Regularly Irregular Atrial Tachycardia Following an Orthotopic Heart Transplant: What Is the Mechanism?
Article first published online: 10 SEP 2013
© 2014 Wiley Periodicals, Inc.
Journal of Cardiovascular Electrophysiology
Volume 25, Issue 1, pages 105–106, January 2014
How to Cite
YAMADA, T., KUMAR, V. and KAY, G. N. (2014), Regularly Irregular Atrial Tachycardia Following an Orthotopic Heart Transplant: What Is the Mechanism?. Journal of Cardiovascular Electrophysiology, 25: 105–106. doi: 10.1111/jce.12258
- Issue published online: 8 JAN 2014
- Article first published online: 10 SEP 2013
- Accepted manuscript online: 17 AUG 2013 10:30AM EST
- Manuscript Accepted: 2 AUG 2013
- Manuscript Received: 30 JUL 2013
- atrial tachycardia;
- heart transplant;
- recipient to donor atrial conduction;
- radiofrequency catheter ablation
A 54-year-old man with atrial tachycardia (AT) that occurred 2 months after an orthotopic heart transplant with
bicaval anastomoses underwent an electrophysiological study and catheter ablation. At baseline, a regularly irregular AT persisted with 2 different cycle lengths of 740 and 370 milliseconds and exhibited negative P waves in the inferior leads and positive P waves in lead V1 (Fig. 1). During the AT, the atrial activation within the coronary sinus (CS) was the earliest at its posterior aspect (Fig. 1). Activation mapping was transseptally performed in the donor left atrium (LA) during the AT, and it revealed a centrifugal activation pattern from the middle of the inferior suture line (Fig. 2). What is the mechanism of this AT?
It has been reported that atrial arrhythmias occur in nearly 10% of patients after an orthotopic cardiac transplantation. These atrial arrhythmias are associated with macroreentrant and focal mechanisms. They usually occur in the donor heart, but on rare occasions they can occur in a recipient heart with a recipient to donor atrial conduction.[1, 2] In this case, the AT was regularly irregular with 2 different cycle lengths. One of the AT cycle lengths was twice as long as the other. Any mechanisms of ATs in the donor heart would unlikely cause this type of AT. Therefore, activation mapping in the recipient LA was performed during the AT. In the recipient LA, a regular faster AT persisted with a cycle length of 185 milliseconds, which was exactly one-fourth and half of the AT cycle lengths in the donor LA (Fig. 3). These findings suggested that the AT originating from the recipient LA likely conducted to the donor LA with 2:1 and 4:1 conduction. When the cycle length of the AT in the recipient LA slightly increased, the cycle length of the AT in the donor LA accordingly increased. At that time, the AT cycle lengths in the donor LA were exactly 2 and 3 times as long as the AT cycle length in the recipient LA (Fig. 3). These findings suggested that the donor LA should be passively activated by the AT in the recipient LA with variable multiples of conduction block in recipient to donor atrial conduction. A single radiofrequency application was delivered at the site of the earliest atrial activation along the inferior suture line in the donor LA, resulting in restoration of sinus rhythm (Fig. 2). Following this, the AT in the recipient LA was mapped and successfully ablated near the inferior suture line.
Another possible mechanism to explain a regularly irregular AT in a donor heart would be a regular AT with multiple separate breakthrough sites of the recipient to donor atrial conduction. If the refractory periods of these breakthroughs are different, the donor atrium may be activated with different cycle lengths, resulting in a regularly irregular AT in the donor heart. If the atrial activation sequences in the donor heart change in accordance with the changes in the AT cycle lengths, this mechanism would be likely operative.
This case demonstrated that a regular AT in a recipient heart with variable multiples of conduction block in recipient to donor atrial conduction could cause a regularly irregular AT in a donor heart.