Electrophysiologic characteristics of paroxysmal and chronic atrial fibrillation in human right atrium
Bernhard Zrenner, MDa,
Gjin Ndrepepa, MDa,
Martin R. Karch, MDa,
Michael A. E. Schneider, MDa,
J.ürgen Schreieck, MDa,
Albert Schömig, MDa and
Claus Schmitt, MDa
a Deutsches Herzzentrum München and 1. Medizinische Klinik, Klinikum rechts der Isar, Technische Universität München, Munich, Germany
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Figure 1 Fluoroscopic appearance of basket catheters and coronary sinus (CS) catheters in the left anterior oblique coronary artery 45° projection. A andB identify the basket splines having markers 7/8 and 6/7 positions.
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Figure 2 Three types of activation observed in the right atrium (RA). Three surface electrocardiographic leads, 56 bipolar basket catheter electrograms and CS electrograms are shown. (Left) Homogeneously regular activation. During a homogeneously regular pattern, the entire RA was activated from a single wave front emerging from the high anteroseptal area (electrode B 1/2). (Middle) Nonhomogeneous activation. Type II and III atrial fibrillation (AF) are observed along the posterior and septal regions of the RA (splines A to D), whereas the lateral wall (splines G and H) is activated by type I AF. (Right) Homogeneously irregular activation. Complex activity (AF type II and III) is observed throughout the RA. Splines E and F were located across the tricuspid annulus.
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Figure 3 Three-dimensional activation patterns in a patient with paroxysmal atrial fibrillation. Isochrones are drawn every 5 ms. Splines A and B are located in the posterior wall, splines B, C and D in the septal wall, spline E across the tricuspid annulus and splines G and H are located in the lateral wall of the right atrium (RA). Electrode pairs 1/2 are located in the upper RA, whereas electrode pairs 7/8 are located in the lower RA. Grey ellipse shows position of the tricuspid valve. Red represents the head of activation front. At time 0, an early breakthrough is observed in the high septal region. After 74 ms, almost the entire RA was activated from that spot. At the level of electrode pair B 6/7 (low posterior region), the main wave front is divided into two wave fronts heading toward the low posterior (electrode B 7/8) and posteroseptal (electrode C 5/6) regions. After 107 ms, the lateral wave front crossed the isthmus region and emerged at the low septal region, whereas the posteroseptal wave front activated most of the posteroseptal area. At 174 ms, two wave fronts are just re-entering the posterior and the lateral regions again.
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Figure 4 Random re-entry in a patient with chronic atrial fibrillation. A time window of 100 ms is shown. Spline locations were: splines A and B in the posterior wall, splines C and D in the septal wall, spline E across the tricuspid annulus and splines F, G and H in the lateral wall. At time 0, two wave fronts in the right atrium were observed. After 20 ms, the posterior wave front goes up the posterior wall, whereas the lateral wave front is divided into two wave fronts going up and down the lateral wall. After 40 ms the posterior activation front reaches the high right atrium. The lateral wave fronts move toward the higher and lower areas. A new wave front moves toward the tricuspid annulus (electrode pair G 5/6). At 60 ms, posterior and lateral wave fronts enter the high septal region. At 80 ms, a collision of wave fronts is observed in the high septal region, and a new division is observed in the low lateral region. At 100 ms, one of the lateral wave fronts crossed the isthmus region and entered the septal region, whereas the other wave front re-enters the midlateral wall. Meanwhile, the septal wave front is divided into two wave fronts, heading for collision with the wave front coming through the isthmus and the other one (electrode pair A 3/4) moving toward the midposterior section.
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