Neurocardiology: translational advancements and potential DOI Creative Commons
Neil Herring, Olujimi A. Ajijola,

Robert D. Foreman

et al.

The Journal of Physiology, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 27, 2024

Abstract In our original white paper published in the The Journal of Physiology 2016, we set out knowledge structural and functional organization cardiac autonomic control, how it remodels during disease, approaches to exploit such for regulation therapy. aim this update is build on blueprint, highlighting significant progress which has been made field since major challenges opportunities that exist with regard translation. Imbalances responses, while beneficial short term, ultimately contribute evolution pathology. As understanding emerges where target terms actuators (including heart intracardiac nervous system (ICNS), stellate ganglia, dorsal root ganglia (DRG), vagus nerve, brainstem, even higher centres), there also a need develop sensor technology respond appropriate biomarkers (electrophysiological, mechanical, molecular) closed‐loop therapies can evolve. goal work endogenous control systems, rather than opposition them, improve outcomes. image

Language: Английский

Neutrophils incite and macrophages avert electrical storm after myocardial infarction DOI Creative Commons
Jana Grune, Andrew Lewis,

Masahiro Yamazoe

et al.

Nature Cardiovascular Research, Journal Year: 2022, Volume and Issue: 1(7), P. 649 - 664

Published: July 11, 2022

Abstract Sudden cardiac death, arising from abnormal electrical conduction, occurs frequently in patients with coronary heart disease. Myocardial ischemia simultaneously induces arrhythmia and massive myocardial leukocyte changes. In this study, we optimized a mouse model which hypokalemia combined infarction triggered spontaneous ventricular tachycardia ambulatory mice, showed that major subsets have opposing effects on conduction. Neutrophils increased via lipocalin-2 whereas neutrophilia associated patients. contrast, macrophages protected against arrhythmia. Depleting recruited Ccr2 −/− mice or all macrophage Csf1 receptor inhibition both fibrillation. Higher burden mortality Cd36 Mertk viewed together reduced mitochondrial integrity accelerated cardiomyocyte death the absence of macrophages, indicated receptor-mediated phagocytosis protects lethal storm. Thus, modulation function provides potential therapeutic pathway for reducing risk sudden death.

Language: Английский

Citations

64

The Impact of Mental Stress on Cardiovascular Health—Part II DOI Open Access
Michael Y. Henein,

Sergio Vancheri,

Giovanni Longo

et al.

Journal of Clinical Medicine, Journal Year: 2022, Volume and Issue: 11(15), P. 4405 - 4405

Published: July 28, 2022

Endothelial dysfunction is one of the earliest manifestations atherosclerosis, contributing to its development and progression. Mental stress induces endothelial through increased activity sympathetic nervous system, release corticotropin-releasing hormone from hypothalamus, inhibition nitric oxide (NO) synthesis by cortisol, levels pro-inflammatory cytokines. Mental-stress-induced output system concomitant withdrawal parasympathetic inflammatory reflex results in systemic inflammation activation a neural–hematopoietic–arterial axis. This includes brainstem subcortical regions network, bone marrow activation, leukocytes into circulation their migration arterial wall atherosclerotic plaques. Low-grade, sterile involved all steps atherogenesis, coronary plaque formation destabilisation rupture. Increased tone may cause smooth-muscle-cell proliferation, resulting vascular hypertrophy, thus hypertension. Emotional events also instability cardiac repolarisation due brain lateralised imbalance autonomic stimulation, which lead asymmetric arrhythmia. Acute emotional can provoke severe catecholamine release, leading direct myocyte injury calcium overload, known as myocytolysis, microvascular vasoconstriction, an increase left ventricular afterload. These changes trigger heart failure syndrome mimicking acute myocardial infarction, characterised transient apical ballooning, (Takotsubo) cardiomyopathy. Women are more prone than men develop mental-stress-induced ischemia (MSIMI), probably reflecting gender differences patterns during mental stress. Although guidelines on CV prevention recognise psychosocial factors risk modifiers improve prediction decision making, evidence that assessment treatment will prevent CAD needs further evaluation.

