Reduced functional connectivity between ventromedial prefrontal cortex and insula relates to longer corrected QT
Roger C McIntosh1, Dominic C Chow2, Corey J Lum3
1Department of Health Psychology, University of Miami, Coral Gables, FL 33124, USA.
Insights
QT interval prolongation in Human Immunodeficiency Virus (HIV) is linked to autonomic nervous system changes. This study found specific ventromedial prefrontal cortex (VMPFC) functional connectivity patterns associated with QT interval length in HIV+ individuals.
Area of Science:
- Neuroscience
- Cardiology
- Infectious Disease
Background:
- QT interval prolongation is a risk factor for fatal cardiac arrhythmias in Human Immunodeficiency Virus (HIV) patients.
- This cardiac issue is associated with autonomic nervous system dysregulation.
- The ventromedial prefrontal cortex (VMPFC) plays a role in cardio-autonomic regulation.
Purpose of the Study:
- To investigate the relationship between QT interval length and resting state functional connectivity (rsFC) of the VMPFC.
- To identify brain regions associated with QT interval length and CD4 count in HIV+ individuals.
Main Methods:
- Compared 18 HIV+ men on antiretroviral therapy with 26 HIV-negative controls.
- Utilized seed-based rsFC analysis of the VMPFC.
- Examined group differences in connectivity and correlations with corrected QT (QTc) interval and CD4 count.
Main Results:
- HIV-negative adults exhibited greater VMPFC rsFC with default mode network structures.
- Greater rsFC between VMPFC and left anterior insula correlated with shorter QTc intervals.
- Greater VMPFC rsFC with right posterior insula correlated with longer QTc intervals.
- In HIV+ patients, longer QTc intervals and lower CD4 counts were linked to weaker VMPFC connectivity with the dorsal striatum.
Conclusions:
- QTc interval length is associated with distinct VMPFC rsFC patterns involving the insula.
- Specific VMPFC connectivity alterations in HIV+ individuals may underlie cardiac risks.
- A forebrain control mechanism might suppress cardiovagal influence, increasing arrhythmia risk in HIV+ individuals.
Objective:
Prolongation of the QT interval, i.e., measure of the time between the start of the Q wave and the end of the T wave, is a precursor to fatal cardiac arrhythmias commonly observed in individuals infected with the Human Immunodeficiency Virus (HIV), and is related to dysregulation of the autonomic nervous system. We investigated the relationship between QT interval length and resting state functional connectivity (rsFC) of the ventromedial prefrontal cortex (VMPFC), a core region of the brain that is involved with cardio-autonomic regulation.
Method:
Eighteen HIV+ men on antiretroviral therapy and with no history of heart disease were compared with 26 HIV-negative control subjects who had similar demographic and cardio-metabolic characteristics. A seed-based rsFC analysis of the right and left VMPFC was performed at the individual subject level, and 2nd-level analyses were conducted to identify the following: group differences in connectivity, brain regions correlating with corrected (QTc) interval length before and after controlling for those group differences, and regions where seed-based rsFC correlates with CD4 count and QTc interval within HIV+ individuals.
Results:
HIV-negative adults showed greater rsFC between the VMPFC seed regions and several default mode network structures. Across groups greater rsFC with the left anterior insula was associated with shorter QTc intervals, whereas right posterior insula connectivity with the VMPFC correlated with greater QTc intervals. HIV patients with lower CD4 counts and higher QTc intervals showed greater rsFC between the right VMPFC and the right posterior insula and dorsal cingulate gyrus.
Conclusions:
This study demonstrates that QTc interval lengths are associated with distinct patterns of VMPFC rsFC with posterior and anterior insula. In HIV patients, longer QTc interval and lower CD4 count corresponded to weaker VMPFC connectivity with the dorsal striatrum.
Significance:
A forebrain control mechanism may be implicated in the suppression of cardiovagal influence that confers risk for ventricular arrhythmias and sudden cardiac death in HIV+ individuals.
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