Heart and Brain: A Complex Relationship

Winklewski PJ* and Frydrychowski AF

Institute of Human Physiology, Medical University of Gdansk, Poland

*Corresponding author: Pawel J. Winklewski,Institute of Human Physiology, Medical University of Gdansk, Tuwima Str. 15, 80-210 Gdansk, Poland

Received: April 24, 2015; Accepted: May 05, 2015; Published: May 07, 2015

Editorial

Macey and colleagues have shown that heart rate (HR) responses are blunted and delayed in obstructive sleep apnoea (OSA) subjects. The blunted HR responses were observed during handgrip and cold test, which require integration of cold temperature, pain and proprioceptive input, and are representative for everyday activities. Such delay indicative of impaired autonomic processing in medulla and thalamic regions is consistent with the known structural brain changes in OSA [1]. Therefore, the brain impairment in OSA has an direct impact on cardiac function. However, how does heart affect brain in OSA? To respond to this question we need to summarize the most recent physiological research advances in this area.

For the first time long term brain microcirculation adaptation to decreased cardiac output has been reported in chronic left ventricle failure by Georgiadis et al [2]. Georgiadis et al. [2] found a significant relationship between the decline in left ventricle ejection fraction (LVEF) and the reduction in cerebrovascular reactivity. Ogoh et al. [3] demonstrated in an elegant study that blood flow velocity in the middle cerebral artery response to a rapid decline in systemic BP was highly related to unloading of the arterial baroreceptors, which suggests cardiac output involvement in the regulation of cerebral blood flow (CBF). One year later, our team reported positive correlations between changes in pial artery pulsation and LVEF, and between the systolic–diastolic cerebral blood volume fraction and LVEF in an animal model with stable blood pressure (BP) [4].

Introduction of wavelet transform analysis to cardiovascular research opened new area to investigate the cardiac contribution to cerebral perfusion [5,6]. Li et al. [7] reported a negative correlation between cerebral oxygenation and CBF velocity at respiratory and cardiac frequencies. Cui et al. [8] used wavelet coherence analysis to assess the relationship between spontaneous oscillations in changes in BP and the cerebral tissue oxyhemoglobin concentration (HbO2); this analysis demonstrated a significant increase in wavelet coherence in elderly compared to young subjects at frequencies of 0.4–2.0 Hz, while no change in wavelet phase coherence was found at the same frequencies. Cui et al. [8] argued that increased sympathetic drive and diminished heart rate variability may results in increased cardiac contribution to spontaneous BP/HbO2 oscillations in the elderly.

Very recent data coming from our lab suggest that cardiac contribution to the BP pial artery pulsation oscillations diminish during apnoea in healthy subjects [9]. In this study we used novel methodology that allows for non-invasive assessment of pial artery pulsation in humans [10]. We considered two potential explanations for our results. During apnea, the influence of the autonomic nervous system on the heart is characterized by co-activation of both branches of the autonomic nervous system and an increase in both sympathetic and parasympathetic outflow to the heart [11,12]. Increased parasympathetic outflow to the heart may result in decreased cardiac activity.

Alternatively, apnoea results in hypercapnia, hypoxia and augmented sympathetic activation, which in turn increases BP contribution to CBF [13,14]. Furthermore, hypercapnia dilates cerebral arteries [15-17] and can alter the pulse wave transmission characteristics of the cerebral vasculature by altering their Windkessel properties [17]. Progressive carbon dioxide retention results in the increase in intracranial pressure [18,19]. Increased intracranial pressure may, in turn, impair jugular outflow and does not allow for dampening the pulsation energy and actually exaggerates the pulsatile flow [20,21]. As a consequence of all factors mentioned above the relative cardiac contribution to BP cc-TQ oscillations may decrease. Interestingly, HR, together with carbon dioxide and BP, significantly modulate intracranial pressure [22].

Taken together, there is an increasing evidence that heart directly influences cerebral perfusion, brain microcirculation and intracranial pressure. Briefly discussed possibility of noninvasive assessment of pial artery function and intracranial pressure seems to be very well suited for OSA research. Recent advancement in physics, in particular the development of theory of chronotaxic systems [23,24], when applied to cardiovascular research, will most likely further increase our understanding about CBF control in human. The above described findings, coming mostly from young, healthy volunteers cannot be directly translated into OSA pathophysiology. Nevertheless, they may open new era in OSA research in the very near future.

Heart and Brain: A Complex Relationship

Editorial

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