Healthy biological systems exhibit complex patterns of variability that can be described by mathematical chaos. Heart rate variability (HRV) consists of changes in the time intervals between consecutive heartbeats called interbeat intervals (IBIs). A healthy heart is not a metronome. The oscillations of a healthy heart are complex and constantly changing, which allow the cardiovascular system to rapidly adjust to sudden physical and psychological challenges to homeostasis. This article briefly reviews current perspectives on the mechanisms that generate 24 h, short-term (~5 min), and ultra-short-term (<5 min) HRV, the importance of HRV, and its implications for health and performance. The authors provide an overview of widely-used HRV time-domain, frequency-domain, and non-linear metrics. Time-domain indices quantify the amount of HRV observed during monitoring periods that may range from ~2 min to 24 h. Frequency-domain values calculate the absolute or relative amount of signal energy within component bands. Non-linear measurements quantify the unpredictability and complexity of a series of IBIs. The authors survey published normative values for clinical, healthy, and optimal performance populations. They stress the importance of measurement context, including recording period length, subject age, and sex, on baseline HRV values. They caution that 24 h, short-term, and ultra-short-term normative values are not interchangeable. They encourage professionals to supplement published norms with findings from their own specialized populations. Finally, the authors provide an overview of HRV assessment strategies for clinical and optimal performance interventions.

/pdf/an-overview-of-heart-rate-variability-metrics-and-norms-sd8bxpnvjg.pdf

An Overview of Heart Rate Variability Metrics and Norms.

Heart rate variability (HRV), the change in the time intervals between adjacent heartbeats, is an emergent property of interdependent regulatory systems that operate on different time scales to adapt to challenges and achieve optimal performance. This article briefly reviews neural regulation of the heart, and its basic anatomy, the cardiac cycle, and the sinoatrial and atrioventricular pacemakers. The cardiovascular regulation center in the medulla integrates sensory information and input from higher brain centers, and afferent cardiovascular system inputs to adjust heart rate and blood pressure via sympathetic and parasympathetic efferent pathways. This article reviews sympathetic and parasympathetic influences on the heart, and examines the interpretation of HRV and the association between reduced HRV, risk of disease and mortality, and the loss of regulatory capacity. This article also discusses the intrinsic cardiac nervous system and the heart-brain connection, through which afferent information can influence activity in the subcortical and frontocortical areas, and motor cortex. It also considers new perspectives on the putative underlying physiological mechanisms and properties of the ultra-low-frequency (ULF), very-low-frequency (VLF), low-frequency (LF), and high-frequency (HF) bands. Additionally, it reviews the most common time and frequency domain measurements as well as standardized data collection protocols. In its final section, this article integrates Porges’ polyvagal theory, Thayer and colleagues’ neurovisceral integration model, Lehrer et al.’s resonance frequency model, and the Institute of HeartMath’s coherence model. The authors conclude that a coherent heart is not a metronome because its rhythms are characterized by both complexity and stability over longer time scales. Future research should expand understanding of how the heart and its intrinsic nervous system influence the brain.

/pdf/a-healthy-heart-is-not-a-metronome-an-integrative-review-of-49cjuoyp79.pdf

A healthy heart is not a metronome: an integrative review of the heart's anatomy and heart rate variability.

Cytokine production by the immune system contributes importantly to both health and disease. The nervous system, via an inflammatory reflex of the vagus nerve, can inhibit cytokine release and thereby prevent tissue injury and death. The efferent neural signaling pathway is termed the cholinergic antiinflammatory pathway. Cholinergic agonists inhibit cytokine synthesis and protect against cytokine-mediated diseases. Stimulation of the vagus nerve prevents the damaging effects of cytokine release in experimental sepsis, endotoxemia, ischemia/reperfusion injury, hemorrhagic shock, arthritis, and other inflammatory syndromes. Herein is a review of this physiological, functional anatomical mechanism for neurological regulation of cytokine-dependent disease that begins to define an immunological homunculus.

