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Insular cortex and QT correction interval: an effect of hemispheric lateralization?

We read the interesting study by Turri et al. [1], who reported that increased insular cortex (Ic) lesion volume and decreased Ic thickness had significant negative associations with QT correction (QTc) interval in patients with multiple sclerosis. In a dog model, the adjusted QT interval at high parasympathetic or low sympathetic tone was significantly longer than that at low parasympathetic or high sympathetic tone [2]. However, recent studies have supported the notion that the cardiovascular system is regulated by a cortical network consisting of the Ic, anterior cingulate gyrus and amygdala [3]. Several points should be taken into account when interpreting these results reported by Turri et al. [1]. First, in an earlier study [4], right hemispheric inactivation induced an increase of high frequency of heart rate and blood pressure, and left inactivation induced an increase of low frequency of heart rate and blood pressure in patients with drug-refractory epilepsy. These results suggest that the left hemisphere, including the left Ic, is predominantly associated with parasympathetic autonomic tone. In the study reported by Turri et al. [1], there were no descriptions of the hemispheric lateralization for Ic lesion volume and Ic thickness. The patients with increased right Ic lesion volume or increased left Ic thickness might have longer QTc intervals. Second, Oppenheimer et al. [5] identified a site of cardiac representation within the Ic. Bradycardia or depressor effects were significantly more common after stimulation of the left Ic. The degree of bradycardia was significantly greater on stimulation of the left posterior than the left anterior Ic [5]. Thus, the posterior portion of the left Ic might have a strong association with parasympathetic nervous system activity. In the study reported by Turri et al. [1], there were no descriptions of the relationship between Ic and QTc interval in relation to the anterior versus posterior Ic of the left hemisphere. Until now, there have been few reports assessing the Ic and QTc interval according to hemispheric laterality and anterior versus posterior portion of the Ic. The data presented in Turri et al. [1] would be of much more importance if the exact mechanism underlying that relationship were provided.