Download A view of cardio-cortical connections

JACC Vol . 14, No .
August 1989 :5 8-9
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EDITORIALS
A View of Cardio-Cortical Connections*
JOHN JAY KORIATH, PHD
Tempe, Arizona
In recent decades, a growing body of research that focuses
on the interrelated dynamics of complex systems has surfaced in many disciplines (1, ) . One aspect of such research
that may be of particular interest to cardiologists involves
the integration of the cardiovascular system with the autonomic and central nervous systems . The findings suggest
that an exclusively "top down" view of the brain controlling
the body may need reshaping in light of evidence that
activity of the heart modulates potentials of the brain .
The Lacey hypothesis . For nearly a quarter of a century,
John and Beatrice Lacey reported cardiac cycle timing
effects during a variety of behavioral situations (3) . Their
observations led to a hypothesis concerning the role of
cardiovascular afferent fibers . The following scenario serves
to clarify the hypothesis . After each ventricular contraction,
the systolic bolus of blood travels through the arterial
system . Along its journey through the thoracic and neck
region it encounters the spray-type nerve endings of pressure-sensitive baroreceptors . Baroreceptors are in particularly high density in the arterial walls of the carotid sinus .
Stimulated by the systolic bolus after each beat of the heart,
baroreceptor discharge results in relay of information by
way of Hering's nerve and the glossopharyngeal nerve to the
vasomotor center in the lower third of the pons and upper
two thirds of the medulla . This afferent feedback loop is well
established and serves the homeostatic function of reducing
daily variation in arterial blood pressure (4) . According to
the Laceys, baroreceptor activity is not only relayed to the
vasomotor center in the brainstem, but to higher brain
centers as well . They suggest that cortical activity is briefly
inhibited as a result of baroreceptor activity .
Animal studies provide indirect support for this notion .
Stimulation of baroreceptors in the carotid sinus leads to
decreased motor activity and prolonged sleep (5), shifts in
electrocortical activity from low voltage fast waves to high
voltage slow waves (6) and depression of the activity of
pyramidal tract cells in the motor cortex (7) . Some early
*Editorials published in Journal of the American College of Cardiology
reflect the views of the authors and do not necessarily represent the views of
JACC or the American College of Cardiology .
From the Department of Psychology, Arizona State University, Tempe,
Arizona .
Address for reprints : John Jay Koriath, Department of Psychology,
Arizona State University, Tempe, Arizona 85 87 .
©1989 by the American College of Cardiology
clinical reports have suggested that brain activity in humans
varies in relation to cardiovascular events . Average evoked
brain potentials change as heart rate (8) and carotid pressure
fluctuate (9) .
Cardio-cortical integration . For the last several years, my
research in the Lindholm Laboratory at Arizona State University has focused on the role that cardiovascular events
play in modulating human brain activity . We have applied a
strategy that compares electroencephalographic (EEG) activity time-locked to cardiovascular events with EEG activity sampled at random times in the same cardiac cycles . The
procedure is as follows : The EEG is recorded ; simultaneously, two cardiovascular measures are taken, the electrocardiogram (ECG) and the pulse pressure waveform . The
pulse pressure waveform is transduced from the ear lobe by
photoplethysmography . By utilizing these two recordings to
measure the amount of time that elapses between ventricular
contraction and the arrival of the systolic bolus of blood at
the ear lobe, an assessment that reflects beat to beat changes
in both heart rate and blood pressure can be obtained .
Through computer analysis, a waveform that we call
"cardiac EEG" is formed . It is generated by taking EEG
samples locked in time to the arrival of the systolic bolus of
blood at the ear . Samples from consecutive cardiac cycles
are averaged to form the cardiac EEG waveform . In similar
fashion a control EEG waveform is obtained by averaging
EEG samples taken at randomly selected times in the same
cardiac cycles .
Statistical analysis indicates that the two waveforms
differ significantly (10) . The "cardiac EEG" waveform,
which reflects the systematic influence of heart rate, blood
pressure and baroreceptor discharge, comprises slower frequencies than those of the control EEG waveform . These
findings support the Lacey hypothesis .
In further laboratory investigations we have varied heart
rate and blood pressure levels by having subjects pedal a
bicycle ergometer at varying work loads . With increases in
mean heart rate, the "cardiac EEG" waveform displays
power increases in the slow frequency components (11) .
