Brain-heart Connection Research Articles

Evaluating the Effects of Different Cognitive Tasks on Autonomic Nervous System Responses: Implementation of a High-Precision, Low-Cost Complementary Method.

We developed a low-cost, user-friendly complementary research tool to evaluate autonomic nervous system (ANS) activity at varying levels of cognitive workload. This was achieved using visual stimuli as cognitive tasks, administered through a specially designed computer-based test battery. To assess sympathetic stress responses, skin conductance response (SCR) was measured, and electrocardiograms (ECG) were recorded to evaluate heart rate variability (HRV), an indicator of cardiac vagal tone. Twenty-five healthy adults participated in the study. SCR and ECG recordings were made during both tonic and phasic phases using a computer-based system designed for visual stimuli. Participants performed a button-pressing task upon seeing the target stimulus, and the relationship between reaction time (RT) and cognitive load was evaluated. Analysis of the data showed higher skin conductance levels (SCLs) during tasks compared to baseline, indicating successful elicitation of sympathetic responses. RTs differed significantly between simple and cognitive tasks, increasing with mental load. Additionally, significant changes in vagally mediated HRV parameters during tasks compared to baseline highlighted the impact of cognitive load on the parasympathetic branch of the ANS, thereby influencing the brain-heart connection. Our findings indicate that the developed research tool can successfully induce cognitive load, significantly affecting SCL, RTs, and HRV. This validates the tool's effectiveness in evaluating ANS responses to cognitive tasks.

Unveiling the heart's silent whisperer: study of stress and the brain-heart connection in Europe.

Unveiling the heart's silent whisperer: study of stress and the brain-heart connection in Europe.

Relationship between Alzheimer dementia and QT interval: A meta-analysis.

While the link between aging and mortality from dementia is widely appreciated, the mechanism is not clear. The objective of this study was to determine whether there is a direct relationship between Alzheimer dementia (AD) and the QT interval, because the latter has been related to cardiac mortality. A systematic review and meta-analysis were conducted after a Medline and EMBASE search using terms "Alzheimer disease or Dementia AND QT interval, QT dispersion or cardiac repolarization." Four studies with control groups were identified. There were significant differences in QT interval between individuals with AD vs individuals without dementia (controls) (odds ratio (OR)1.665 [random effects model] and 1.879 [fixed effect model]) (p < 0.001). There were significant differences in QT interval between individuals with AD vs individuals with mild cognitive impairment (MCI) (OR 1.760 [random effects] and 1.810 [fixed effect]) (p < 0.001). A significant (p <0.001) correlation exists between the QTc and the Mini-Mental State Exam (MMSE), a test of cognitive function. Two studies examined QT variability (the difference between the longest and shortest QT interval on a 12 lead ECG); the OR for QT variability AD vs MCI was 3.858 [random effects model] and 3.712 [fixed effects model] (p < 0.001). When compared to the control group, the OR for QT dispersion in AD was 6.358 [random effects model] or 5.143 ( P< 0.001) [fixed effects model]. A qualitative analysis of the data raised questions about paucity of data defining the nature of the control groups, the pathophysiologic mechanism, and the uniform use of a poor QT heart rate correction factor. The longer QT in AD, greater QT variability in AD, and the direct relationship between QT interval and AD severity supports a brain-heart connection in AD that might be fundamental to aging-induced AD and mortality. Issues with defining the control group, limited number of studies, conflicting data in population studies, and the lack of a strong electrophysiological basis underscore the need for additional research in this field.

A framework for quantifying the coupling between brain connectivity and heartbeat dynamics: Insights into the disrupted network physiology in Parkinson's disease.

Parkinson's disease (PD) often shows disrupted brain connectivity and autonomic dysfunctions, progressing alongside with motor and cognitive decline. Recently, PD has been linked to a reduced sensitivity to cardiac inputs, that is, cardiac interoception. Altogether, those signs suggest that PD causes an altered brain-heart connection whose mechanisms remain unclear. Our study aimed to explore the large-scale network disruptions and the neurophysiology of disrupted interoceptive mechanisms in PD. We focused on examining the alterations in brain-heart coupling in PD and their potential connection to motor symptoms. We developed a proof-of-concept method to quantify relationships between the co-fluctuations of brain connectivity and cardiac sympathetic and parasympathetic activities. We quantified the brain-heart couplings from electroencephalogram and electrocardiogram recordings from PD patients on and off dopaminergic medication, as well as in healthy individuals at rest. Our results show that the couplings of fluctuating alpha and gamma connectivity with cardiac sympathetic dynamics are reduced in PD patients, as compared to healthy individuals. Furthermore, we show that PD patients under dopamine medication recover part of the brain-heart coupling, in proportion with the reduced motor symptoms. Our proposal offers a promising approach to unveil the physiopathology of PD and promoting the development of new evaluation methods for the early stages of the disease.

