scholarly journals Sympathetic Blockade for Dysrhythmia Management in Heart Failure: Rationale and Therapeutic Progression to Intervention

10.5772/66517 ◽  
2017 ◽  
Author(s):  
Daryl I. Smith ◽  
Albert O. Duah
Keyword(s):  
Heart Failure ◽  
Sympathetic Blockade

scholarly journals Manejo anestésico de la tormenta arrítmica mediante bloqueo simpático

2020 ◽  
Vol 11 (12) ◽  
pp. 1
Author(s):  
Laura Laso Ramírez ◽  
María José Rodríguez Pérez ◽  
Elisabeth Agudelo Montoya
Keyword(s):  
Heart Failure ◽  
Ventricular Tachycardia ◽  
Anaesthetic Management ◽  
Sympathetic Blockade ◽  
Sympathetic Block ◽  
Apical Hypertrophic Cardiomyopathy ◽  
Thoracic Sympathectomy ◽  
Cardioverter Defibrillator ◽  
Insuficiencia Cardiaca ◽  
Pharmacological Control

La tormenta arrítmica se define por la presencia de tres o más episodios de taquicardia ventricular, fibrilación ventricular y/o descargas de un desfibrilador automático implantable (DAI) en un periodo de 24 horas. En su manejo es esencial la identificación y corrección de factores desencadenantes, como isquemia miocárdica, alteraciones hidroelectrolíticas, descompensación de la insuficiencia cardíaca, así como el adecuado control del tono simpático. Presentamos el caso de un varón de 43 años con miocardiopatía hipertrófica apical, portador de DAI en prevención primaria que ingresa por tormenta arrítmica de difícil control farmacológico y ablación ineficaz, con repercusión clínica importante. Ante posible componente de descarga adrenérgica, se decide implante de catéter epidural alto alcanzándose bloqueo simpático con perfusión de lidocaína y reducción de los episodios arrítmicos. Posteriormente se realizó simpatectomía bilateral torácica con evolución favorable. ABSTRACT  Anaesthetic management of arrhythmic storm by sympathetic block The arrhythmic storm is defined by the presence of three or more episodes of ventricular tachycardia, ventricular fibrillation and / or discharges of an implantable cardioverter defibrillator (ICD) in a 24-hour period. In its management, the identification and correction of triggering factors is essential, such as myocardial ischemia, hydroelectrolyte alterations, decompensation of heart failure, as well as the adequate control of sympathetic tone. We present the case of a 43-year-old man with apical hypertrophic cardiomyopathy, carrier of ICD in primary prevention who arrives due to an arrhythmic storm with difficult pharmacological control and ineffective ablation, with important clinical repercussions. Before possible component of adrenergic discharge, it was decided to implant a high epidural catheter reaching sympathetic blockade with lidocaine perfusion and reduction of arrhythmic episodes. Subsequently, bilateral thoracic sympathectomy with favorable evolution was performed.

EFFECTS OF SYMPATHETIC BLOCKADE ON RESPONSIVENESS TO VNS IN PATIENTS WITH HEART FAILURE AND REDUCED EJECTION FRACTION

2020 ◽  
Vol 75 (11) ◽  
pp. 780
Author(s):  
Inderjit Anand ◽  
Jeffrey L. Ardell ◽  
Douglas Gregory ◽  
Imad Libbus ◽  
Lorenzo Dicarlo ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Sympathetic Blockade ◽  
Reduced Ejection Fraction ◽  
Patients With Heart Failure

Mitochondria in Cardiomyopathy: Alterations in Size, Number and Internal Structures

1968 ◽  
Vol 26 ◽  
pp. 126-127
Author(s):  
George Hug ◽  
William K. Schubert
Keyword(s):  
Heart Failure ◽  
Biochemical Analysis ◽  
Left Ventricular ◽  
Size Number ◽  
Internal Structures ◽  
Left Ventricular Outflow ◽  
Chest X Ray ◽  
Myocardial Fibers ◽  
Muscle Biopsies ◽  
Needle Liver Biopsy

A white boy six months of age was hospitalized with respiratory distress and congestive heart failure. Control of the heart failure was achieved but marked cardiomegaly, moderate hepatomegaly, and minimal muscular weakness persisted.At birth a chest x-ray had been taken because of rapid breathing and jaundice and showed the heart to be of normal size. Clinical studies included: EKG which showed biventricular hypertrophy, needle liver biopsy which showed toxic hepatitis, and cardiac catheterization which showed no obstruction to left ventricular outflow. Liver and muscle biopsies revealed no biochemical or histological evidence of type II glycogexiosis (Pompe's disease). At thoracotomy, 14 milligrams of left ventricular muscle were removed. Total phosphorylase activity in the biopsy specimen was normal by biochemical analysis as was the degree of phosphorylase activation. By light microscopy, vacuoles and fine granules were seen in practically all myocardial fibers. The fibers were not hypertrophic. The endocardium was not thickened excluding endocardial fibroelastosis. Based on these findings, the diagnosis of idiopathic non-obstructive cardiomyopathy was made.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Protective role of peroxiredoxin-4 in heart failure

2020 ◽  
Vol 134 (1) ◽  
pp. 71-72
Author(s):  
Naseer Ahmed ◽  
Masooma Naseem ◽  
Javeria Farooq
Keyword(s):  
Heart Failure ◽  
Cardiac Fibroblasts ◽  
Protective Role ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Galectin 3 ◽  
Consequent Increase ◽  
And Oxidative Stress

Abstract Recently, we have read with great interest the article published by Ibarrola et al. (Clin. Sci. (Lond.) (2018) 132, 1471–1485), which used proteomics and immunodetection methods to show that Galectin-3 (Gal-3) down-regulated the antioxidant peroxiredoxin-4 (Prx-4) in cardiac fibroblasts. Authors concluded that ‘antioxidant activity of Prx-4 had been identified as a protein down-regulated by Gal-3. Moreover, Gal-3 induced a decrease in total antioxidant capacity which resulted in a consequent increase in peroxide levels and oxidative stress markers in cardiac fibroblasts.’ We would like to point out some results stated in the article that need further investigation and more detailed discussion to clarify certain factors involved in the protective role of Prx-4 in heart failure.

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