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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Usually there are no symptoms, but there may be weakness and the effects of cardiac arrhythmias. Ultimately, ventricular arrhythmias and ventricular fibrillation can cause a cardiac arrest.
Swarm Intelligence and Evolutionary Algorithms for Heart Disease Diagnosis
Published in Sandeep Kumar, Anand Nayyar, Anand Paul, Swarm Intelligence and Evolutionary Algorithms in Healthcare and Drug Development, 2019
Cardiac arrhythmias (CA): This cardiovascular disease is caused due to abnormality in the heart beat rhythm. The characteristics of arrhythmias are (1) increased heart beat rhythm greater than 100bpm; (2) decrease in the heart beat rhythm less than 60bpm; (3) asynchronous functioning of heart chambers; and (4) irregular rate of heart pumping. The health conditions that result due to cardiac arrhythmias are (1) decrease in the performance of hemodynamics; (2) natural cardiac pacemaker exhibits abnormal pumping rate; (3) blood conduction process interruption due to blockage of blood vessel pathways; and (4) random heart part takes self-alternative responsibility to control pumping rate of blood.
Mitochondrial Dysfunction and Heart Diseases
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
The capacity of mitochondria to uptake and release Ca2+ can have substantial impact on the spatial and temporal dynamics of Ca2+ signaling in cardiomyocytes. Impaired mitochondrial function has been reported to cause alterations of calcium transient by affecting the capacity of the mitochondrial Ca2+ handling.130 This change increases susceptibility to cardiac arrhythmias. Increased ROS has also been shown to alter mitochondrial Ca2+ concentration131 by modulating mitochondrial NCX function or cytosolic Ca2+ levels, contributing to the perturbation of intracellular Ca2+.115,132 Ischemia-induced ROS can lead to collapse of mitochondrial membrane potential and release Ca2+ into via a reverse transport mode through mitochondrial NCX,133 resulting in [Ca2+] overload.134 Conversely, Ca2+ overload can induced mitochondrial ROS production. Mitochondrial Ca2+ is known to stimulate oxidative phosphorylation, which also increase the chance of respiratory chain electron leakage leading to ROS production.135 Ca2+ is also known to activate nitric oxide synthase to generate NO, which may inhibit complex IV and enhance ROS production.136 Increased Ca2+ can affect cytochrome c dislocation by competing for cardiolipin binding sites, which may cause complex III inhibition and increased ROS production.137
Gene therapy to terminate tachyarrhythmias
Published in Expert Review of Cardiovascular Therapy, 2022
Kohei Kawajiri, Kensuke Ihara, Tetsuo Sasano
Gene therapy targeting cardiac arrhythmias has been studied for many years, but few clinical applications have been made. Currently, the most commonly used treatments for cardiac arrhythmia are antiarrhythmic drugs, ablative therapy, and implantable devices. Antiarrhythmic drugs, which have been studied for a long time, have shown some efficacy in treating tachyarrhythmias [1]. Ablative therapy is making progress and is particularly effective in treating paroxysmal and early stage of supraventricular arrhythmias [2]. Implantable devices are used to prevent sudden death [3,4]. However, it is difficult to treat all arrhythmias effectively with these therapies [5]. In particular, persistent atrial fibrillation (AF), which is often encountered in daily practice, is difficult to treat using the methods listed above [6], and the treatment of catheter ablation or antiarrhythmic drugs may lead to iatrogenic arrhythmias [7–9]. Once implanted, Implantable Cardioverter-Defibrillators (ICDs) are effective in preventing sudden death from ventricular tachycardia (VT) and ventricular fibrillation (VF), but it is difficult to treat the arrhythmia itself and suppress its onset. It can also cause device infections in the long term [10].
Unravelling the health effects of fasting: a long road from obesity treatment to healthy life span increase and improved cognition
Published in Annals of Medicine, 2020
Françoise Wilhelmi de Toledo, Franziska Grundler, Cesare R. Sirtori, Massimiliano Ruscica
The practice of LF has reached a wide network of utilisation in Europe. Among 1422 subjects who followed fasting periods (daily calorie intake of 200–250 kcal accompanied by a multidisciplinary lifestyle programme) lasting between 4 and 21 days, there were significant reductions in body weight, between 3.2 ± 0.0 kg after 5 and 8.6 ± 0.3 kg after 20 days of fasting, as well as in abdominal circumference, i.e. between 4.6 ± 0.1 cm and 8.8 ± 0.8 cm, respectively. BP decreased for the whole group from 131.6 ± 0.7 to 120.7 ± 0.4 for systolic BP and from 83.7 ± 0.4 to 77.9 ± 0.3 for diastolic BP [24]. A reduction of total cholesterol (−0.4 ± 0.0 mmol/L), triglycerides (−0.4 ± 0.0 mmol/L), glucose (−0.7 ± 0.1 mmol/L) and HbA1c (−1.2 ± 0.1 mmol/mol) was reported. The absence of hunger feeling, documented in 93.2% of the subjects and an increase of emotional and physical well-being was documented. None of the subjects dropped out of the fasting procedure. Adverse effects, e.g. cardiac arrhythmia, were reported in less than 1% and mild symptoms like headache and fatigue occurred rarely and mainly in the first days. In another study on 174 hypertensive patients, who underwent a water-only fasting programme (approximately 10 days), 90% of the subjects achieved a reduction of BP to below 140/90 mm Hg [121].
Identification of Swimmers in Distress Using Unmanned Aerial Vehicles: Experience at the Mont-Tremblant IRONMAN Triathlon
Published in Prehospital Emergency Care, 2020
Valerie Homier, François de Champlain, Michael Nolan, Richard Fleet
A triathlon involves a swim leg (750–3,800 m), followed by a bicycle leg (20–180 km), and a run (5–42 km). The mortality rate for triathletes is 1.7 per 100,000, with the majority of deaths occurring during the swim leg (16, 17). The exact cause of sudden death during the swim portion remains elusive. Cardiac arrhythmia is the most likely cause, although this is not definitive as the quality of available studies is limited (16, 18). In addition, cases of swimming-induced pulmonary edema (SIPE) can occur within minutes of the swim start (16). Triathletes run the risk of rapidly losing consciousness and disappearing in a crowd of swimmers, especially at the race start, and it can be challenging for lifeguards to distinguish victims amongst a large group of swimmers. Early identification of swimmers in distress is becoming a growing priority (19).