Preface

Chapter 6 **Thrombogenesis in Atrial Fibrillation 127** Hanan Ahmed GalalAzzam

José Joaquín Rieta and Raúl Alcaraz

Raúl Alcaraz and José Joaquín Rieta

**Coronary Artery Disease 229** Atila Bitigen and Vecih Oduncu

Chapter 9 **New Oral Anticoagulants in Atrial Fibrillation 207** Lucía Cid-Conde and José López-Castro

**of Atrial Fibrillation 181**

**Section 4 Anticoagulation Therapy 205**

Chapter 7 **Applications of Signal Analysis to Atrial Fibrillation 155**

Chapter 8 **The Contribution of Nonlinear Methods in the Understanding**

Chapter 10 **Anticoagulant Therapy in Patients with Atrial Fibrillation and**

**Section 3 Signal Analysis 153**

**VI** Contents

Atrial fibrillation is a rapidly evolving epidemic associated with increased cardiovascular morbidity and mortality, and its prevalence has increased during the past few decades. In the past few years, the recent understanding of the diverse mechanisms of this arrhythmia has led to the improvement of our therapeutic strategies. However, many clinicians have still felt the frustration in management of this commonly encountered arrhythmia.

This book contains a spectrum of different topics from bench to bedside in atrial fibrillation. We try to introduce the most recent advancement of mechanisms and treatment of AF including genetics, calcium signaling, thrombogenesis, signal analysis, upstream therapies focus on re‐ nin-angiotensin-aldosterone system inhibitors, antioxidants and n-3 polyunsaturated fatty acids, and anticoagulation issues. I strongly believe that scientists, cardiologists and electro‐ physiologists will find this book very informative and useful. The references cited in each chapter will definitely act as additional source of information for readers.

I am grateful to the all the authors who contributed to this book with their valuable experi‐ ence. I also appreciate the great help from InTech editorial office, Ms. Mirna Cvijic and Mr. Dejan Grgur, who guided me through the publication process step by step. I would also like to thank for the important contributions from the co-editors of this book – Prof. Guangping Li, my mentor, and Dr. Panagiotis Korantzopoulos, my best friend who guided me to ex‐ plore the wonderful world of arrhythmia. Finally, special thanks to my family – wife, Lijian, and son, Yujie, who provided continuous inspiration and support to my work.

#### **Tong Liu, MD, PhD**

Department of Cardiology, Tianjin Institute of Cardiology Second Hospital of Tianjin Medical University, Tianjin People's Republic of China

**Section 1**

**Pharmacological Management**

**Pharmacological Management**

**Chapter 1**

**Atrial Fibrillation and the Renin-Angiotensin-**

Atrial fibrillation (AF) is the most common cardiac arrhythmia, affecting approximately 1% of the general population and up to 8% of subjects over the age of 80 years.[1] AF is a major contributor to cardiovascular mortality and morbidity, being associated with de‐ creased quality of life, increased incidence of congestive heart failure,[2] embolic phe‐ nomena, including stroke,[2,3] and a 30 % higher risk of death.[3,4] AF-associated morbidity includes a four- to five-fold increased risk for stroke, [2,5] a two-fold in‐ creased risk for dementia,[6,7] and a tripling of risk for heart failure.[5] According to the Framingham Study, the percentage of strokes attributable to AF increases steeply from 1.5% at 50–59 years of age to 23.5% at 80–89 years of age, [2] and the presence of AF ac‐ counts for a 50–90% increased risk for overall mortality.[3] From the viewpoint of the AF-related socio-economic burden, it has been estimated that it is consuming between 0.9% and 2.4% of total National Health Service expenditure in the UK,[8] while in the USA, total costs are 8.6–22.6% higher for AF patients in all age- and sex- population strata.[9] Therefore significant clinical, human, social and economical benefits are there‐

It has to be noted that although multiple treatment options are currently available, no single modality is effective for all patients.[10] AF can occasionally affect a structurally normal heart of otherwise healthy individuals (so-called "lone AF")[11], but most typically it occurs in subjects with previous cardiovascular damage due to hypertension, coronary artery dis‐ ease and diabetes. Moreover, it can be associated with clinical conditions such as hyperthyr‐ oidism, acute infections, recent cardiothoracic or abdominal surgery, and systemic

> © 2013 Perlini et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use,

© 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

distribution, and reproduction in any medium, provided the original work is properly cited.

and reproduction in any medium, provided the original work is properly cited.

fore expected from any improvement in AF prevention and treatment.

**Aldosterone System**

Stefano Perlini, Fabio Belluzzi,

http://dx.doi.org/10.5772/53917

**1. Introduction**

Francesco Salinaro and Francesco Musca

Additional information is available at the end of the chapter
