Number of P-wave fragmentations on P-SAECG correlates with infiltrated atrial fat.

2014 
An estimated 2.23 million people in the United States have diagnosed atrial fibrillation (AF)1. AF increases the risk of stroke and death 2;3 and leads to important socioeconomic consequences such as chronic disease management, disability, and increased hospital admissions. Moreover, the AF burden is increasing due to the aging US population since AF tends to be more prevalent in the elderly 4;5. While our understanding of AF pathophysiology has significantly advanced over the last two decades, the treatment of AF is rarely curative, and in many cases AF progresses from paroxysmal AF to persistent AF 6. The development of a strategy for the primary prevention of AF is urgently needed. However, the substrate and the mechanisms of early AF genesis are not fully understood. Underlying structural heart diseases, such as coronary heart disease (CHD), hypertensive heart disease, valvular heart disease, cardiomyopathy, and heart failure (HF), predispose patients to AF7. Atrial fibrosis8 is associated with clinically manifest AF. Epicardial fat was shown associated with AF9,10. In the Framingham Heart Study (FHS) epicardial fat was associated with prevalent AF11. Experiments showed paracrine properties of epicardial fat and release of pro-inflammatory and pro-fibrotic substances12. At the same time, autopsy studies demonstrated that fat can infiltrate myocardium13. However, infiltrated atrial fat has not been previously studied in-vivo in patients with paroxysmal AF and in individuals at risk of AF. Only recently technology to quantify in-vivo infiltrated myocardial fat became available14. Electrophysiologic studies have shown that an abnormally prolonged and fractionated atrial electrogram, which is a sign of delayed and non-uniform conduction through the atria, is characteristic of patients with AF 15;16. Modeling studies have shown that atrial electrogram fractionation is a measure of fibrosis and discontinuous conduction17. Abnormally prolonged P-waves on signal-averaged electrocardiograms (P-SAECGs) predicted AF paroxysms in HF patients 18 and patients after cardiac surgery 19. Still, very few studies have explored atrial electrophysiological properties and atrial structural characteristics in patients at risk of AF, without clinically manifest AF. We hypothesized that number of P-wave fragmentations on P-SAECG correlates with infiltrated atrial fat and represents early substrate of AF.
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