THE AGING BRAIN: A NEUROVISCERAL INTEGRATION PERSPECTIVE

Abstract Healthy aging is associated with significant changes in both the brain and the heart. The changes between these, the two most important organs of the body, are linked via the vagus nerve. Using a model of Neurovisceral Integration I will describe how autonomic imbalance and decreased parasympathetic tone in particular may be the final common pathway linking negative affective states and conditions to ill health. The central nervous system network that regulates autonomic balance is closely related and partially overlaps with networks serving executive, social, affective, cognitive, and motivated behavior. This inhibitory cortico-subcortical circuit may structurally as well as functionally, link psychological processes with health-related physiology. When the prefrontal cortex is taken “offline” for whatever reason, parasympathetic inhibitory action is withdrawn and a relative sympathetic dominance associated with disinhibited defensive circuits is released, which can be pathogenic when sustained for long periods. This state is indicated by low heart rate variability (HRV), which is a marker for low parasympathetic activation and prefrontal hypoactivity. In this presentation, I examine the normative changes with aging and the effect that stress may have on how the brain–heart connection changes with age. I will present data linking peripheral physiology to brain structure and function. I conclude by noting that significant sex and ethnic differences exist but that future studies are needed to more fully explicate how they may influence the aging brain and its association with the cardiovascular system.

Understanding the brain-heart connection through a case of wounded glioma syndrome

Understanding the brain-heart connection through a case of wounded glioma syndrome

Research on atrial fibrillation mechanisms and prediction of therapeutic prospects: focus on the autonomic nervous system upstream pathways.

Atrial fibrillation (AF) is the most common clinical arrhythmia disorder. It can easily lead to complications such as thromboembolism, palpitations, dizziness, angina, heart failure, and stroke. The disability and mortality rates associated with AF are extremely high, significantly affecting the quality of life and work of patients. With the deepening of research into the brain-heart connection, the link between AF and stroke has become increasingly evident. AF is now categorized as either Known Atrial Fibrillation (KAF) or Atrial Fibrillation Detected After Stroke (AFDAS), with stroke as the baseline. This article, through a literature review, briefly summarizes the current pathogenesis of KAF and AFDAS, as well as the status of their clinical pharmacological and non-pharmacological treatments. It has been found that the existing treatments for KAF and AFDAS have limited efficacy and are often associated with significant adverse reactions and a risk of recurrence. Moreover, most drugs and treatment methods tend to focus on a single mechanism pathway. For example, drugs targeting ion channels primarily modulate ion channels and have relatively limited impact on other pathways. This limitation underscores the need to break away from the "one disease, one target, one drug/measurement" dogma for the development of innovative treatments, promoting both drug and non-drug therapies and significantly improving the quality of clinical treatment. With the increasing refinement of the overall mechanisms of KAF and AFDAS, a deeper exploration of physiological pathology, and comprehensive research on the brain-heart relationship, it is imperative to shift from long-term symptom management to more precise and optimized treatment methods that are effective for almost all patients. We anticipate that drugs or non-drug therapies targeting the central nervous system and upstream pathways can guide the simultaneous treatment of multiple downstream pathways in AF, thereby becoming a new breakthrough in AF treatment research.

Increased neurocardiological interplay after mindfulness meditation: a brain oscillation-based approach.

