Pathophysiology and therapy of Takotsubo syndrome. Letter regarding the article ‘Pathophysiology of Takotsubo syndrome – a joint scientific statement from the Heart Failure Association Takotsubo Syndrome Study Group and Myocardial Function Working Group of the European Society of Cardiology – Part 1: overview and the central role for catecholamines and sympathetic nervous system’

2022 ◽  
Author(s):  
John E. Madias
Keyword(s):  
Heart Failure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
European Society ◽  
Myocardial Function ◽  
Study Group ◽  
Takotsubo Syndrome ◽  
Scientific Statement ◽  
Sympathetic Nervous ◽  
European Society Of Cardiology

scholarly journals Magnesium Dynamics and Sympathetic Nervous System Activity in Patients With Chronic Heart Failure

1999 ◽  
Vol 63 (4) ◽  
pp. 267-273 ◽  
Author(s):  
Hisanori Samejima ◽  
Kazuhiko Tanabe ◽  
Noriyuki Suzuki ◽  
Kazuto Omiya ◽  
Masahiro Murayama
Keyword(s):  
Heart Failure ◽  
Nervous System ◽  
Chronic Heart Failure ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous System Activity ◽  
System Activity ◽  
Nervous System Activity ◽  
Sympathetic Nervous

The 2009 Carl Ludwig Lecture: pathophysiology of the human sympathetic nervous system in cardiovascular diseases: the transition from mechanisms to medical management

2010 ◽  
Vol 108 (2) ◽  
pp. 227-237 ◽  
Author(s):  
Murray Esler
Keyword(s):  
Heart Failure ◽  
Nervous System ◽  
Heart Disease ◽  
Essential Hypertension ◽  
Sympathetic Nervous System ◽  
Clinical Translation ◽  
Organ Specific ◽  
Circulatory Control ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

Sympathetic nervous system responses typically are regionally differentiated, with activation in one outflow sometimes accompanying no change or sympathetic inhibition in another. Regional sympathetic activity is best studied in humans by recording from postganglionic sympathetic efferents (multiunit or single fiber recording) and by isotope dilution-derived measurement of organ-specific norepinephrine release to plasma (regional “norepinephrine spillover”). Evidence assembled in this review indicates that sympathetic nervous system abnormalities are crucial in the development of cardiovascular disorders, notably heart failure, essential hypertension, disorders of postural circulatory control causing syncope, and “psychogenic heart disease,” heart disease attributable to mental stress and psychiatric illness. These abnormalities involve persistent, adverse activation of sympathetic outflows to the heart and kidneys in heart failure and hypertension, episodic or ongoing cardiac sympathetic activation in psychogenic heart disease, and defective sympathetic circulatory reflexes in disorders of postural circulatory control. An important goal for clinical scientists is translation of knowledge of pathophysiology, such as this, into better treatment for patients. The achievement of this “mechanisms-to-management” transition is at differing stages of development with the different conditions. Clinical translation is mature in cardiac failure, knowledge of cardiac neural pathophysiology having led to introduction of β-adrenergic blockers, an effective therapy. With essential hypertension, perhaps we are on the cusp of effective translation, with recent successful testing of selective catheter-based renal sympathetic nerve ablation in patients with resistant hypertension, an intervention firmly based on demonstration of activation of the renal sympathetic outflow. With psychogenic heart disease and postural syncope syndromes, knowledge of the neural pathophysiology is emerging, but clinical translation remains for the future.

scholarly journals New Approaches in the Management of Sudden Cardiac Death in Patients with Heart Failure—Targeting the Sympathetic Nervous System

2019 ◽  
Vol 20 (10) ◽  
pp. 2430 ◽  
Author(s):  
Márcio Galindo Kiuchi ◽  
Janis Marc Nolde ◽  
Humberto Villacorta ◽  
Revathy Carnagarin ◽  
Justine Joy Su-Yin Chan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Nervous System ◽  
Sudden Cardiac Death ◽  
Sympathetic Nervous System ◽  
Clinical Data ◽  
Cardiac Death ◽  
Electrical Storm ◽  
Emission Computed Tomography ◽  
Sympathetic Outflow ◽  
Sympathetic Nervous

