China
Africa
Explore chapters and articles related to this topic
Neuroendocrine Factors
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Catecholamines are potent cardiac stimulants, with both inotropic and chronotropic effects mediated by β1 receptors on the sinoatrial (SA) node and conducting tissues (108, 219). Heart rate can be accelerated through an increase in the slow depolarization of the SA nodes during diastole (219). It is generally believed that increased heart rate after β-adrenergic stimulation is caused by modulation of ionic channels, particularly Ca++ channels, located in the surface membrane of conduction fibers (39). Ventricular arrhythmias, including premature ventricular contractions (PVCs), tachycardia, and fibrillation, can be caused by endogenous release of catecholamines, particularly EPI, in a sensitized heart (43, 132, 219). Increased blood pressure (BP) can be a myocardial sensitizing factor for catecholamine-induced arrhythmias; thus, factors such as exercise that simultaneously increase catecholamines and BP may induce arrhythmias among susceptible individuals (11, 219). Epinephrine can also cause a decreased T wave amplitude, and large doses can cause S-T segment depression (EKG) (204, 219).
Ventricular Arrhythmias in Heart Failure
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Antonis S. Manolis, Antonis A. Manolis, Theodora A. Manolis
In patients with LV dysfunction suspected to be caused by PVCs or NSVTs (“PVC- or tachycardia-induced CM”) catheter ablation should be considered (Table 21.2).61,106,107 A high PVC burden (>24% or >10,000/24 h) in patients with LV dysfunction and a rather short coupling interval of the PVCs (<300 ms) suggest PVC-induced cardiomyopathy.1,108 In such patients, catheter ablation can suppress PVCs and restore LV function.43
Cardiovascular Drugs during Pregnancy
Published in “Bert” Bertis Britt Little, Drugs and Pregnancy, 2022
Premature ventricular contractions (PVCs) are relatively common and may actually be increased during pregnancy. They generally do not require therapy, especially in asymptomatic pregnant women. Frequent PVCs should alert the clinician to possible organic heart disease, but medical therapy is rarely necessary for infrequent PVCs. Agents to treat frequent or asymptomatic PVCs include lidocaine, procainamide, quinidine, or disopyramide.
Acute effect of outflow tract premature ventricular complex ablation on QT dispersion, Tp-e interval and Tp-e/QT ratio
Published in Acta Cardiologica, 2021
Abdulkadir Uslu, Ayhan Kup, Kamil Gulsen, Serdar Demir, Batur Gonenc Kanar, Gokay Taylan, Münevver Sari, Taylan Akgun, Alper Kepez
A total of 180 patients (49.2 ± 13.6 years, 74 male) without any exclusion criteria who had undergone outflow tract PVC ablation between 01.01.2015 and 01.11.2018 constituted our study population. PVC ablation had been considered for patients with symptomatic frequent (more than 10,000 PVCs on 24-h Holter recording) monomorphic PVCs resistant to medical therapy. Ablation was also considered for patients with suspected PVC-related cardiomyopathy. Detailed medical history and electrocardiography (ECG) acquired before and after ablation procedure on the same day was retrospectively obtained from patient files for each patient. Prior Holter recordings that directed patient for ablation and electrophysiological study (EPS) recordings acquired during ablation procedure were also obtained for evaluation of the presence of outflow tract VT that has the same morphology with clinical outflow tract PVC. Patients with atrial fibrillation/flutter, paced rhythm and/or complete/incomplete bundle branch block were excluded from the study. Other exclusion criteria were history of prior myocardial infarction, hypertrophic cardiomyopathy and having any kind of systemic disease that may increase tendency of development of outflow tract PVCs and/or VT as anaemia and thyroid disease. Local ethics committee has approved the study protocol.
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
Following extrication and over the ensuing 20 min, the patient’s heart rhythm was NSR. Patient reassessment found wheezing in all lung fields. A Metered Dose Inhaler (MDI) adapter was placed on the airway tree and over 2 min, 6 100 mcg MDI doses of albuterol (also known as salbutamol) were administered. Subsequent reassessment revealed that the wheezes had resolved. Approximately one min after albuterol administration was completed, the patient developed uniform premature ventricular contractions (PVCs), which quickly increased in frequency over the ensuing minute until the patient was in ventricular bigeminy. Periods of ventricular bigeminy alternated with NSR, which ultimately evolved to include polymorphic PVCs (Figure 3a), short bursts of bidirectional ventricular tachycardia (Figure 3b), and ultimately Polymorphic Ventricular Tachycardia (PVT) (also known as torsades de pointes) (Figure 3c), which occurred approximately 5 min after albuterol administration.
Computational modelling of mechano-electric feedback and its arrhythmogenic effects in human ventricular models
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Yongjae Lee, Barış Cansız, Michael Kaliske
The function of the heart is achieved as a result of mutual interaction between the propagation of electrical wave and the mechanical deformation, which operates bidirectional coupling: excitation–contraction coupling and mechano-electric feedback (MEF). The former refers to the process by which the electrically activated cardiac myocytes result in the myocardial contraction (Bers and Despa 2013), and the latter refers to the reverse coupling through which the electrophysiological changes may result from the regional mechanical stretch or global hemodynamic overload (Franz et al. 1989). Ions flow through stretch activated channels (SACs) that are opened and closed in response to the myocardial stretch, which consequently leads to the variation of the voltages through the cell membrane and the depolarization of cardiomyocyte. As a result, the generated electricity due to stretches affects the cardiac electrophysiology, which has the potential to modulate heart rate and rhythm through auto-regulatory mechanisms in response to beat-to-beat changes in venous return (Kohl et al. 1999). By contrast, with acute mechanical alteration, MEF has the potential to disturb the cardiac rhythm and to increase risk of arrhythmia including heart failure. For example, a critical fibrillation can be caused by a moderate precordial impact to the heart without any morphological damage, which is attributed to MEF and is called commotio cordis (Kohl et al. 2001). Also, MEF is one of the causes of premature ventricular contraction (PVC), where a beat is initiated from outside of the atrioventricular (AV) node, e.g. by Purkinje fibres (Franz 1996; Adams et al. 2012).