By Hauw T. Sie, Giuseppe D'Ancona, Fabio Bartolozzi, Willem Beukema, Donald B. Doty
In recent times, a myriad of surgical protocols were built to control atrial traumatic inflammation, expanding the confusion over that are the simplest techniques. This well timed e-book offers a multidisciplinary, foreign staff of experts who've reviewed the facts on the way to identify which surgical techniques will be used less than which circumstances.Divided into 5 elements, the e-book not just explores surgical procedure of atrial traumatic inflammation, it additionally deals an entire knowing of its underlying causes:Anatomy, Pathophysiology, and Electrophysiologic foundation of Atrial traumatic inflammation Surgical method of Atrial traumatic inflammation: The Cox-Maze method changes of the Cox-Maze, Use of other Surgical styles, and effort resources The Invasive heart specialist technique Perioperative problems, Reporting effects, and Statistical AnalysisWith its transparent presentation and research of the present findings in surgery of atrial traumatic inflammation, this booklet issues the way in which in the direction of a systematic strategy for the surgical medication of atrial traumatic inflammation and is key examining for all cardiac surgeons.
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Additional info for Manual of Surgical Treatment of Atrial Fibrillation
Example text
These include hypertension, coronary artery disease, heart failure, valvular dysfunction, pericardial disease, and cardiac surgery. Arrhythmogenesis is postulated to be mediated by altered vascular compliance, impaired ventricular relaxation, elevated filling pressures, and left atrial (LA) stretch. This disease entity tends to be associated with a dysfunctional cardiovascular substrate and is associated with a higher incidence of complications, such as systemic thromboembolism. A smaller proportion of cases (approximately 15%) occur in patients without structural cardiac or vascular diseases.
It has been identified in families with hypertrophic cardiomyopathy [12], skeletal myopathies [13], familial amyloidosis [14], and in monogenic diseases predisposing to atrial abnormalities. In these cases, the disease is probably related to morphological changes in the atria caused by the underlying cardiac pathology. The disease can also be present in other ion channelopathies like Long QT 4 [15], Brugada syndrome [16], and Short QT syndrome [17]. In the latter, the mutations described in HERG cause a gain of function of IKr , responsible for sudden cardiac death.
Multiple electrophysiologic mechanisms have been proposed as the basis for focal PV firing, including abnormal automaticity, triggered activity, and micro-reentry; however, the exact mechanism for conversion of the focal PV activity into AF is still unknown. There is increasing evidence that local autonomic innervation of the PVs plays an important role in the modulation of PV foci output and the transduc- Pathophysiology of atrial fibrillation 25 tion of these impulses into a propagated arrhythmia.