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The cardiac myocyte: excitation and contraction
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
The overloaded Ca2+ store is prone to spontaneous, partial discharge during early diastole, possibly exacerbated by increased leakiness of the Ca2+ release channels (RyR2) due to p-adrenoceptor-driven phosphorylation. The diastolic rise in sarcoplasmic Ca2+ stimulates Ca2+ expulsion by the sarcolem- mal 3Na+/1Ca2+ exchanger. Since this entails a net inward flow of positive charge, it causes a depolarization after the action potential (Figure 3.17). If the afterdepolarization reaches a threshold, a premature action potential follows and may trigger an arrhythmia. Afterdepolarization may occur after the cell has fully repolarized (delayed afterdepolarization) or during its repolarization phase (early afterdepolarization). Delayed afterdepolarizations probably trigger most of the arrhythmias associated with acute cardiac ischaemia, chronic cardiac failure, digoxin toxicity and phosphodiesterase inhibition.
Electrocardiogram
Published in Burt B. Hamrell, Cardiovascular Physiology, 2018
Early afterdepolarizations (Figure 7.32) tend to occur with action potential prolongation. A decrease in heart rate normally is accompanied by prolongation of atrial and ventricular myocyte action potentials, particularly phase 2. Normal prolongation of phase 2 with a low heart rate derives from effects related to IK.
Pinocembrin ameliorates arrhythmias in rats with chronic ischaemic heart failure
Published in Annals of Medicine, 2021
Yan Guo, Cui Zhang, Tianxin Ye, Xiuhuan Chen, Xin Liu, Xiaoli Chen, Yazhou Sun, Chuan Qu, Jinjun Liang, Shaobo Shi, Bo Yang
Autonomic nervous system (ANS) is a crucial role in the pathogenesis of VAs in CIHF. On the one hand, increased sympathetic activation can lead to increased automaticity of the ventricular pacemaker cells. On the other hand, ANS also regulates early afterdepolarization (EADs) and delayed afterdepolarization (DADs) [23]. Previous studies have shown that the density of sympathetic nervous in myocardial infarction area of spontaneous VAs patients was higher than that of non-spontaneous VAs patients [24]. It is reported that the density of nervous in left stellate ganglion increased significantly after myocardial infarction caused by coronary artery balloon occlusion [25]. Moreover, sympathetic activation reduces ERP and QTc, which could be a prerequisite for circus-type re-entry [26]. Furthermore, sympathetic neurotransmitters increase excitation and conduction heterogeneity and lead to susceptibility to VAs by interacting with cardiac ion channels. Sustained sympathetic activation inhibits Kv4.3, depolarizes L-type calcium channels, and resulting in APD shortening [27, 28]. Our electrophysiological data support these published findings. At the molecular level, autonomic nerves not only acted on ion channels, but also interacted with connexin proteins extensively. Yang et al. found that the neural chemorepellent semaphoring 3a inhibits neural remodelling, reducing the accumulation of dephosphorylated Cx43, and improving the inductivity of VAs [29]. These findings are consistent with our observation that up-regulated Cx43 were parallel with the reduced incidence of VTs following pinocembrin treatment.
Pharmacotherapy in inherited and acquired ventricular arrhythmia in structurally normal adult hearts
Published in Expert Opinion on Pharmacotherapy, 2019
Staniel Ortmans, Charline Daval, Martin Aguilar, Pablo Compagno, Julia Cadrin-Tourigny, Katia Dyrda, Lena Rivard, Rafik Tadros
The long QT syndrome is characterized by delayed ventricular cardiomyocyte repolarization manifesting on the surface ECG by a prolonged corrected QT (QTc) interval. Ventricular arrhythmia physiopathology in LQTS involves early afterdepolarization-mediated triggered activity. β-adrenergic stimulation accentuates the phenotype by increasing ICa (Figure 3). In untreated patients, the rate of SCD ranges between 0.3% and 0.9% per year [23]. The risk of cardiac events is about 10% between birth and age 40 in asymptomatic carriers of a pathogenic mutations [24]. Based on the 2013 international expert consensus statement, LQTS is diagnosed in the presence of either 1) a risk score ≥ 3.5 in the absence of secondary cause of QT prolongation [25], 2) an unequivocally pathogenic mutation or 3) a QTc interval ≥ 500 ms in repeated 12-lead ECGs and in the absence of a secondary cause for QT prolongation. LQTS can also be diagnosed in the presence of a QTc between 480 ms and 499 ms in repeated 12-lead ECGs in a patient with unexplained syncope [3]. Mutations in 3 genes underlie ~85% of definite LQTS cases [26]: loss of function mutations in the potassium channel genes KCNQ1 and KCNH2 cause LQT1 and LQT2, respectively, while gain of function mutations in SCN5A that cause impaired inactivation cause LQT3. LQTS can be classified as either isolated or accompanied with extra-cardiac features.
Effects of antiarrhythmics and hypokalemia on the rate adaptation of cardiac repolarization
Published in Scandinavian Cardiovascular Journal, 2018
In normal conditions, heart rate acceleration during exercise or emotional stress provokes a reduction in ventricular action potential duration [1], an effect that ensures sufficiently long diastolic interval in order to allow an adequate ventricular filling and maintain coronary blood flow. The prolonged diastolic interval also eliminates the possibility for encroachment of the next ventricular depolarization on the T wave of a preceding beat (the “R-on-T phenomenon”), which would otherwise initiate arrhythmia. Importantly, attenuated shortening of ventricular repolarization in tachycardia can result in the “too long” action potential duration for a given level of increased heart rate, an effect that favors arrhythmogenic early afterdepolarizations [1,2]. The impaired rate adaptation of ventricular repolarization, therefore, is likely to be maladaptive and contributing to cardiac electrical instability.