Introduction:
Transcranial Magnetic Stimulation (TMS) is a non-invasive technique for brain stimulation.
Repetitive TMS (rTMS) over the medial Prefrontal Cortex (mPFC), Broadman Area 10
(BA10) may stimulate transynaptically perigenual Anterior Cingulate Cortex (pACC,
BA 33), insula, amigdala, hypothalamus and connected branches of the Autonomic Nervous
System (ANS) involved in stressorevoked cardiovascular reactivity. Stressors are
associated with an increase in sympathetic cardiac
control, a decrease in parasympathetic control, or both, and, consequently,
an increase in systolic/stroke volume, total vascular impedance/resistance and heart
rate, a decrease of baroreflex sensitivity, i.e.,
an increase in blood pressure/arterial tension. Objectives and Aims: The present
work aims, using TMS and accordingly to Gianaros modeling, based on functional neuroimaging
studies and previous neuroanatomical data from animal models, to probe the connectivity
of brain systems involved in stressor-evoked cardiovascular reactivity and to explore
TMS potential as a tool for detection and stratification of individual differences
concerning this reactivity and hemorreological risk factors correlated with the
development of Coronary Heart Disease (CHD). Methods: Both subjects, a 52 years old male and a 40 years old female
with previous increased Low Frequency (LF)/High Frequency (HF) Heart Rate Variability
(HRV) ratios (respectively, 4.209/3.028)
without decompensated cardiorespiratory symptoms, gave informed consent,
and ethico-legal issues have been observed. Electroencephalographic (EEG) monitoring
has been performed for safety purposes. Immediately after administration, over the
mPFC, of 15 pulses of rTMS, during 60 second, with an inductive electrical current,
at the stimulating coil, of 85.9 Ampère per μsecond and 66 Ampère per μsecond, respectively, for male and female
subjects (a “figure-of-eight” coil and magnetic stimulator MagLite, Dantec/Medtronic,
have been used), HRV spectrum analysis (cStress software) has been performed (during
5 minutes, in supine position). Results: In both subjects, LF power, HF power and
LF/HF ratio results, before and after rTMS administration, pointed towards sympathetic
attenuation and parasympathetic augmentation (respectively, in male/female subject:
decreased LF power—65.1 nu/69.3 nu, before rTMS; 56.1 nu/41.6 nu, after rTMS; increased
HF power—15.5 nu/22.9 nu, before rTMS; 30.9 nu/45.5 nu, after rTMS). Conclusions:
In this preliminary investigation, the existence of a link between “mind” and heart’s
function has been put in evidence, through a reversible “virtual” lesion, of brain
systems involved in cardiovascular control, caused by TMS. Repetitive TMS over mPFC
decreased brain function involved in stressorevoked cardiovascular reactivity, suggesting
the importance of TMS in the management of stress-related cardiovascular disorders.