Key result
Various pathophysiological substrates, including macroreentrant and microreentrant circuits, cause sustained monomorphic ventricular tachycardia after myocardial infarction and may require tailored ablation.
Answers are grounded in this paper and cite their sources.
This review highlights the diverse pathophysiological substrates of ventricular tachycardia in chronic myocardial infarction and discusses the potential mechanisms by which catheter ablation modifies these circuits.
Several pathophysiological substrates may be responsible for ventricular tachycardia (VT) occurring in the chronic phase of a myocardial infarction. Reentrant circuits can have anatomical or functional characteristics. Macroreentrant or microreentrant circuits have been described. Activation maps have shown that the circuit can be represented as a single loop or as a figure-of-eight reentrant pattern. All these different substrates have in common that they result in sustained monomorphic VT. The adequate treatment will probably be different for each one of them. In this article, some possible pathophysiological substrates of VT occurring in the chronic phase of a myocardial infarction are reviewed. Finally, we speculate on how catheter ablation may modify each one of the substrates.
No takes yet. Share an insight, caveat, or question.
Brugada et al. (1993) conducted a review in Ventricular tachycardia in the chronic phase of myocardial infarction. Catheter ablation was evaluated. Various pathophysiological substrates, including macroreentrant and microreentrant circuits, cause sustained monomorphic ventricular tachycardia after myocardial infarction and may require tailored ablation.
Synapse has enriched 10 related papers. Consider them for comparative context: