arthur Garson
Keyword(s):  
At Risk ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Sudden Death ◽  
Tetralogy Of Fallot ◽  
Ventricular Arrhythmias ◽  
Congenital Heart ◽  
Antiarrhythmic Drugs ◽  
Premature Ventricular Contractions

Sudden death occurs in patients after repair of congenital heart disease. In those with tetralogy of Fallot, or a similar lesion, ventricular tachycardia has been hypothesized as the major arrhythmic mechanism for sudden death. It would be desirable to identify individuals at risk for sudden death, to determine which arrhythmia would be likely to cause sudden death, and to treat those individuals with an appropriate antiarrhythmic to prevent sudden death. For the last 10 years, physicians have been treating patients with antiarrhythmic drugs, based on a number of criteria, the most common of which is the presence of premature ventricular contractions.1,2 The practice has recently been called into question by the CAST trial. It is the purpose of this paper to review the evidence that repair causes ventricular arrhythmias, that ventricular arrhythmias cause sudden death, and that ventricular arrhythmias should be treated prophylactically.

scholarly journals Ventricular arrhythmias and sudden death in tetralogy of Fallot

2017 ◽  
Vol 110 (5) ◽  
pp. 354-362 ◽  
Author(s):  
Philippe Maury ◽  
Frederic Sacher ◽  
Anne Rollin ◽  
Pierre Mondoly ◽  
Alexandre Duparc ◽  
...  
Keyword(s):  
Sudden Death ◽  
Tetralogy Of Fallot ◽  
Ventricular Arrhythmias

Sudden Death and Tetralogy of Fallot

Circulation ◽  
1995 ◽  
Vol 92 (2) ◽  
pp. 158-159 ◽  
Author(s):  
J. Timothy Bricker
Keyword(s):  
Sudden Death ◽  
Tetralogy Of Fallot

Abstract 248: Age-specific Differences in Outcomes Following Isoproterenol-induced Sudden Cardiac Death in Guinea Pigs

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Kathleen C Woulfe ◽  
Sarah Chau ◽  
Lori A Walker ◽  
Christine Tompkins ◽  
Carmen C Sucharov ◽  
...  
Keyword(s):  
Sudden Death ◽  
Guinea Pigs ◽  
Ventricular Arrhythmias ◽  
Molecular Mechanisms ◽  
Calcium Handling ◽  
Initial Exposure ◽  
Age Related ◽  
Volatile Anesthesia ◽  
Pediatric Heart Failure ◽  
Guinea Pig Model

Background: The pathophysiological mechanisms involved in adult and pediatric heart failure (HF) are unique. One example of clinical differences in these two patient populations is the need for primary prevention implantable defibrillators (ICDs) in adults with HF, whereas pediatric HF patients infrequently have ventricular arrhythmias and rarely require ICDs. To better understand the age-specific molecular mechanisms involved in HF, we are developing a guinea pig model of pediatric HF. We have found age-specific differences in guinea pigs acutely treated with isoproterenol (ISO). Additionally, initial exposure to ISO leads to sudden death in guinea pigs. This sudden death has previously been reported as an interaction with an inhaled volatile anesthesia. We hypothesized that isoproterenol is leading to sustained ventricular arrhythmias in guinea pigs. Methods: Adult (n= 11) and young (n= 50) guinea pigs were treated with vehicle, 16 mg/kg/day or 32 mg/kg/day of ISO by osmotic pump (Alzet) implanted under isoflurane anesthesia. Cardiac rhythm was monitored in a subset via simultaneously implanted Linq recorders (Medtronic, n= 12). Results: Acute exposure to ISO in the presence or absence of isoflurane resulted in sudden death in adult and young guinea pigs. Four of the 6 adult guinea pigs exposed to ISO died even with attempts at resuscitation. In contrast, 61% (22 out of 36) of the young guinea pigs treated with ISO arrested and 60% (13 out of 22) were rescued with chest compressions. Analysis of the heart rhythms demonstrated that the guinea pigs experienced ventricular fibrillation. The arrhythmia was transient in the young guinea pigs, but sustained in the adult. Conclusions: Acute ISO leads to age-dependent differences in arrhythmias and sudden death in guinea pigs. Contrary to prior reports, this response occurs independently of isoflurane. These age-specific differences suggest unique mechanisms in calcium handling, which can lead to arrhythmias. Guinea pigs may be a useful model for the age-related differences in HF arrhythmias seen in humans. A better understanding of these differences may lead to the development of therapies to protect adult HF patients from arrhythmias.

Sign in / Sign up

Export Citation Format

Share Document