The insular cortex is known to be involved in central sympathovagal regulation. Both right and left insular lesions have been associated with cardiac derangements.

Previous stroke studies suggest that right insular lesions may cause reduced inhibition of sympathetic activity resulting in tachyarrhythmias, ECG changes, elevation of troponin T (TnT) and serum catecholamine levels, decreased heart rate variability, higher occurrence of sudden death and overall death rate within 3 months.

In contrast, recent data indicate a significant role of the left insula in mediating the parasympathetic tone, and therefore lesions in this region may be associated with a shifted balance towards sympathetic activity.1 In patients surgically treated for epilepsy, direct stimulation of the right insular cortex mainly resulted in sympathetic cardiovascular responses whereas stimulation of the left insula mainly caused parasympathetic reactions (bradycardia).2 This is in agreement with the observation that barbiturate infusion into the human left carotid artery produced tachycardia whereas infusion into the right carotid artery generated bradycardia.3

Left insular lesions may be associated with decreased parasympathetic tone, shifting the balance towards enhanced sympathetic outflow and decreased heart rate variability.1 Left insular strokes have been associated with adverse cardiac outcome, suggesting this mechanism.

Nevertheless, it is possible that both …