Brain oscillations facilitate interaction within the brain network and between the brain and heart activities, and the alpha wave, as a prominent brain oscillation, plays a major role in these coherent activities. We hypothesize that mindfully breathing can make the brain and heart activities more coherent in terms of increased connectivity between the electroencephalogram (EEG) and electrocardiogram (ECG) signals. Eleven participants (28-52 years) attended 8 weeks of Mindfulness Based Stress Reduction (MBSR) training. EEG and ECG data of two states of mindful breathing and rest, both eye-closed, were recorded before and after the training. EEGLAB was used to analyze the alpha band (8-12 Hz) power, alpha peak frequency (APF), peak power and coherence. FMRIB toolbox was used to extract the ECG data. Heart coherence (HC) and heartbeat evoked potential (HEP) were calculated for further correlation analysis. After 8 weeks of MBSR training, the correlation between APF and HC increased significantly in the middle frontal region and bilateral temporal regions. The correlation between alpha coherence and heart coherence had similar changes, while alpha peak power did not reflect such changes. In contrast, spectrum analysis alone did not show difference before and after MBSR training. The brain works in rhythmic oscillation, and this rhythmic connection becomes more coherent with cardiac activity after 8 weeks of MBSR training. Individual APF is relatively stable and its interplay with cardiac activity may be a more sensitive index than power spectrum by monitoring the brain-heart connection. This preliminary study has important implications for the neuroscientific measurement of meditative practice.

Neurogenic Cardiac Outcome in Patients with Acute Ischemic Stroke: The Brain-Heart Connection (S35.005)

Neurogenic Cardiac Outcome in Patients with Acute Ischemic Stroke: The Brain-Heart Connection (S35.005)

The Association Between Standard Electrocardiography and Cerebral Small Vessel Disease in a Memory Clinic Study.

P-wave terminal force in lead V1 (PTFV1) on electrocardiography has been associated with atrial fibrillation and ischemic stroke. To investigate whether PTFV1 is associated with cerebral small vessel disease (CSVD) markers and etiological subtypes of cognitive impairment and dementia. Participants were recruited from ongoing memory clinic study between August 2010 to January 2019. All participants underwent physical and medical evaluation along with an electrocardiography and 3 T brain magnetic resonance imaging. Participants were classified as no cognitive impairment, cognitive impairment no dementia, vascular cognitive impairment no dementia, and dementia subtypes (Alzheimer's disease and vascular dementia). Elevated PTFV1 was defined as > 4,000μV×ms and measured manually on ECG. Of 408 participants, 78 (19.1%) had elevated PTFV1 (37 women [47%]; mean [SD] age, 73.8 [7.2] years). The participants with elevated PTFV1 had higher burden of lacunes, cerebral microbleeds (CMB), and cortical microinfarcts. As for the CMB location, persons with strictly deep CMB and mixed CMB had significantly higher PTFV1 than those with no CMB (p = 0.005, p = 0.007). Regardless of adjustment for cardiovascular risk factors and/or heart diseases, elevated PTFV1 was significantly associated with presence of CMB (odds ratio, 2.26; 95% CI,1.33-3.91). Elevated PTFV1 was associated with CSVD, especially deep CMB. PTFV1 in vascular dementia was also higher compared to Alzheimer's disease. Thus, PTFV1 might be a potential surrogate marker of brain-heart connection and vascular brain damage.

Brain, heart, and sudden death.

During the past 30 years, rate of coronary artery disease (CAD), as the main cause of sudden death (SD), has decreased more than rate of SD. Likewise, cause of SD remains elusive in not a trivial portion of its victims. One possible reason is attention to only one organ, the heart, as the cause of SD. In fact, SD literature focuses more on the heart, less on the brain, and seldom on both. A change is required. In this paper, we first review the pathological findings seen in heart autopsies of SD victims after psychological stressors such as physical assault victims without internal injuries. Then, we summarize new studies investigating brain areas, like the insula, whose malfunctions and injuries are related to SD. Next, we review prototypes of neurological diseases and psychological stressors associated with SD and look at heart failure (HF)-related SD providing evidence for the brain-heart connection. Finally, we propose a new look at SD risk factors considering both brain and heart in their association with SD, and review strategies for prevention of SD from this perspective.

Sex Differences in the Co-Occurrence of PTSD and Cardiovascular Disease

Posttraumatic stress disorder (PTSD) is a highly impairing psychiatric condition, and women are twice as likely as men to receive a diagnosis. It is thought that chronic arousal and physiological stress place individuals with PTSD at greater risk for cardiovascular disease (CVD). Sex differences in CVD are also well established. For example, premenopausal women have lower CVD risk compared to men, and this is partly explained by higher levels of estradiol in premenopausal women. Estradiol is considered to be a protective factor against PTSD as well; therefore, it is important to understand the role of sex hormones in PTSD and CVD, including whether or not there is shared impact of sex hormones on the co-occurrence of these diseases. In this review, we discuss sex differences in PTSD and CVD, as well as the brain-heart connection in the PTSD-CVD link and current treatment approaches, considering sex as a biological variable. [ Psychiatr Ann . 2022;52(1):26–30.]

