Key result
This letter discusses the potential role of hemispheric lateralization and the insular cortex in regulating autonomic tone and cerebral blood flow in patients with heart failure.
This letter highlights the need to consider hemispheric lateralization and specific regions of the insular cortex when evaluating the relationship between reduced cerebral blood flow and autonomic deficits in heart failure.
We read the interesting study by Roy et al.,1 who reported that heart failure (HF) patients showed lower and lateralized cerebral blood flow (CBF) in autonomic regulatory sites, and that reduced CBF was suggested to lead to autonomic deficits. In the recent meta-analysis of functional magnetic resonance imaging studies, right hemispheric dominance emphasized information processing with the posterior insular cortex (Ic), serving as the major gateway for cardioception.2 On the other hand, recent studies have supported the notion that the cardiovascular system is regulated by a central autonomic network consisting of Ic, anterior cingulate gyrus and amygdala.3 Several points should be taken into account when interpreting the results reported by Roy et al.1 First, in an earlier study,4 right hemispheric inactivation induced an increase in high-frequency heart rate and blood pressure, and left hemispheric inactivation induced an increase in low-frequency heart rate and blood pressure in patients with drug-refractory epilepsy. These results suggest that the right hemisphere including right Ic is predominantly associated with sympathetic autonomic tone. In the study reported by Roy et al.,1 there were little descriptions about hemispheric lateralization for the relationship between reduced CBF and autonomic deficits in HF. The patients with reduced right hemispheric CBF might have lower sympathetic outflows to the heart, although most of those patients with HF were on renin–angiotensin system inhibitors or beta-blockers, which may affect regional CBF. Second, Oppenheimer et al.5 identified a site of cardiac representation within the Ic. Bradycardia or depressor effect was significantly more common after stimulation of the left Ic. The degrees of bradycardia and depressor were 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 Roy et al.,1 there were no descriptions about the relationship of left CBF in Ic with lower blood pressure in HF, although activation of the Ic was suggested to have an important role among the central autonomic network in regulating the cardiovascular system. Until now, there have been few reports assessing reduced regional CBF and HF according to hemispheric laterality and the anterior vs. posterior portion of Ic. The data presented in the manuscript by Roy et al.1 would make much more importance if the exact mechanism underlying that relationship were provided.
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Nagai et al. (2017) conducted a letter in Heart failure. This letter discusses the potential role of hemispheric lateralization and the insular cortex in regulating autonomic tone and cerebral blood flow in patients with heart failure.
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