Epicardial mapping in chronic atrial fibrillation during open chest surgery

Chronic atrial fibrillation (AF) is a frequently encountered arrhythmia in
clinical practice. Atrial dilatation, e.g. secondary to mitral regurgitation,
is an important and independent risk factor for development of AF. On the other
hand, persisting AF itself leads to atrial dilatation. So AF and atrial
dilatation are mutually dependent. Much research has been done to study the
relationship between AF and atrial dilatation, however mostly in animal models.
Not much is known about the appearance of AF in humans with chronic AF and
dilated atria. Also the effect of acute dedilatation and dilatation in subjects
with chronic AF has never been studied.

The goal of the proposed study is to study the relationship between chronic
atrial dilatation and the electrophysiological properties of the atria in
subjects with chronic AF. Furthermore, we would like to study the effect of
acute atrial dilatation and dedilatation on the electro-physiological
properties of the atria in part of the study population.

The design of the study is observational.

Nature and extent of the burden and risks associated with participation
During open chest surgery we will perform high-density mapping on the
epicardial surface of the right and the left atrium, just after opening of the
pericardium, on a beating heart during normothermia. The measurements will take
approximately 10 minutes. In 10 patients we will also vary the left atrial
pressure by means of the extracorporal circulation from approximately 3-5 mmHg
to a maximum of 25 mmHg. Maximal left atrial pressure will be 25 mmHg to
prevent pulmonary edema. At baseline pressure, minimal pressure and maximal
pressure a steady state will be kept for 2 minutes. The only side effect of the
dilatation protocol is a change in pressure in the pulmonary vessels. Low
pulmonary pressure during a couple of minutes is not a problem at all. The
effect of high pulmonary pressures can be that pulmonary edema occurs. However,
pulmonary edema only occurs when the pulmonary pressures rise for a longer
period of time above 25 mmHg. To prevent this, we won't accept that the
pulmonary pressure rises above 25 mmHg. Furthermore, the time pulmonary
pressures are someawhat elevated ís short, only a couple of minutes, making the
occurrence of edema even less unlikely.
Even so, when pulmonary edema does occur, it is quickly noticed due to the
normal hemodynamic monitoring during open heart surgery, and also quickly
corrected.
The follow up of the patients will be the usual care.