These findings provide preliminary evidence to suggest that
factors that initiate change in heart rate and blood pressure
also play a role in modulating electrical potentials of the
higher brain centers . These factors may include structural
and functional aberrations of the cardiovascular system or
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JACC Vol . 14, No .
August 1989:5 8-9
interventions of a pharmacologic, cognitive or emotional
nature . The implication is that information relayed by the
cardiovascular afferents not only serves to maintain homeostasis of the cardiovascular system, but also plays a role in
regulating a more global homeostasis of the human organism .
Clinical implications . For the clinician, new considerations emerge . Do patients with elevated heart rate or blood
pressure, or both, seem susceptible to depression or cognitive deficits during the period when baroreceptors are adapting to changes in cardiodynamics? Is the patient who reports
mood and cognitive changes that accompany the use of
drugs that modify heart rate and blood pressure experiencing
a pharmacologic side effect or adaptive changes in a more
global homeostasis? What reassessments of treatment protocol are necessitated by patient-initiated changes in life
style habits known to influence cardiodynamics, such as
nutrition, exercise and coping style? What systemic changes
beyond cardiovascular homeostasis result from procedures
that employ the severing of cardiovascular afferent fibers?
Although fundamentally sound research highlights these
concerns, substantive answers remain to be generated . The
process requires a generation of research studies that employ a multidisciplinary focus and can be facilitated by the
astute observations of experienced clinicians who collaborate with researchers .
Conceptual direction . The contribution that integrative
cardiovascular research makes to understanding the global
dynamics of the human organism suggests it may be time to
expand our working concept of cardiovascular fitness . A
cardiovascular system whose events play a role in shaping
brain activity fits in the larger context of findings emerging
from the fields of psychoneuroimmunology and psychobiology (1 ) . These fields have identified a growing array of
neurotransmitters that not only serve to carry information
from neuron to neuron in the brain, but also function as
messenger molecules circulating in the bloodstream . Many
of these neuropeptides are produced by the white blood
KORIATH
EDITORIAL
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cells, and these cells have receptor and secretor sites for the
molecules on their membrane surface . In such a context,
cardiovascular fitness seems to have much more extensive
implications than the efficient and functional transport of
oxygen and nutrients . The cardiovascular system is an
information transport system as well .
As cardiovascular caretakers we are asked to assume
guardianship of humankind's most tangible representation of
the centuries-old "stream of consciousness ." Whereas
many dimensions of this task remain to be explained in the
1st century, we may be prudent to consider the issues now .
The upcoming decade will lead us not only into a new
century, but also into a new millenium of evolution for the
human organism .
References
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55 :46-57.
. Gleick J . Chaos : making of a new science . New York : Viking, 1987 :3-5 .
3 . Lacey J, Lacey B . Two way communication between the heart and the
brain . Am Psychol 1978 ;33 :99-113 .
4 . Guyton A . Human Physiology and Mechanisms of Disease . Philadelphia :
WB Saunders, 198 :173 .
5 . Koch E . Die Irradiation der pressoreceptorischen Kreislaufrelexe . Klin
Wochenschr193 ;11 : 55-7.
6 . Bonvallet M, Dell P, Hiebel G . Tonus sympathique et activite electrique
corticale . Electroencephalogr Clin Neurophysiol 1954 ;6 :119-44 .
7 . Coleridge H, Coleridge J, Rosenthal F . Prolonged inactivation of cortical
pyramidal tract neurons in cats by distension of the carotid sinus . J
Physiol (Lond) 1976; 56 :635-49.
8 . Walker B, Sandman C . Relationship of heart rate on the visual evoked
potential . J Comp Physiol Psychol 1979 ;93 :717- 9 .
9 . Walker B, Sandman C . Visual evoked potentials change as heart and
carotid pressure change . Psychophysiology 198 ;19:5 0-7 .
10 . Koriath J, Lindholm E. Cardiac related cortical inhibition during a fixed
foreperiod reaction time task . Int J Psychophysiol 1986 ;4 :183-95 .
11 . Koriath J, Lindholm E, Landers D . Cardiac related cortical activity
during variations in mean heart rate . Int J Psychophysiol 1987 ;5 : 89-99.
1 . Rossi E . The Psychobiology of Mind-Body Healing . New York : Norton,
1986 :1 5-8 .