China
Africa
Explore chapters and articles related to this topic
Rosmarinic Acid: A Boon in the Management of Cardiovascular Disease
Published in Mahfoozur Rahman, Sarwar Beg, Mazin A. Zamzami, Hani Choudhry, Aftab Ahmad, Khalid S. Alharbi, Biomarkers as Targeted Herbal Drug Discovery, 2022
Md. Adil Shaharyar, Mahfoozur Rahman, Kumar Anand, Chowdhury Mobaswar Hossain, Imran Kazmi, Sanmoy Karmakar
Acute myocardial infarction (AMI) and arrhythmia are a menace to the society and a great cause of hospitalization and mortality respectively. The cellular calcium level is regulated by both Sarcoplasmic reticulum Ca2+ ATPase (SERCA2) and Ryanodine receptor (RyR2), respectively. The protocol was designed in such a way so as to investigate whether rosmarinic acid can safeguard cardiac functions against AMI and arrhythmia induced by Isoproterenol, modulated by both SERCA2 and RyR2 genotypically. For mechanism of rosmarinic acid in myocardial infarction refer to Figure 10.1 (Javidanpour et al., 2018).
Roles of Daily Diet and Beta-Adrenergic System in the Treatment of Obesity and Diabetes
Published in Nilanjana Maulik, Personalized Nutrition as Medical Therapy for High-Risk Diseases, 2020
Ebru Arioglu Inan, Belma Turan
However, Lima-Leopoldo et al. reported that feeding with a hypercaloric diet did not cause any impairment in beta-adrenergic responsiveness mediated by isoprenaline in the papillary muscles of obese Wistar rats (Lima-Leopoldo, Leopoldo et al. 2011). Furthermore, in this study, cyclic adenosine monophosphate (cAMP) phosphorylation of proteins associated with Ca2+ handling such as SERCA2a and phospholamban was not changed in obesity. Cardiomyocyte contraction amplitude was shown to be decreased in Fisher rats fed with a protein restricted feed after weaning (Penitente, Novaes et al. 2014). Both mean arterial pressure and heart rate were increased significantly in the protein restricted group. This effect was attributed to structural alterations in the cardiovascular system due to reduced amino acid bioavailability. In this study, the fact that the beta AR mediated contractile response mediated by isoprenaline was also depressed has been suggested to arise from reduced sympathetic responsiveness due to low protein intake. Ca2+ sparks amplitude was lower and frequency was higher in the protein restricted group which was attributed to altered Ryanodine receptor (RyR2) function. Furthermore, the SERCA2a expression decrease in the restricted group is consistent with inhibited Ca2+ intake to SR during cardiomyocyte relaxation, thus contributing to prolongation of relaxation time.
Genetically Determined Ventricular Arrhythmias
Published in Andrea Natale, Oussama M. Wazni, Kalyanam Shivkumar, Francis E. Marchlinski, Handbook of Cardiac Electrophysiology, 2020
Houman Khakpour, Jason S. Bradfield
Two variants of CPVT have been described based on their genetic mutation and mode of transmission. CPVT1 has a mutation in the ryanodine 2 receptor gene (RyR2) which leads to delayed afterdepolarization (DAD)-induced extrasystolic activity from defective calcium handling. The resulting transmural dispersion of repolarization provides the substrate for the development of re-entrant tachyarrhythmias.13,76 The RyR2 gene shows autosomal dominant inheritance. CPVT2 is defined by a mutation in the calsequestrin (CASQ2) gene and has an autosomal recessive inheritance. Other unidentified genes are also believed to result in CPVT. The ryanodine receptor is located on the sarcoplasmic reticulum and allows the release of calcium into the cell, thus facilitating excitation contraction coupling in the myocardium. Calsequestrin gene mutations interfere with sarcoplasmic calcium storage.13
Cardiac arrhythmias in pregnant women: need for mother and offspring protection
Published in Current Medical Research and Opinion, 2020
Theodora A. Manolis, Antonis A. Manolis, Evdoxia J. Apostolopoulos, Despoina Papatheou, Helen Melita, Antonis S. Manolis
CPVT is a rare inherited cardiac arrhythmia caused by an imbalance in the homeostasis of intracellular calcium, and characterized by catecholamine-sensitive polymorphic VT, which can present with palpitations and/or syncope and can lead to SCD83. Patients with CPVT typically have a normal resting ECG and a structurally normal heart. Polymorphic VT is triggered by exertion or emotional stress. CPVT is caused by mutations in the cardiac ryanodine receptor (RyR2) gene, responsible for the autosomal dominant form, or in the sarcoplasmic reticulum protein calsequestrin 2 gene (CASQ2), responsible for the recessive form. Beta blockers remain the cornerstone of therapy in these patients, aided by flecainide, which has an adjunctive role in those not responding to beta blocker84. Implantation of a defibrillator and/or cardiac sympathetic denervation might also be alternative therapeutic options in certain cases.
Catecholaminergic Polymorphic Ventricular Tachycardia: An Unusual Case of Fright-Induced Prehospital Cardiac Arrest in a Healthy 6-Year-Old Child
Published in Prehospital Emergency Care, 2020
Michael Wilson, Steven Schwartz, P. Richard Verbeek
The most common form of CPVT is caused by genetic mutations in the Ryanodine receptor gene (RYR2), responsible for the coding of the ryanodine receptor in cardiac muscle (2). The ryanodine receptor controls the release of intracellular calcium from the sarcoplasmic reticulum, generally in response to an action potential. Spontaneous calcium releases (called “sparks”) occur naturally, but are normally not propagated. Catecholamines, such as epinephrine, sensitize the ryanodine receptors and increase the concentration of calcium in the sarcoplasmic reticulum which, in the presence of abnormal ryanodine receptors, can result in a spontaneous calcium wave being propagated throughout the heart (6). These calcium waves leave the cell via the sodium/calcium exchanger and cause a membrane potential change known as an afterdepolarization, which can lead to sustained ventricular arrhythmias in severe cases (7).
Malignant syndromes: current advances
Published in Expert Opinion on Drug Safety, 2021
Minghua Tao, Jiyuan Li, Xuefeng Wang, Xin Tian
Mutations in the RYR2 gene have been shown to cause catecholaminergic polymorphic ventricular tachycardia (CPVT), which can present with episodes of syncope, sudden cardiac arrest, or sudden cardiac death due to either fast polymorphic ventricular tachycardia (VT) or bidirectional VT [36]. RYR3 is ubiquitously expressed but is less well studied. According to one study, RYR3 variants are associated with hypertension, diabetes, and Alzheimer’s disease [37]. In addition, a recent study indicated that RYR3 is important for extraocular muscle (EOM) function. The authors observed strong RYR3 expression in human and murine EOM, which is mainly responsible for focusing the eye, and thus functional defects in EOM may result in poor vision [38].