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JACC Vol . 14, No . August 1989 :5 8-9 5 8 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 0735-10971891$3 .50 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 5 9 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 1 . Crutchfield J, Farmer J, Packard N, Shaw R . Chaos . Sci Am 1986 ; 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 .