The postcryomaze coronary CTA demonstrated that 95% of the patients had a completely patent circumflex artery. Significant stenosis was seen in only one patient (right dominant circulation), with a 30% to 40% tubular stenosis of the circumflex artery (Fig. 5). However, this lesion corresponded to the P1 area of the mitral annulus and was significantly proximal on the circumflex artery to the P3 area, where the cryoprobe was applied during the cryomaze procedure.
As cryotechnology continues to evolve and becomes more widely accepted in clinical practice, its risk to the coronary arteries that are in anatomic proximity to the areas of targeted ablation remains an issue of debate. Although a rare complication, coronary artery injury has been previously associated with cryoablation in the literature.10–17 Although more recent reports, mostly single patient, have investigated the potential damage of cryothermy to the coronary arteries, the literature is largely devoid of any major studies. Speculation about possible cryothermy-mediated coronary injury, based on random case reports, calls for a proper investigation to search for any occult coronary artery stenosis after the cryomaze procedure.
At a minimum, all cryomaze lesion sets include the Cox-maze III lesions made in the left atrium because of the observations that a left-sided maze alone decreases the incidence of AF18 by 85% to 90%. In the left atrium, a complete set of cryomaze lesions includes a box lesion around all four pulmonary veins, an endocardial mitral isthmus lesion, a “mirror-image” epicardial mitral isthmus lesion that includes the coronary sinus, and closure of the left atrial appendage os. In the right atrium, a cavotricuspid isthmus lesion has been made as the lone right-sided lesion. In fact, this was our preferred lesion during the era from April 2005 to December 2006. However, in view of the fact that macroreentrant circuits can develop in the upper two thirds of an enlarged right atrium despite a well-constructed cavotricuspid isthmus lesion, more recently, our preference is a complete set of Cox-maze III right-sided lesions. The cryolesions across the AV groove that are present in the complete right atrial lesion set can potentially freeze the RCA. However, the limited number of complete right-sided lesions in this study makes drawing conclusions regarding the RCA and cryothermic injury difficult. Nevertheless, none of the CTAs or stress tests in this study support RCA injury.
The circumflex artery courses near the anterolateral commissure, and the coronary sinus is adjacent to the annulus of the posterior mitral valve leaflet; both vessels lie within the left AV groove. This is even more clinically relevant in the left dominant coronary system in which the circumflex artery runs in the AV groove on the posterior surface of the heart and terminates in the posterior descending artery. The RCA runs in the AV groove on the anterior surface of the heart and normally terminates in the posterior descending artery in a right dominant or codominant circulation. On the basis of these observations, it is hypothesized that, during the left-sided cryomaze, when an epicardial lesion is made over the coronary sinus (to ensure transmurality of the counter endocardial mitral isthmus lesion), the circumflex artery is at risk for injury.
To reliably cure long-standing persistent AF, a transmural mitral isthmus lesion that includes the coronary sinus at that level is crucial. Failure to achieve this lesion can produce atypical left atrial flutter that is notoriously difficult to manage, either medically or with catheter intervention. From our current understanding of cardiac anatomy and available power sources, reliably producing a transmural mitral isthmus lesion requires cardiopulmonary bypass. In Cox’s original description, the mitral isthmus lesion was created by extending the inferior limb of the left atriotomy to the P3 portion of the mitral annulus. The coronary sinus was exposed after the fat pad was dissected and then epicardial ablation was carried out with a cryoprobe. This reusable device (Frigitronics; Cooper Surgical, Pleasanton, CA USA) used nitrous oxide and achieved temperatures of −60°C. No reports of coronary injury were ever documented with this approach. In addition, nearly all procedures reproducing the Cox-maze III lesion set, including those using bipolar RF, generally use cryothermy when creating lesions around the coronary sinus as well as the mitral and tricuspid annuli. Again, there are no reports of coronary injury associated with these procedures.
The previously mentioned case reports make apparent that the exact pathophysiology of any potential vessel injury and the final manifestation of the injury remain unclear. As such, a comprehensive approach to identify potential injury is warranted. For example, if the injury manifests itself as physical vessel damage, as in the case report by Doguet et al,19 it would be detected by coronary CTA. On the other hand, if the damage comes in the form of predisposition to coronary vasospasm under stress, as in the case report by Berreklouw et al,20 a stress ECG would likely detect that derangement. Only with documented evidence of the vessels being intact anatomically and physiologically can the true safety of the procedure begin to be assessed.
In light of our findings, it is possible that the underlying cause of circumflex vessel injury in the case reports of Doguet et al19 and Raza et al16 is from suture-related injury secondary to the concomitant mitral valve surgery. Rajbanshi et al17 reported a case of RCA spasm after ablation at the vicinity of the right atrial lesion. The coronary spasm was successfully reversed with the use of intracoronary nitroglycerin, indicating that the cause of spasm may have had other contributing factors. Recently, Wong et al21 reported circumflex artery injury after catheter ablation. In this report, 15 of the 54 patients undergoing ablation had subclinical narrowing that reversed upon administration of intracoronary glycerine trinitrate. We conducted a detailed literature search on postablation vascular injury. The most significant studies that met our criteria are summarized in Table 5.
Although one case of coronary stenosis in our series is debatable, it could have several contributing factors. Because of its location in the circumflex artery, we believe its etiology to be the normal ongoing progression of CAD in an octogenarian. At discharge, the patient had a normal sinus rhythm. Two years after surgery, she had a negative stress test and continued NSR. This circumflex lesion corresponded to the area of the posterior mitral annulus near the P1 area. Therefore, it was unlikely to have been caused by the cryoprobe because the ablation was applied at P3, which was anatomically remote from the site of coronary stenosis.