Stress and aging: A neurovisceral integration perspective.

Darwin emphasized the intimate relationship between the brain and the heart over 150years ago. Healthy aging is associated with significant changes in both the brain and the heart. The changes between these, the two most important organs of the body, are linked via the vagus nerve. In this review, we examine the normative changes with aging and the effect that stress may have on how the brain-heart connection changes with age. We provide a framework based on the concept of neurovisceral integration and propose that stress regulation is emotion regulation. As such, studies that have investigated emotion regulation may yield insights into successful stress regulation that helps protect people from age-related decline. In addition, interventions that improve brain health also improve heart health and vice versa. We conclude by noting that significant sex and ethnic differences exist but that future studies are needed to more fully explicate how they may moderate the associations between stress and aging.

Blood Pressure Correlates Asymmetrically with Neuropeptidase Activities of the Left and Right Frontal Cortices

It was suggested that the brain-heart connection is asymmetrically organized. However, evidence connecting neurochemical factors from each brain hemisphere with changes in cardio-vascular functions have not yet been reported. In order to analyze potential asymmetrical connections between brain neurochemical factors with cardio-vascular functions, we studied the level of correlations between the left and right frontal cortex (FC) soluble (Sol) and membrane-bound (MB) neuropeptide-degrading enzymes alanyl (AlaAP), cystinyl (CysAP), and glutamyl (GluAP) aminopeptidase activities, involved among others in the metabolism of angiotensins, with heart rate (HR), systolic (SBP), and diastolic (DBP) blood pressure, in rats treated or not with hypotensive or hypertensive drugs such as captopril, propranolol or L-NAME. The present study suggests the existence of a bidirectional asymmetrical connection between these brain neuropeptidases and cardio-vascular functions. Specifically, depending on treatment, in control group, Sol AlaAP from the left FC correlates negatively with SBP and DBP. In captopril-treated animals, MB CysAP and MB GluAP from the right FC correlate negatively with HR. In L-NAME treated rats, Sol CysAP from the right FC correlates negatively with DBP. No significant correlations were observed in the propranolol group. Considering together all the values obtained from the left or the right cortex of the four groups regardless of drug treatment, the results demonstrated significant negative correlations between these neuropeptidase activities, mainly from the left frontal cortex, with the levels of systolic and diastolic blood pressure. Remarkably, these findings contrast drastically with previously reported results indicating significant positive correlations between the left frontal cortex with other peripheral functions such as water intake and diuresis. Both results represent noteworthy information that strongly supports the concept of a bidirectional asymmetric organization of neurovisceral integration involving left and right brain neurochemical processes with peripheral physiological functions, most probably mediated by the autonomic nervous system. Overall, the present results suggest that cognitive functions involving the frontal cortex may be asymmetrically connected with peripheral physiological processes, and vice versa.

The Microbiota-Gut-Brain Axis-Heart Shunt Part II: Prosaic Foods and the Brain-Heart Connection in Alzheimer Disease.

There is a strong cerebrovascular component to brain aging, Alzheimer disease, and vascular dementia. Foods, common drugs, and the polyphenolic compounds contained in wine modulate health both directly and through the gut microbiota. This observation and novel findings centered on nutrition, biochemistry, and metabolism, as well as the newer insights we gain into the microbiota-gut-brain axis, now lead us to propose a shunt to this classic triad, which involves the heart and cerebrovascular systems. The French paradox and prosaic foods, as they relate to the microbiota-gut-brain axis and neurodegenerative diseases, are discussed in this manuscript, which is the second part of a two-part series of concept papers addressing the notion that the microbiota and host liver metabolism all play roles in brain and heart health.

The Brain-Heart Connection in Takotsubo Syndrome: The Central Nervous System, Sympathetic Nervous System, and Catecholamine Overload.

Takotsubo syndrome (TTS), also known as stress cardiomyopathy, is a type of acute heart failure syndrome triggered by intense psychological or physiological stress. TTS typically manifests as acute chest pain, dyspnea or syncope that mimics an acute myocardial infarction but does not involve coronary artery obstruction. The current understanding of the pathogenesis of TTS suggests that sympathetic nervous system (SNS) activation plays a central role. Specifically, stress can activate the SNS and lead to the over-release of catecholamine, which have toxic effects on myocardial tissue when present at excessive levels. However, the brain changes associated with TTS and the connection between the brain and the heart in patients with this disease remain unclear. In recent years, several published reports have revealed the role of this brain-heart connection in the pathogenesis of TTS. This review summarizes recent studies regarding SNS activation, catecholamine overload, and the brain-heart connection in patients with TTS from both pathophysiological and mechanistic aspects.

