ஜர்னல் ஆஃப் இன்டர்வென்ஷனல் மற்றும் ஜெனரல் கார்டியாலஜி

The description of atrial fibrillation (AF) as a functional electrical condition ignores the significant underlying structural abnormalities. The muscular sleeve of the atrium and the pulmonary vein (PV) undergo microstructural alterations, resulting in a weak foundation for AF maintenance. Current data indicate that this arrhythmia typically requires a trigger for start and a weak electrophysiological or anatomical substrate for maintenance, despite the lack of knowledge regarding the anatomical and functional foundations of AF. Whether the trigger mechanisms are focused improved automaticity, prompted activity, or micro re-entry from cardiac tissue is currently unknown. AF onset can be sped up by both sympathetic and parasympathetic stimuli, which appear to also play a role in AF maintenance. A mechanism that may involve cellular ageing, apoptosis, and subsequent atrial fibrosis and inflammation is linked to both new-onset and recurrent AF, according to growing clinical data.

Arrhythmias in the fetus are a common occurrence with rather intricate causes. The diagnosis and treatment of fetal arrhythmias during pregnancy are still the subject of debate. The retrieved, compiled, and analyzed literature from the past two decades on prenatal diagnosis and treatment of fetal arrhythmias. The types or etiologies of fetal arrhythmias as well as fetal conditions determine the outcomes of intrauterine therapy for fetal tachyarrhythmia’s. The majority can be treated with the first-line antiarrhythmic through a trans placental procedure. In cases of drug resistance or thermodynamic impairment, fetal cardiac pacing’s can successfully restore sinus rhythm. In refractory cases, implantation of an immediate postnatal pacemaker is required.