Pathophysiologic mechanisms of cardiac arrhythmias
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Cited by (115)
Wide Complex Tachycardias
2022, Emergency Medicine Clinics of North AmericaCitation Excerpt :VT is termed sustained when there is hemodynamic instability, or it lasts for greater than 30 seconds.22 The underlying mechanisms of VT, similar to other tachyarrhythmias, can be divided into 3 broad categories: reentrant, triggered activity, or abnormal automaticity.23 Reentry requires a trigger (eg, PVC) and a “loop” or 2 connected pathways (eg, scar or fibrosis from prior MI, surgery, cardiomyopathy) that differ in conduction speed and refractoriness to initiate and sustain the arrhythmia, respectively.
Ventricular Arrhythmias
2019, Medical Clinics of North AmericaCitation Excerpt :Repetitive MMVT refers to short bursts of nonsustained VT occurring in waves of higher frequency followed by lower frequency of occurrence (Fig. 1B, Table 1). There are 3 main mechanisms of MMVT: abnormal automaticity, triggered activity, and reentry.3,4 Focal VT often ensues from triggered activity or abnormal automaticity (see Table 1).
Neonatal and Pediatric Arrhythmias: Clinical and Electrocardiographic Aspects
2018, Cardiac Electrophysiology ClinicsCitation Excerpt :Cardiac arrhythmias are determined by a disorder in the generation or conduction of the electrical impulse. As for adult patients, also in pediatric patients (neonates, children, and adolescents) tachyarrhythmias are caused by enhanced automaticity, triggered activity or reentry mechanism, whereas bradyarrhythmias derive from missing generation of the impulse, or a slow or blocked conduction through the specific conduction system of the heart.8–11 In pediatric patients, a diagnosis of bradycardia depends on the age.12,13
Human placenta hydrogel reduces scarring in a rat model of cardiac ischemia and enhances cardiomyocyte and stem cell cultures
2017, Acta BiomaterialiaCitation Excerpt :Optical mapping experiments showed that hpECM not only increased the amount of surviving cardiac muscle tissue, but that this tissue was also fully functional from an electrophysiological point of view (Fig. 7). This finding is important, because insufficiently repaired tissue could lead to slow conduction, changes in action potential duration, and unidirectional block, which together could provide a substrate for arrhythmias that could be even worse than a larger infarct [36]. Induction of arrhythmia is a notable concern, as other approaches to restore ischemic myocardial tissue have reported aberrant electrical activity in the heart, including recent use of embryonic stem cell (ESC)-derived cardiomyocytes in primates [37].
The Ca-calmodulin dependent kinase II: A promising target for future antiarrhythmic therapies?
2013, Journal of Molecular and Cellular Cardiology