Is there a link between depression, neurochemical asymmetry and cardiovascular function?

Although at present depression is one of the most disabling disorders in our social environment, the understanding of its pathogenesis and the resources for its treatment are still unsatisfactory. The importance of brain asymmetry in the pathogenesis of disorders in brain function, including mood disorders such as depression, is a highly unexplored, sometimes underrated, and even ignored topic. It is important to note that the basal and pathological functional lateralization must have an underlying neurochemical substrate. It is also necessary to indicate that the brain asymmetry extends to a neurovisceral integration whose behavior may also be lateralized. One of the most studied axis from the functional point of view is the brain-heart connection, in whose operation there are observations that suggest an asymmetric behavior in basal conditions that is modified by central and peripheral changes, as well as by pharmacological treatments. There are evidences that connect cardiovascular function, neurochemical asymmetries, and depression. A deep understanding of the bilateral behavior of the brain following pathophysiological changes in blood pressure as well as pharmacologically induced, can provide us with therapeutic suggestions for the treatment of depression. In this article, we analyze remarkable results of some representative selected contributions, with which we discuss our proposal on the relationship between hypertension, depression and neurochemical asymmetry.

Neurocardiology: the brain-heart connection in Takotsubo syndrome.

Neurocardiology: the brain-heart connection in Takotsubo syndrome.

Surge of corticocardiac coupling in SHRSP rats exposed to forebrain cerebral ischemia.

Sudden death is an important but underrecognized consequence of stroke. Acute stroke can disturb central control of autonomic function and result in cardiac dysfunction and sudden death. Previous study showed that bilateral common carotid artery ligation (BCCAL) in the spontaneously hypertensive stroke-prone rat strain (SHRSP) is a well-established model for forebrain ischemic sudden death. This study aims to investigate the temporal dynamic changes in electrical activities of the brain and heart and functional interactions between the two vital organs following forebrain ischemia. EEG and ECG signals were simultaneously collected from nine SHRSP and eight Wistar-Kyoto (WKY) rats. RR interval was analyzed to investigate the cardiac response to brain ischemia. EEG power and coherence (CCoh) analysis were conducted to study the cortical response. Corticocardiac coherence (CCCoh) and directional connectivity (CCCon) were analyzed to determine brain-heart connection. Heart rate variability (HRV) was analyzed to evaluate autonomic functionality. BCCAL resulted in 100% mortality in SHRSP within 14 h, whereas no mortality was observed in WKY rats. The functionality of both the brain and the heart were significantly altered in SHRSP compared with WKY rats after BCCAL. SHRSP, but not WKY rats, exhibited intermittent surge of CCCoh, which paralleled the elevated CCCon and reduced HRV, following the onset of ischemia until sudden death. Elevated brain-heart coupling invariably associated with the disruption of the autonomic nervous system and the risk of sudden death. This study may improve our understanding of the mechanism of forebrain ischemia-induced sudden death. NEW & NOTEWORTHY This study demonstrates a marked surge of corticocardiac coupling in rats dying from focal cerebral ischemia, consistent with our earlier data in rats exposed to fatal asphyxia. Since the bidirectional electrical signal coupling (corticocardiac coherence) and communication (corticocardiac connectivity) between the brain and the heart are only identified in dying animals, they could be used as potential biomarkers to predict the risk of sudden death.

Association of prolonged QTc interval with Takotsubo cardiomyopathy: A neurocardiac syndrome inside the mystery of the insula of Reil.

The Takotsubo cardiomyopathy is often considered autochthonous to the heart, although the primary problem may be not in the heart muscle itself. Instead, similar to several Takotsubo-like cardiac pathologies seen in acute neurological diseases, it may reflect the capacity of the nervous system to injure the heart. Persuasive evidence exists that shocking emotional stress promotes direct heart injuries. Moreover, clinical and laboratory research shows that cardiac structural damage can occur in the presence of a normal heart, especially in the context of seizures, stroke, and traumatic brain injury or under conditions of psychological stress. The aim of this review is to summarize the clinical implications of these observations, several of which focus on the pivotal role of the insula of Reil in the brain-heart connection, to unravel the mystery of Takotsubo cardiomyopathy pathogenesis.