Brain, behavior, mental stress, and the neurocardiac interaction (original) (raw)
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Heart-brain interactions in mental stress-induced myocardial ischemia
Current Cardiology Reports, 2009
Myocardial ischemia, which results from emotional provocation, occurs in as many as 30-50% of patients with CAD during the discourse of their daily lives. This emotionally provoked or mental stress ischemia is associated with the poor prognosis, with emerging treatment strategies. This chapter will outline the conceptual constructs which support the pathophysiologic underpinnings, and biobehavioral aspects associated with this mental stress ischemia. We will review a biobehavioral model where cognitive stress is transduced in the brain. The response of the brain to psychosocial stress is a highly sophisticated and integrated process by which sensory inputs are evaluated and appraised for its importance in relation to previous experience and current goals. The biologic consequences of such stress transduced in the CNS has its effect upon the cardiovascular flow and function through changes in autonomic balance, which result in various biologic processes that culminate in the perturbation of flow and function of the heart. NIH Public Access
Neural and cardiovascular responses to emotional stress in humans
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2008
Sympathetic neural responses to mental stress are well documented but controversial, whereas sympathetic neural responses to emotional stress are unknown. The purpose of this study was to investigate neural and cardiovascular responses to emotional stress evoked by negative pictures and reexamine the relationship between muscle sympathetic nerve activity (MSNA) and perceived stress. Mean arterial pressure (MAP), heart rate (HR), MSNA, and perceived stress levels were recorded in 18 men during three randomized trials: 1) neutral pictures, 2) negative pictures, and 3) mental stress. MAP and HR increased during mental stress (Δ14 ± 2 mmHg and Δ15 ± 2 beats/min, P < 0.001) but did not change during viewing of negative or neutral pictures. MSNA did not change during viewing of neutral (Δ1 ± 1 burst/min, n = 16) or negative (Δ0 ± 1 burst/min, n = 16) pictures or during mental stress (Δ1 ± 2 burst/min, n = 13). Perceived stress levels were higher during mental stress (3 ± 0 arbitrary un...
Reflections on the past four decades of mental stress research in autonomic cardiology
Clinical Autonomic Research, 2021
This commentary with some reflections and summary of my experience in the field of mental stress research is my contribution to celebrate the thirtieth anniversary of Clinical Autonomic Research, a journal that, over the past years, has become the benchmark publication for all those interested in the autonomic nervous system, regardless of their primary medical specialty, which, in my case, is cardiology. In 1977, after 4 years of postgraduate research and clinical training with Prof. Stevo Julius in the Hypertension Division of the University of Michigan Medical Center, I returned to the Baker Medical Research Institute and the Alfred Hospital in Melbourne, Australia, where I worked as a clinical cardiologist and established a cardiovascular neuroscience laboratory. In my early clinical practice in Melbourne, I remember being struck by how the presentation of patients with myocardial infarction or ventricular arrhythmias was sometimes precipitated by emotional turmoil. I saw patients in whom a heart attack had been triggered by armed robbery, assaults, and even an owner's racehorse winning by a "nose". With this clinical exposure, I was pleased to accept, in 1985, an invitation to participate in what I anticipated would be an influential national panel to explore the relationship between mental stress and heart disease. I was, however, not ready for the opening statement of the meeting chair (whose name I won't say): "There is no evidence that stress causes heart disease, nor will there ever be". I was disappointed though not discouraged, as of course this could not be true-where was his crystal ball?-although the statement did capture the pessimism that was common in the cardiology of that era.
