Issue: February 2009
February 01, 2009
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Clinical science integrated into AF therapies and research

Issue: February 2009
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Recent discoveries have advanced knowledge of the mechanisms of atrial fibrillation in humans while raising new questions.

Nicholas S. Peters, MD, PhD, professor of cardiology at the Imperial College in London, discussed some of the clinical information about the mechanisms and assessment of AF that has been integrated into practice.

“About 10 years ago, it was very simple … Today we have triggers vs. substrates, and the concept was that there was a natural progression of patients with clinical syndrome paroxysmal to persistent AF,” Peters said.

One of the issues investigators have been exploring is the difference between paroxysmal and long-standing persistent AF. While the differences have been established, Peters indicated that there needed to be greater distinction between the two.

“If we look at the American College of Cardiology/American Heart Association guidelines, you will see that there is not a great deal of acknowledgement that there is a difference between new-onset persistent AF and long-lasting persistent AF in terms of the paradigms and guidelines throughout their clinical practice,” Peters said.

Another potential area for further exploration is of the structure and function of the myocardium. Although tools exist for the assessment of histology and conduction in the laboratory, clinical equivalents like high-resolution cardiac MRI can be used for assessing “virtual” histology. Conduction can be assessed clinically by examining an electrogram.

For more information:

  • Peters N. Thursday afternoon scientific session.

PERSPECTIVE

Regarding atrial fibrillation, Dr. Peters is correct to emphasize how much more we have to learn about the relationship between trigger and substrate, and the pathophysiology of the different clinical presentations and progressions of AF. This, importantly, includes an understanding of the mechanism or mechanisms of AF. Animal models suggest that an important mechanism is the presence of one or more drivers. In patients, we know that drivers can exist in the pulmonary veins, but while it has been suggested that drivers develop in the atrial substrate, that is uncertain. The multiple reentrant wavelet canine model of AF suggests that AF can persist in the absence of a driver or drivers. But, again, in patients, we don't know. Very high resolution atrial mapping during AF would provide important data in this regard, but the techniques to do that are not readily available for use in patients. So, we need advances in understanding the pathophysiology of AF, and we need improved techniques to obtain these answers.

Albert Waldo, MD
Cardiology Today Editorial Board member