TY - JOUR
T1 - Prevention of sudden cardiac death
T2 - the ICD, or an electrical end‐point with preceding opportunities for intervention?
AU - Tonkin, Andrew M.
PY - 1992/10
Y1 - 1992/10
N2 - Sudden cardiac death (SCD) is usually due to monomorphic ventricular tachycardia and/or ventricular fibrillation. However, in the vast majority of patients these arrhythmias are associated with advanced structural disease. In our society, this is usually due to coronary artery disease (CAD). The implantable cardioverter – defibrillator is the logical approach to management in survivors of SCD. Its rational use must be guided by electrophysiology study. However, a realistic and cost‐effective approach to the prevention of a first cardiac arrest must be multifaceted and take cognisance of other aspects including primary prevention. Limitation of the size of myocardial infarction (MI) is vital. Trials already suggests that effective thrombolysis may impinge long‐term on arrhythmic end‐points. Following infarction, ventricular arrhythmias and sudden death may also be decreased by aspirin, beta‐blockers, and possibly angiotensin converting enzyme inhibitors and amiodarone. Many post‐infarction studies employ a combined end‐point of death and clinical arrhythmias. However, death is usually confined to those with an ejection fraction <35%. In them, treatment of associated heart failure is often a consideration and if the ejection fraction < 15–20%, depending on donor availability, transplantation may even be the preferred therapeutic option to the cardioverter‐defibrillator.
AB - Sudden cardiac death (SCD) is usually due to monomorphic ventricular tachycardia and/or ventricular fibrillation. However, in the vast majority of patients these arrhythmias are associated with advanced structural disease. In our society, this is usually due to coronary artery disease (CAD). The implantable cardioverter – defibrillator is the logical approach to management in survivors of SCD. Its rational use must be guided by electrophysiology study. However, a realistic and cost‐effective approach to the prevention of a first cardiac arrest must be multifaceted and take cognisance of other aspects including primary prevention. Limitation of the size of myocardial infarction (MI) is vital. Trials already suggests that effective thrombolysis may impinge long‐term on arrhythmic end‐points. Following infarction, ventricular arrhythmias and sudden death may also be decreased by aspirin, beta‐blockers, and possibly angiotensin converting enzyme inhibitors and amiodarone. Many post‐infarction studies employ a combined end‐point of death and clinical arrhythmias. However, death is usually confined to those with an ejection fraction <35%. In them, treatment of associated heart failure is often a consideration and if the ejection fraction < 15–20%, depending on donor availability, transplantation may even be the preferred therapeutic option to the cardioverter‐defibrillator.
KW - Arrhythmia
KW - implantable defibrillator
KW - sudden death
UR - http://www.scopus.com/inward/record.url?scp=0026939224&partnerID=8YFLogxK
U2 - 10.1111/j.1445-5994.1992.tb00491.x
DO - 10.1111/j.1445-5994.1992.tb00491.x
M3 - Article
C2 - 1449453
AN - SCOPUS:0026939224
SN - 0004-8291
VL - 22
SP - 631
EP - 635
JO - Australian and New Zealand Journal of Medicine
JF - Australian and New Zealand Journal of Medicine
IS - 5
ER -