Key result
Arrhythmias are linked to heightened posterior insula activation and ventricular coupling during angry contexts.
Why the study?
While anger triggers sympathetic hyperactivity and insular stimulation can induce cardiac arrhythmias, little is known about the interplay between anger and the insula as the underlying emotional-brain-body link that triggers neurogenic cardiac events in patients with cardiovascular diseases.
Does exposure to an angry context and isometric handgrip exercise elicit greater insular reactivity and altered functional connectivity in patients with cardiac arrhythmias compared to healthy controls?
Case-Control (n=40)
No
Does exposure to an angry context and isometric handgrip exercise elicit greater insular reactivity and altered functional connectivity in patients with cardiac arrhythmias compared to healthy controls?
Patients with cardiac arrhythmias exhibit heightened posterior insular reactivity and unique insula-ventricular functional coupling during anger processing and sympathetic activation, highlighting a central neurobiological mechanism linking emotional stress to arrhythmogenesis.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for neurocardiac stress pathways in arrhythmias; leaves open causality and requires prospective validation before practice implications.
Anger is a well-known risk factor in cardiovascular diseases (CVDs) since it triggers a sympathetic hyperactivity of peripheral autonomic nervous system (ANS). As our previous findings showed, facing an angry situation instead of a joyful one elicits in healthy participants an affective engagement that involved mainly the insular reactivity and its connectivity. On the other hand, stimulating the insula, the key neural hub of the cardiovascular brain, can induce cardiac arrhythmias. Unfortunately, still little is known about the interplay between the anger and the insula as the underlying emotional-brain-body link that can trigger or precipitate a series of neurogenic cardiac events in CVDs patients. To address this question, we employed a multimodal method combining neuroimaging, behavioral and blood data to gain a more complete picture of the insula activity and its connectivity in patients with different types of heart arrhythmias. The present findings show a greater generalized involvement of the bilateral posterior insulae in the patients group both when facing angry context and squeezing the handgrip device, suggesting an automatic engagement of the sympathetic nervous system/SNS. Moreover, the bilateral insulae were functionally coupled with the bilateral lateral ventricles selectively under angry conditions, suggesting an insular role in glymphatic dysfunction and CSF dynamics due to the neurovascular coupling. Clearly, understanding this anger-insula-heart link may factually contribute to lower the probability of adverse cardiac outcomes in orienting the necessary treatment of the person, taking into account the emotion-related cardiovascular pathologies and the psychological health.
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Mazzola et al. (2026) conducted a case-control in Heart arrhythmias (n=40). Heart arrhythmias during fMRI emotional (angry vs. joyful) and isometric handgrip tasks vs. Healthy age- and gender-matched controls was evaluated on Bilateral posterior insula activation and functional connectivity with lateral ventricles during angry fMRI context and isometric handgrip (p=<0.05 FWE corrected). Patients with heart arrhythmias exhibited significantly greater bilateral posterior insula activation and functional coupling with the lateral ventricles during angry contexts (p<0.05 FWE).
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