Cardiovascular diseases (CVDs) have been considered the most predominant cause of death and one of the most critical public health issues worldwide. In the past two decades, cardiovascular (CV) mortality has declined in high-income countries owing to preventive measures that resulted in the reduced burden of coronary artery disease (CAD) and heart failure (HF). In spite of these promising results, CVDs are responsible for ~17 million deaths per year globally with ~25% of these attributable to sudden cardiac death (SCD). Pre-clinical data demonstrated that renal denervation (RDN) decreases sympathetic activation as evaluated by decreased renal catecholamine concentrations. RDN is successful in reducing ventricular arrhythmias (VAs) triggering and its outcome was not found inferior to metoprolol in rat myocardial infarction model. Registry clinical data also suggest an advantageous effect of RDN to prevent VAs in HF patients and electrical storm. An in-depth investigation of how RDN, a minimally invasive and safe method, reduces the burden of HF is urgently needed. Myocardial systolic dysfunction is correlated to neuro-hormonal overactivity as a compensatory mechanism to keep cardiac output in the face of declining cardiac function. Sympathetic nervous system (SNS) overactivity is supported by a rise in plasma noradrenaline (NA) and adrenaline levels, raised central sympathetic outflow, and increased organ-specific spillover of NA into plasma. Cardiac NA spillover in untreated HF individuals can reach ~50-fold higher levels compared to those of healthy individuals under maximal exercise conditions. Increased sympathetic outflow to the renal vascular bed can contribute to the anomalies of renal function commonly associated with HF and feed into a vicious cycle of elevated BP, the progression of renal disease and worsening HF. Increased sympathetic activity, amongst other factors, contribute to the progress of cardiac arrhythmias, which can lead to SCD due to sustained ventricular tachycardia. Targeted therapies to avoid these detrimental consequences comprise antiarrhythmic drugs, surgical resection, endocardial catheter ablation and use of the implantable electronic cardiac devices. Analogous NA agents have been reported for single photon-emission-computed-tomography (SPECT) scans usage, specially the 123I-metaiodobenzylguanidine (123I-MIBG). Currently, HF prognosis assessment has been improved by this tool. Nevertheless, this radiotracer is costly, which makes the use of this diagnostic method limited. Comparatively, positron-emission-tomography (PET) overshadows SPECT imaging, because of its increased spatial definition and broader reckonable methodologies. Numerous ANS radiotracers have been created for cardiac PET imaging. However, so far, [11C]-meta-hydroxyephedrine (HED) has been the most significant PET radiotracer used in the clinical scenario. Growing data has shown the usefulness of [11C]-HED in important clinical situations, such as predicting lethal arrhythmias, SCD, and all-cause of mortality in reduced ejection fraction HF patients. In this article, we discussed the role and relevance of novel tools targeting the SNS, such as the [11C]-HED PET cardiac imaging and RDN to manage patients under of SCD risk.

The contribution of the renin-angiotensin system to limb vasoregulation in patients with heart failure: observations during orthostasis and α-adrenergic blockade

1985 ◽  
Vol 68 (6) ◽  
pp. 659-667 ◽  
Author(s):  
Mark A. Creager ◽  
David P. Faxon ◽  
Susan M. Rockwell ◽  
Haralambos Gavras ◽  
Jay D. Coffman
Keyword(s):  
Heart Failure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Patients With Heart Failure ◽  
Sympathetic Nervous ◽  
Forearm Vascular Resistance

1. In patients with congestive heart failure, both the sympathetic nervous system and renin-angiotensin system are often stimulated. In order to assess the contribution of the renin-angiotensin system to limb vascular resistance, the forearm haemodynamic response to captopril was studied in 13 patients with heart failure. 2. Seven subjects were studied while supine and during 60° head-up tilt. To eliminate α-adrenergic effects, six additional patients with heart failure were pretreated with intra-arterial phentolamine and then given captopril. Venous occlusion plethysmography was used to determine forearm blood flew and forearm vascular resistance. 3. Tilt did not significantly increase pretreatment plasma renin activity or plasma noradrenaline concentration, nor did it decrease forearm blood flow. Furthermore, captopril did not alter forearm vascular resistance during supine or upright posture. During the phentolamine infusion, however, captopril reduced forearm vascular resistance by 19% (P < 0.05). 4. Despite increased plasma renin activity, captopril did not cause forearm vasodilatation during supine or upright posture in these patients with heart failure. When the contribution of the sympathetic nervous system was eliminated, captopril decreased forearm vascular resistance. Therefore, in patients with congestive heart failure, the sympathetic nervous system is important in limb vasoregulation, and the contribution of the renin-angiotensin system is apparent only after α-adrenergic blockade.

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