Although this subset of patients was selected from a much larger cohort, the results did support our contention that cryomaze was highly effective in relieving AF burden. In addition, despite mitral valve repair and the lack of coronary grafts to improve left ventricular function, the ejection fraction did not deteriorate with surgery (50.26% ± 10.07% preoperatively vs 51.68 ± 8.49% postoperatively), as stated earlier in the Results section. This was probably a reflection of the preponderance of mitral repairs rather than replacements as well as the previously documented salutary effect of a successful maze on left ventricular function.
Cryomaze can reliably produce a full set of transmural lesions and, thus, greatly simplify the creation of an effective operation to cure AF. However, concerns that the mitral isthmus lesions are producing occult injuries to the circumflex arteries have been raised. It is hoped that the results of this study, albeit based on a relatively small number of patients, will begin to allay those fears. It is encouraging that all of these patients had no significant AF burden by 24-hour Holter or pacemaker interrogation despite all patients having a long preoperative history of AF. In addition, none of the CTAs or stress tests are consistent with cryothermy-induced coronary injury. The location of the stenosis in the lone patient with a 30% to 40% circumflex lesion is in the P1 area. This area is never frozen during the procedure, and thus, the lesion is not consistent with a cryomaze injury. Expanding the enrollment of patients into this study protocol, particularly those with left dominant circulation, is crucial in confirming our preliminary conclusions.
A secondary observation of this study is the uniform lack of postoperative AF burden. We believe that the success rate of our study in achieving AV synchrony has been due to the cryomaze technique faithfully replicating most lesions of the Cox-maze III lesion set.
Although the data from this small study do not show any adverse complications from cryoablation, in no way do we advocate the carte blanche freezing of coronary arteries. Some laboratory and anecdotal clinical evidence supports cryothermia-induced coronary injury, so we believe that avoiding the intentional freezing of coronary arteries is prudent. Although larger studies are needed to definitively investigate the possibility of vessel injury in cryomaze, this is the first formally designed study investigating the phenomenon in humans. Nevertheless, this small cohort of patients demonstrates no evidence of cryothemia-related coronary injury and is consistent with our much larger overall experience with cryomaze. We have yet to recognize acute or chronic coronary injury associated with cryomazes performed on our patients. However, the scope of this study is restricted to only midterm follow-up, which precludes us from drawing any conclusions of the effects of cryoenergy on the development of CAD in the long-term. Whether cryoablation gives rise to the development of arteriosclerotic plaques over an extended period and whether cryolesions form a nidus for such plaque formation are questions that cannot currently be answered because of the inadequate length of this study. Thus, the relatively small numbers and the midterm follow-up dictate that we continue to exercise caution when freezing in the vicinity of the coronary arteries. Understanding well the limitations of studying only 20 patients, our long-term goal is to add to this study protocol. Because our current policy for persistent and permanent AF is a complete biatrial lesion set, we will also include the RCA as an additional site of investigation for potential injury.
In conclusion, our preliminary data from this relatively small cohort suggest that cryomaze is safe with regard to coronary artery injury. Barring one case of partial circumflex stenosis, likely due to the ongoing normal progression of CAD, these data derived from a limited prospective trial suggest that epicardial application during the cryomaze procedure does not cause anatomic or physiological compromise of the circumflex artery. The results of this study, albeit based on a relatively limited sample size, will begin to allay the fears that the transmural mitral isthmus lesions are producing occult injuries to the circumflex arteries. Whereas these data confirm the safety of cryoablation, in no way do the authors advocate the carte blanche freezing of coronary arteries. Caution should be exercised when applying cryothermy in the vicinity of coronary arteries while creating the Cox-maze III lesion set.
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This is an interesting clinical series examining whether epicardial application of a cryoprobe over the coronary sinus and the atrioventricular groove could injure the circumflex coronary artery. In this prospective study, 20 consecutive patients with normal results of preoperative angiograms were followed after a cryomaze procedure. Postoperatively, all patients underwent a computed tomographic angiogram (CTA), and, in 95% of the patients, there was a patent circumflex artery. There was a stenosis in one patient. The CTAs were performed at a minimum of 6 months after the ablation, with a mean of 2.7 years.
This study suggests that, during a reasonably short follow-up period, the cryomaze procedure, as described in this article, did not injure the circumflex artery. However, this study has a number of important limitations. First of all, it is unclear whether, in any of the patients, the cryoprobe was positioned directly over the circumflex artery. In fact, in a typical right dominant system, the epicardial cryoablation would not be near the circumflex coronary artery. Only five patients in this series had a left or codominant system in which there was even a possibility of an injury. Moreover, there are convincing data that cryoablation of coronary arteries causes intimal hyperplasia in experimental models (Holman WL, Ikeshita M, Ungerleider RM, Smith PK, Ideker RE, Cox JL. Cryosurgery for cardiac arrhythmias: acute and chronic effects on coronary arteries. Am J Cardiol. 1983;51:149–155. Mikat EM, Hackel DB, Harrison L, Gallagher JJ, Wallace AG. Reaction of the myocardium and coronary arteries to cryosurgery. Lab Invest. 1977;37:632–641). This type of injury probably would not be identified on CTA, particularly at this short of a follow-up period, and would likely result in stenoses years after ablation. It is the strong opinion of the Editor that cryoablation should never be performed over coronary arteries. These arteries can almost always be avoided with careful examination of preoperative coronary angiograms. This study does not provide enough data to suggest that cryoablation is safe around coronary arteries, and great caution should be exercised in their vicinity.