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DOI: 10.1148/radiol.2461071406
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(Radiology 2008;246:108-109.)
© RSNA, 2008


Cardiac Imaging

Clinician's Commentary on Saremi et al1

Tristram D. Bahnson, MD

1 From the Duke Cardiovascular Research Institute, Duke University Medical Center, Box 2959 Med Ctr, Durham, NC 27710. Received August 6, 2007; final version accepted August 7. Address correspondence to the author (e-mail: Bahns001{at}mc.duke.edu).

Normal heart rhythm depends on normal impulse initiation in the sinuatrial node (SAN) and impulse propagation through the atrium, atrioventricular node (AVN), and His-Purkinje system. Collectively, these specialized cardiac tissues are referred to as the cardiac conduction system. Injury or disease of the SAN results in bradycardia, sinus arrhythmia, or sinus arrest. Likewise, injury or disease of the AVN or His-Purkinje system results in atrioventricular block or aberrant atrioventricular conduction (eg, bundle-branch block). Ischemia is one potential mechanism of injury to the cardiac conduction system. For example, both SAN dysfunction and atrioventricular block are clinically relevant rhythm disturbances that have been described in association with acute myocardial infarction (1), and both are believed, in many instances, to be caused by interruption of the arterial blood supply to conduction system tissue (2). Abnormalities of the cardiac conduction system often produce hemodynamic compromise because of effects on cardiac output and require permanent pacemaker implantation (3).

The armamentarium of contemporary cardiovascular therapeutics includes surgical procedures for coronary bypass, cardiac valve replacement, and treatment of cardiac arrhythmias. Further, endocardial catheter ablation of cardiac tissue continues to advance as an important therapy to treat virtually all tachyarrhythmias, including atrioventricular nodal reentry, atrial tachycardias, and atrial fibrillation. Most important, each of these therapeutic modalities has the potential to injure the cardiac conduction system either directly or by injury to epicardial coronary arteries. By their nature, atriotomy for valve surgery and arrhythmia surgery, as well as surgical epicardial ablation to achieve modification of intraatrial impulse propagation, produce injury to the myocardium and epicardial structures. Although rare, endocardial catheter ablation can result in injury to adjacent epicardial structures, such as the phrenic nerve (4), esophagus (5), and epicardial coronary arteries (6). Accordingly, knowledge about the specific course of epicardial coronary vessels feeding the SAN and AVN is of potential importance to optimize lesion delivery or atriotomy placement during these procedures.

In this issue of Radiology, Saremi et al (7) report findings of sinuatrial and atrioventricular nodal artery imaging with multidetector CT. In this study, 102 patients of a 110-patient cohort referred for imaging of epicardial coronary arteries are described; eight patients had uninterpretable images because of artifacts. The authors report that these vessels were well visualized by using the described imaging techniques and that the origin and course of both arteries were variable and consistent with results of previous cadaveric and angiographic studies. Accordingly, feasibility of multidetector CT to help provide detailed information about the sinuatrial and atrioventricular nodal arteries has been demonstrated, which opens the possibility of applying these in vivo imaging techniques to define an individual's arterial anatomy prior to surgical procedures. Indeed, the authors consider optimal placement of surgical atriotomy for valve surgery in two of their figures (7).

Of interest is that Saremi et al describe that a single sinuatrial nodal artery originated from the left circumflex artery in 27.4% of the individuals, and that, in 18% (5.9% of the total cohort), it passed through the epicardial sulcus between the base of the left atrial appendage and the left superior pulmonary vein ostium (7). Furthermore, the authors describe that in 47.5% of the individuals, the terminal portion of the sinuatrial nodal artery, whether originating from the right or left coronary arteries, passed posterior to the superior vena cava immediately adjacent to the septal margin of the right superior pulmonary vein ostium. These two regions, anterior and adjacent to the ostia of right and left superior pulmonary veins, respectively, are invariably targeted with surgical and catheter ablation procedures for the cure of atrial fibrillation (812) because electrical isolation of the pulmonary veins by encircling lesions has been shown to be an important end point to achieving procedure efficacy (11,12). A recent study (8) on patient outcome after the cut-and-sew maze III procedure revealed that the incidence of permanent pacemaker implantation for bradycardia was 4.7%, with other outcome studies (10) of this technique revealing a requirement for permanent pacemaker implantation in up to 24% of cases. Surgical maze procedures to treat atrial fibrillation are often performed in conjunction with valve or bypass surgery, which raises the likelihood that some instances of bradycardia are due to direct mechanical injury of the SAN, AVN, or His bundle; however, results of another case series (13) also showed postprocedural bradyarrhythmias requiring permanent pacemaker implantation in patients undergoing a "stand-alone" procedure targeting the arrhythmia only. Thus, inadvertent injury to the sinuatrial nodal artery could well be an important cause of this complication.

There is a potential for catheter ablation to affect the sinuatrial nodal artery; however, clinical experience thus far suggests that this is a rare or nonexistent occurrence (14). In contradistinction, two centers (15,16) report that there is a decrease in the need for permanent pacemaker implantation for SAN dysfunction after endocardial catheter ablation for atrial fibrillation, perhaps owing to modification of cardiac autonomic nerve ganglia after endocardial radiofrequency energy delivery (17).

In conclusion, the current study highlights a potential mechanism for reported bradyarrhythmias that complicate surgical procedures for valve repair or treatment of atrial fibrillation, namely, injury to the sinuatrial or atrioventricular nodal artery. Perhaps future studies relating multidetector CT–defined arterial anatomy with the occurrence of clinically important bradyarrhythmias after specific epicardial surgical lesion sets for atrial fibrillation or other heart ailments will reveal new techniques to minimize this complication.


    FOOTNOTES
 
See also the preceding article by Saremi et al.

Author stated no financial relationship to disclose.


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Related Article

Arterial Supply to Sinuatrial and Atrioventricular Nodes: Imaging with Multidetector CT
Farhood Saremi, Amir Abolhoda, Oganes Ashikyan, Jeffrey C. Milliken, Jagat Narula, Swaminatha V. Gurudevan, Khushboo Kaushal, and Aidan Raney
Radiology 2007 246: 99-107. [Abstract] [Full Text] [PDF]




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