Language: Английский

Citations

40

RNA modification in cardiovascular disease: implications for therapeutic interventions DOI Creative Commons
Cong Wang,

Xuyang Hou,

Qing Guan

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: Oct. 27, 2023

Abstract Cardiovascular disease (CVD) is the leading cause of death in world, with a high incidence and youth-oriented tendency. RNA modification ubiquitous indispensable cell, maintaining cell homeostasis function by dynamically regulating gene expression. Accumulating evidence has revealed role aberrant expression CVD caused dysregulated modification. In this review, we focus on nine common modifications: N 6 -methyladenosine (m A), 1 5-methylcytosine 5 C), 7 -methylguanosine G), 4 -acetylcytosine (ac pseudouridine (Ψ), uridylation, adenosine-to-inosine (A-to-I) editing, modifications U34 tRNA wobble. We summarize key regulators their effects expression, such as splicing, maturation, transport, stability, translation. Then, based classification CVD, mechanisms which occurs progresses through are discussed. Potential therapeutic strategies, therapy, reviewed these mechanisms. Herein, some (such stroke peripheral vascular disease) not included due to limited availability literature. Finally, prospective applications challenges discussed for purpose facilitating clinical Moreover, look forward more studies exploring roles future, there substantial uncultivated areas be explored.

Language: Английский

Citations

31

AIEgen‐Based Covalent Organic Frameworks for Preventing Malignant Ventricular Arrhythmias Via Local Hyperthermia Therapy DOI
Liang Zhang,

Fuding Guo,

Saiting Xu

et al.

Advanced Materials, Journal Year: 2023, Volume and Issue: unknown

Published: Aug. 3, 2023

The engineering of aggregation-induced emission luminogens (AIEgen) based covalent organic frameworks (COFs), TDTA-COF, BTDTA-COF, and BTDBETA-COF are reported, as hyperthermia agents for inhibiting the occurrence malignant ventricular arrhythmias (VAs). These AIE COFs exhibit dual functionality, they not only directly modulate function neural activity stellate ganglion (SG) through local therapy (LHT) but also induce browning white fat improve neuroinflammation peri-SG microenvironment, which is favorable ischemia-induced VAs. In vivo studies have confirmed that BTDBETA-COF-mediated LHT enhances thermogenesis browning-related gene expression, thereby serving a synergistic role in combating Transcriptome analysis adipose tissue reveals substantial downregulation inflammatory cytokines, highlighting potency ameliorating microenvironment offering myocardial arrhythmia protection. work on COF-based agent VAs inhibition provides new avenue mitigating cardiac sympathetic nerve hyperactivity.

Language: Английский

Citations

28

Molecular and cellular neurocardiology in heart disease DOI
Beth A. Habecker, Donald M. Bers, Susan J. Birren

et al.

The Journal of Physiology, Journal Year: 2024, Volume and Issue: unknown

Published: May 22, 2024

Abstract This paper updates and builds on a previous White Paper in this journal that some of us contributed to concerning the molecular cellular basis cardiac neurobiology heart disease. Here we focus recent findings underpin autonomic development, novel intracellular pathways neuroplasticity. Throughout highlight unanswered questions areas controversy. Whilst neurochemical are already demonstrating prognostic viability patients with failure, also discuss opportunity better understand sympathetic impairment by using patient specific stem cells provides pathophysiological contextualization study ‘disease dish’. Novel imaging techniques spatial transcriptomics facilitating road map for target discovery may form therapeutic treat dysautonomia. image

Language: Английский

Citations

9

Feasibility of the Absolute Quantification and Left Ventricular Segmentation of Cardiac Sympathetic Innervation in Wild–type Transthyretin Amyloidosis Cardiomyopathy with [123I]-MIBG SPECT/CT: the I–NERVE study DOI Creative Commons
Alwin Tubben, Niek H. J. Prakken, Oleksandra Ivashchenko

et al.

