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Cardiac arrhythmias are defined by their mechanism and
by their anatomy. The anatomic label may merely be a marker of site of origin, but in a
growing number of situations, discreet, anatomical abnormalities are known to be
responsible for the generation of arrhythmias. Thus a variety of common, repetitive
arrhythmias ranging from the reciprocating tachycardias through to post infarction
ventricular tachycardia, are based on pathological structures or disruption of normal
myocardial architecture.
Myocardial structure may also contribute to arrhythmogenesis in more general ways.
Atrial disease is known to predispose to atrial fibrillation1.
Ventricular arrythmias occur most frequently in the setting of ventricular dilatation2,3. Ventricular stretch has been shown to be
arrhythmogenic in animal models4 demonstrating the
relationship between altered myocardial structure and arrythmia5.
In a similar manner, the process of left ventricular hypertrophy is associated with
increased rates of sudden death6-8.
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