Role of Inflammation in Initiation and Perpetuation of Atrial Fibrillation
Role of Inflammation in Initiation and Perpetuation of Atrial Fibrillation
Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Recent studies have indicated that inflammation might play a significant role in the initiation, maintenance, and perpetuation of AF. Inflammatory markers such as interleukin-6 and C-reactive protein are elevated in AF and correlate to longer duration of AF, success of cardioversion, and thrombogenesis. Furthermore, the inflammatory process might be modulated by the use of statins, angiotensin-converting enzyme inhibitors, or glucocorticoids. The purpose of this study is to analyze the current published reports on the relationship between inflammation and AF and the potential therapeutic options available to modulate the inflammatory milieu in AF.
Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. It is often rapid, irregular, and might arise from multiple ectopic atrial foci. Twenty percent of patients with paroxysmal atrial fibrillation (PAF), defined as lasting <7 days (and spontaneous conversion), progress to chronic (persistent or permanent) AF, defined as lasting >30 days. The prevalence of AF—affecting more than 2.3 million people in the U.S.—increases dramatically with age and is seen in as high as 9% of individuals by the age of 80 years. In high-risk patients, the thromboembolic stroke risk can be as high as 9% per year and is associated with a 2-fold increase in mortality. The purpose of this study is to analyze the current published reports on the role of inflammation in the perpetuation and maintenance of AF and potential therapeutic options available to modulate this inflammatory process.
Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Recent studies have indicated that inflammation might play a significant role in the initiation, maintenance, and perpetuation of AF. Inflammatory markers such as interleukin-6 and C-reactive protein are elevated in AF and correlate to longer duration of AF, success of cardioversion, and thrombogenesis. Furthermore, the inflammatory process might be modulated by the use of statins, angiotensin-converting enzyme inhibitors, or glucocorticoids. The purpose of this study is to analyze the current published reports on the relationship between inflammation and AF and the potential therapeutic options available to modulate the inflammatory milieu in AF.
Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. It is often rapid, irregular, and might arise from multiple ectopic atrial foci. Twenty percent of patients with paroxysmal atrial fibrillation (PAF), defined as lasting <7 days (and spontaneous conversion), progress to chronic (persistent or permanent) AF, defined as lasting >30 days. The prevalence of AF—affecting more than 2.3 million people in the U.S.—increases dramatically with age and is seen in as high as 9% of individuals by the age of 80 years. In high-risk patients, the thromboembolic stroke risk can be as high as 9% per year and is associated with a 2-fold increase in mortality. The purpose of this study is to analyze the current published reports on the role of inflammation in the perpetuation and maintenance of AF and potential therapeutic options available to modulate this inflammatory process.
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