/pdf/physiology-and-immunology-of-the-cholinergic-cq02sk4dxl.pdf

Physiology and immunology of the cholinergic antiinflammatory pathway

Heart rate variability, the change in the time intervals between adjacent heartbeats, is an emergent property of interdependent regulatory systems that operates on different time scales to adapt to environmental and psychological challenges. This article briefly reviews neural regulation of the heart and offers some new perspectives on mechanisms underlying the very low frequency rhythm of heart rate variability. Interpretation of heart rate variability rhythms in the context of health risk and physiological and psychological self-regulatory capacity assessment is discussed. The cardiovascular regulatory centers in the spinal cord and medulla integrate inputs from higher brain centers with afferent cardiovascular system inputs to adjust heart rate and blood pressure via sympathetic and parasympathetic efferent pathways. We also discuss the intrinsic cardiac nervous system and the heart-brain connection pathways, through which afferent information can influence activity in the subcortical, frontocortical, and motor cortex areas. In addition, the use of real-time HRV feedback to increase self-regulatory capacity is reviewed. We conclude that the heart's rhythms are characterized by both complexity and stability over longer time scales that reflect both physiological and psychological functional status of these internal self-regulatory systems.

Heart Rate Variability: New Perspectives on Physiological Mechanisms, Assessment of Self-regulatory Capacity, and Health risk.

The term ''adrenergic'' originates from ''adrenaline'' and describes hormones or drugs whose effects are similar to those of epinephrine. Adrenergic stress is mediated by stimulation of adrenergic receptors and activation of post-receptor pathways. Critical illness is a potent stimulus of the sympathetic nervous system. It is undisputable that the adrenergic-driven ''fight-flight response'' is a physiologically meaningful reaction allowing humans to survive during evolution. However, in critical illness an overshooting stimulation of the sympathetic nervous system may well exceed in time and scope its beneficial effects. Comparable to the overwhelming immune response during sepsis, adrenergic stress in critical illness may get out of control and cause adverse effects. Several organ systems may be affected. The heart seems to be most susceptible to sympathetic overstimulation. Detrimental effects include impaired diastolic function, tachycardia and tachyarrhythmia, myocardial ischemia, stunning, apoptosis and necrosis. Adverse catecholamine effects have been observed in other organs such as the lungs (pulmonary edema, elevated pulmonary arterial pressures), the coagulation (hypercoagulability, thrombus formation), gastrointestinal (hypoperfusion, inhibition of peristalsis), endocrinologic (decreased prolactin, thyroid and growth hormone secretion) and immune systems (immunomodulation, stimulation of bacterial growth), and metabolism (increase in cell energy expenditure, hyperglycemia, catabolism, lipolysis, hyperlactatemia, electrolyte changes), bone marrow (anemia), and skeletal muscles (apoptosis). Potential therapeutic options to reduce excessive adrenergic stress comprise temperature and heart rate control, adequate use of sedative/analgesic drugs, and aiming for reasonable cardiovascular targets, adequate fluid therapy, use of levosimendan, hydrocortisone or supplementary arginine vasopressin.

Sympathetic Overstimulation During Critical Illness: Adverse Effects of Adrenergic Stress:

Objective:Multiple organ dysfunction syndrome (MODS) is the sequential failure of several organ systems after a trigger event, like sepsis or cardiogenic shock. Mortality rate is high, up to 70%. Autonomic dysfunction may substantially contribute to the development of MODS. Our study aimed to charac

Autonomic dysfunction predicts mortality in patients with multiple organ dysfunction syndrome of different age groups.

Objective
The cardiac chemoreflex sensitivity is a powerful predictor of autonomic dysfunction in chronic heart failure and after myocardial infarction. The objective of the present study was to characterize cardiac chemoreflex sensitivity in patients with multiple organ dysfunction syndrome (MODS). We also aimed to elucidate the effect of the severity of MODS on the assessment of cardiac chemoreflex sensitivity.

Impaired chemoreflex sensitivity in adult patients with multiple organ dysfunction syndrome—the potential role of disease severity

Unser Verstandnis der Pathogenese kardialer Erkrankungen hat in den letzten Jahren einen Wandel von der isolierten Betrachtung des geschadigten Organs hin zur Untersuchung der Auswirkungen der Herzschadigung auf den Gesamtorganismus erfahren: Herzerkrankungen konnen vielfaltige Systemreaktionen auf nervaler, hormoneller und Zytokinebene induzieren. Die Einsicht in die autonomen Regulation ermoglicht es uns, die Pathogenese und die Symptomatik vieler kardiologisch relevanter Erkrankungen besser zu verstehen, Hochrisikopatienten zu identifizieren und neue Behandlungsansatze zu untersuchen. Die Intention dieses Artikels ist es, praxisrelevante Messmethoden zu prasentieren, welche Aufschluss uber die veranderten kardiorespiratorischen Regelkreise bei Herz- und Kreislauferkrankungen geben. Diese Techniken werden zuerst kurz vorgestellt, ihre klinische Anwendbarkeit wird herausgearbeitet, und die Veranderungen dieser Parameter werden anschliesend in den Kontext der Pathogenese des Myokardinfarktes, der Herzinsuffizienz und der Herzschadigung im Rahmen eines Multiorgandysfunktionssyndroms kritisch Kranker gestellt.