Journal of Nuclear Cardiology, Journal Year: 2025, Volume and Issue: unknown, P. 102146 - 102146

Published: Feb. 1, 2025

Cardiac sympathetic neuronal dysfunction is an early marker in wild-type transthyretin amyloidosis cardiomyopathy (ATTRwt-CM). [123I]-MIBG imaging evaluates cardiac innervation but lacks volumetric activity quantification current methods. This study aims to quantify ATTRwt-CM using SPECT/CT and correlate findings with functional structural parameters from echocardiogram magnetic resonance (CMR). We conducted a single-center, descriptive, cross-sectional absolute myocardial function SPECT/CT. Retrospective reconstruction allowed for tracer-uptake of the left ventricle, overall segmented, kBq/mL, SUV percentage injected dose (%ID). Echocardiography, CMR, bone scintigraphy were performed according clinical standards. Segmented values correlated global longitudinal strain (GLSS) on echocardiography, native-T1, extracellular volume (ECV) CMR fused CMR. Twenty-nine patients (75.8±6.6 years, 90% male) prospectively included. All exhibited dysfunction, median late heart-to-mediastinum ratio 1.69[1.45-1.89] washout rate 22.7% (16.4-27.3%). SUVmean, SUVpeak, SUVmax %ID 1.80 ± 0.78, 3.84 1.41, 4.46 1.68 0.46 0.18 respectively, correlating semi-quantitative measures. No correlations found GLSS echocardiography or native T1 ECV The demonstrates feasibility ATTRwt-CM. measures not key confirms sensitivity different aspects pathology. EudraCT ref. 2020-003350-72, retrospectively registered 20 March 2023. https://classic. gov/ct2/show/NCT05776212.

Language: Английский

Citations

1

Neuropeptide Y as a Prognostic Biomarker in Electrical Storm DOI
Jianjun Tang, Chengfeng Liu, Zhuo Wang

et al.

JACC. Clinical electrophysiology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

Citations

1

Influence of Primary Neurologic Disease on Cardiovascular Health in Females DOI

Khaldoun Ali,

Deborah Kerrigan, Janet Berkman

et al.

Circulation Research, Journal Year: 2025, Volume and Issue: 136(6), P. 618 - 627

Published: March 13, 2025

Neurocardiology is an interdisciplinary field that examines the complex interactions between nervous and cardiovascular systems, exploring how neurological processes, such as autonomic system regulation brain-heart communication impact heart function contribute to health disease. Although much of focus on has centered traditional risk factors, influence system, especially in females, increasingly recognized a key determinant outcomes. This article reviews existing literature mechanisms females. Specifically, we analyze primary disorders including cerebrovascular disease, headache disorders, multiple sclerosis have specific downstream effects cardiac function. By understanding relationship health, this review highlights need for sex-specific approaches prevention, diagnosis, treatment disease ultimately encouraging discovery more effective care strategies improving

Language: Английский

Citations

1

Air Pollution and Cardiac Arrhythmias: A Comprehensive Review DOI
Mohammad Amin Shahrbaf, Mohammad Ali Akbarzadeh, Mohammadreza Tabary

et al.

Current Problems in Cardiology, Journal Year: 2020, Volume and Issue: 46(3), P. 100649 - 100649

Published: July 22, 2020

Language: Английский

Citations

65

The Physiology and Pathophysiology of T-Tubules in the Heart DOI Creative Commons
Ingunn E. Setterberg, Christopher Le, Michael Frisk

et al.

Frontiers in Physiology, Journal Year: 2021, Volume and Issue: 12

Published: Sept. 9, 2021

In cardiomyocytes, invaginations of the sarcolemmal membrane called t-tubules are critically important for triggering contraction by excitation-contraction (EC) coupling. These structures form functional junctions with sarcoplasmic reticulum (SR), and thereby enable close contact between L-type Ca 2+ channels (LTCCs) Ryanodine Receptors (RyRs). This arrangement in turn ensures efficient release, contraction. While new data indicate that capable exhibiting compensatory remodeling, they also widely reported to be structurally functionally compromised during disease, resulting disrupted homeostasis, impaired systolic and/or diastolic function, arrhythmogenesis. review summarizes these findings, while highlighting an emerging appreciation distinct roles pathophysiology heart failure reduced preserved ejection fraction (HFrEF HFpEF). this context, we current understanding processes underlying t-tubule growth, maintenance, degradation, underscoring involvement a variety regulatory proteins, including junctophilin-2 (JPH2), amphiphysin-2 (BIN1), caveolin-3 (Cav3), newer candidate proteins. Upstream regulation structure/function cardiac workload specifically ventricular wall stress is discussed, alongside perspectives novel strategies which may therapeutically target mechanisms.

Language: Английский

Citations

55