Abstract

While a great emphasis has been placed on pathophysiological mechanisms underlying the long QT syndromes (LQTS), both congenital and acquired forms, little attention has been focused on the mechanisms whereby a brain damage could induce changes in the QTc interval. Until now, there has been no precise explanation for the frequently observed relationship between acute cerebrovascular events and QTc interval prolongation. Many excellent studies with inductive reasoning proposed QTc effects of insular cortex stimulation [1,2] Few and controversial studies with abductive reasoning investigated an association between prolonged QTc and ischemic insular damage.

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