Die autonome Dysfunktion des Herzkranken


 
 
 Type of funding sources: Public Institution(s). Main funding source(s): Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK)
 
 
 
 Co-existence of atrial fibrillation (AF) and heart failure with preserved ejection fraction (HFpEF) is common and severely affects morbidity and prognosis.
 
 
 
 This study evaluates outcome after cryoballoon-ablation for AF in HFpEF compared to patients without heart failure employing multiple diagnostic modalities.
 
 
 
 A total of 102 patients scheduled for cryoablation of AF with LVEF≥50% were prospectively enrolled. Baseline evaluation included echocardiography, stress echocardiography, six-minute-walk-test, biomarker measurements and quality of life assessment (SF-36). HFpEF was diagnosed according to current guidelines and confirmed applying the HFA-PEFF-Score. Procedural parameters as well as clinical, functional and echocardiographic endpoints at follow-up ≥12 months after AF-ablation were compared between patients with and without HFpEF.
 
 
 
 Patients with HFpEF (n=24) were older (median: 73.5 years [Q25: 66.5 years; Q75: 75.8 years] vs. 64.5 years [Q25: 55.0 years; Q75: 71.3 years], P<0.001) and more often female (83.3% vs. 28.2%). They were characterized by more pronounced AF-related symptoms (median EHRA-score: 3.0 [Q25:3.0; Q75:3.0] vs. 2.0 [Q25: 2.0; Q75: 3.0], P<0.001), reduced distance in six-minute-walk-test (median 487.5m [Q25: 378.1m; Q75: 517.8m] vs. 539.0m [Q25: 489.3m; Q75:589.1 m], P<0.001), and higher mean left atrial (LA)-pressure measured at the needle tip at transseptal puncture (14.0mmHg [Q25: 10.3mmHg; Q75: 21.5mmHg] vs. 10.0 mmHg [Q25: 8.0mmHg; Q75: 13.3mmHg], P=0.008). Procedural parameters were comparable between the two subgroups. Rates of AF-recurrence, repeat AF-ablation and AF-related re-hospitalization were increased in HFpEF (Figure 1A-C), which was confirmed after adjusting for intergroup differences in sex and age distribution by multiple regression analysis. There was no improvement of heart failure-related symptoms and persistent elevation of cardiac biomarkers, even in HFpEF-patients with successful restoration of sinus rhythm at follow-up (Figure 2A-C). Echocardiographic follow-up showed progression of adverse LA-remodeling (LA-volume index at baseline: 35.8ml/m2 [Q25: 32.2ml/m2; Q75: 41.9ml/m2] vs. 12-month follow-up: 40.5ml/m2 [Q25: 36.0ml/m2; Q75: 51.4ml/m2], P=0.017) and no improvement in diastolic function in HFpEF (E/e’ at baseline: 9.7 [Q25: 7.8; Q75: 12.1] vs 12-month follow-up: 10.2 [Q25: 8.4; Q75: 11.8], P=0.874), in particular in patients with HFpEF and AF-recurrence. Quality of life improved in patients without HFpEF in both physical and mental summary scales, however, no beneficial effect was seen in HFpEF.
 
 
 
 Patients with HFpEF constitute a distinct subgroup with an elevated risk for arrhythmia recurrence after cryoablation of AF. Functional hallmarks and heart-failure related symptoms of HFpEF persisted in our cohort, irrespective of rhythm-status at follow-up. Future research is needed to optimize tailored treatment strategies in HFpEF.


Cryoballoon-ablation of atrial fibrillation in patients with heart failure and preserved ejection fraction

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Autonomic dysfunction predicts mortality in patients with multiple organ dysfunction syndrome of different age groups.

Impaired chemoreflex sensitivity in adult patients with multiple organ dysfunction syndrome—the potential role of disease severity

Die autonome Dysfunktion des Herzkranken

Cryoballoon-ablation of atrial fibrillation in patients with heart failure and preserved ejection fraction