Stress, behavior and the heart
Neuroscience & Biobehavioral Reviews, 2017
A broad spectrum of research, spanning epidemiological studies, clinical research, preclinical investigations and animal models, has pointed to a link between psychological factors and cardiovascular dysfunctional states. Acute and chronic life stressors, psychological alterations such as anxiety and depression, personality traits such as anger and hostility, reactive behavioral coping strategies, as well as the absence of social support have all been shown to interfere with and modulate the onset and progression of cardiovascular alterations. These psychological elements, in many instances, appear to be independent risk factors of disease, as important as traditional ones such as cholesterol levels, waist fat, body mass index and poor physical activity. Recently developed research approaches have shed light on the brain substrates, genetic and epigenetic factors, as well as cellular/molecular mechanisms that underlie the tight and complex relationship between stress, behavior and the cardiovascular system. However, despite a growing number of empirical investigations and accumulating clinical evidence, still several issues remain to be clarified about the mechanisms linking stressful events, psychological traits, behavioral coping and cardiovascular risk profiles. This special issue is a collection of 19 selected review papers that present the newest scientific evidence in the multidisciplinary arena intersecting stress, behavior and the cardiovascular system. It gathers the contribution of leading scientists from a variety of disciplines (neuroscience,
A series of meta-analyses was undertaken to determine the contributions of sympathetic and parasympathetic activation to cardiovascular stress reactivity. A literature search yielded 186 studies of sufficient quality that measured indices of sympathetic (n = 113) and/or parasympathetic activity (n = 73). A range of psychological stressors perturbed blood pressure and heart rate. There were comparable aggregate effects for sympathetic activation, as indexed by increased plasma epinephrine and norepinephrine, and shortened pre-ejection period, and parasympathetic deactivation, as indexed by heart rate variability measures. Effect size varied with stress task, sex, and age. In contrast to alpha-adrenergic blockade, beta-blockade attenuated cardiovascular reactivity. Cardiovascular reactivity to acute psychological stress would appear to reflect both beta-adrenergic activation and vagal withdrawal to a largely equal extent.
The reactivity hypothesis postulates that large magnitude cardiovascular reactions to psychological stress contribute to the development of pathology. A key but little tested assumption is that such reactions are metabolically exaggerated. Cardiac activity, using Doppler echocardiography, and oxygen consumption, using mass spectrometry, were measured at rest and during and after a mental stress task and during graded sub maximal cycling exercise. Cardiac activity and oxygen consumption showed the expected orderly association during exercise. However, during stress, large increases in cardiac activity were observed in the context of modest rises in energy expenditure; observed cardiac activity during stress substantially exceeded that predicted on the basis of contemporary levels of oxygen consumption. Thus, psychological stress can provoke increases in cardiac activity difficult to account for in terms of the metabolic demands of the stress task.
The study aimed to: confirm that acute stress elicits metabolically exaggerated increases in cardiac activity; test whether individuals with elevated resting blood pressure show more exaggerated cardiac reactions to stress than those who are clearly normotensive; and explore the underlying mechanisms. Cardiovascular activity and oxygen consumption were measured pre-, during, and post-mental stress, and during graded submaximal cycling exercise in 11 young men with moderately elevated resting blood pressure and 11 normotensives. Stress provoked increases in cardiac output that were much greater than would be expected from contemporary levels of oxygen consumption. Exaggerated cardiac reactions were larger in the relatively elevated blood pressure group. They also had greater reductions in total peripheral resistance, but not heart rate variability, implying that their more exaggerated cardiac reactions reflected greater β-adrenergic activation.
The response of the cardiovascular system to stressful situations has long been considered to have implications for health outcomes. Both exaggerated and diminished cardiovascular reactivity to acute psychological stressors have serious consequences for health. This chapter based on my STAR 2014 Early Career Award talk will compare and discuss my research on both high and low cardiovascular responses to psychological stress. Exaggerated reactions are associated with the development of hypertension, markers of systemic atherosclerosis, and cardiovascular disease. Blunted or low reactivity is related to depression, obesity, and a range of addictions. It has been proposed that an interaction between genetics and the environment contributes to individuals' reactivity to stress. The objective of this talk is to explore cutting edge research on the pathways to the development of disease via alterations in stress reactivity. It will also highlight some of the key environmental, social, and mechanistic pathways from high and low cardiovascular reactivity to health and ill health in later life.