Aortic Dissection Complicating Failed Coronary Stenting<br />

Coronary dissection is a well-known complication of coronary interventions; however, proximal progression of the dissection into the aortic root happens rarely.1 The outcome and therapeutic strategy for this iatrogenic complication need to be established. Case Report. A 75-year-old man with exertional angina was admitted to our hospital for coronary angioplasty. Angiography showed a long stenotic lesion of the mid-right coronary artery and a more proximal mildly stenotic curvature with calcification (Figure 1A). The former required treatment by coronary intervention. There were no other systemic findings except for a fourth heart sound. Routine laboratory examination showed that the patient had hyperglycemia compatible with diabetes mellitus and mild hypercholesterolemia. We elected to implant coronary stents because of the high plaque burden of the lesion. We inserted a 6 French Kimny guiding catheter (Schneider Corporation, Minneapolis, Minnesota) into the right coronary artery via the right radial artery and advanced a 0.014´´ Hi-torque balance wire (Guidant Corporation, Temecula, California). Predilatation was easily performed with a 3.0 mm Adante balloon (Boston Scientific/Scimed, Inc., Maple Grove, Minnesota) without difficulty (Figure 1B). Insertion of a 3.0 x 25 mm NIR stent (Boston Scientific/Scimed, Inc.) was attempted; however, the stent did not cross the proximal curvature. We changed to a stiffer guidewire (Hi-torque extra-support wire; Guidant Corporation) and also attempted the parallel guidewire method. Although the guiding catheter was deeply engaged for sufficient back-up force, it was impossible to advance the stent distally. Angiography after removing the stent delivery system showed a proximal dissection of the right coronary artery (Figures 1C and 1D). To avoid abrupt closure, we implanted a 3.5 x 9 mm NIR stent in the ostium of the right coronary artery (Figure 1E). The inflation pressure was titrated to 12 atmospheres and the artery was almost repaired, but minimal false lumen remained (Figure 1F). The patient immediately complained of chest pain. Angiography revealed a threatened closure of the primary dilated lesion (Figure 1G). We performed balloon dilatation again, but considered that stent implantation would be better to avoid abrupt closure. It was impossible to deliver stents without dilating the proximal curvature; thus, despite the risk of propagating the coronary dissection, we attempted balloon dilatation with an Adante 3.0 mm catheter. However, the dissection become prominent without dilating the true lumen. We tried a S670 stent (AVE, Galway, Ireland), which is more flexible and crossable, but could not advance it into the curvature. The Amplatz-shaped guiding catheter was exchanged for a Guider catheter (Schneider Corporation) to increase the back-up force, but it was difficult to engage the catheter coaxially, and a second attempt at implanting the S670 stent resulted in failure. Immediate angiography revealed a large coronary dissection with retrograde extension to the sinus of Valsalva and ascending aorta (Figures 1H and 1I). Morphine and nitroglycerin were administered to relieve pain and to control the elevated blood pressure. After a few minutes, fluorography revealed that dye in the false lumen had begun to fade (Figure 1J). Aortography was performed by manual injection; this showed neither extension of the dissection nor involvement of the left main coronary artery. We therefore elected to monitor the patient continuously, rather than attempt more surgery. The patient’s pain resolved immediately and systolic blood pressure was maintained below 110 mmHg. About an hour later, angiography showed that abnormal staining of the false lumen had almost disappeared, and the right coronary artery was patent with no reocclusion of the primary dilated lesion (Figure 1K). Aortic regurgitation was trivial. Computed tomography on that day showed a minimum enhancement of false lumen, but this disappeared by the next day (Figure 2). Although levels of C-reactive protein were elevated to 2.6 mg/dl, the patient had an uneventful course and was discharged on the 10th day after intervention. Angiography performed a month after discharge showed that the aortic dissection had completely disappeared. Moreover, both the primary stenotic lesion and the dissected proximal right coronary artery were patent without haziness or restenosis. Discussion. Dissection of the aorta is an infrequent but life-threatening complication of coronary intervention.1,2 Almost all reported dissections result from the retrograde propagation of a proximal coronary dissection, mainly in the right coronary artery.1 As the supravalvular ridge is rich in collagenous fibers,2 dissections usually remain below the sinotubular junction of the aorta; however, they sometimes distend into the ascending aorta as in our patient, or rarely into the entire aorta.3 During the procedure on our patient, the guidewires and the balloon catheter crossed the lesion without difficulty, and the dissection was not observed after predilatation. It appeared either after deep engagement of the guiding catheter or when we attempted to deliver the NIR stent. Thus, we speculate that an intimal tear caused by the tip of the guiding catheter or by the stent struts was the initial cause of the complication. Just before the aortic dissection appeared, we used an Amplatz type guiding catheter. Although this catheter provides appropriate back-up force when it is coaxially engaged into the coronary ostium, the tip may injure the coronary artery if coaxial alignment is not established. In our case, it may have migrated into the pre-existing false lumen; over-vigorous dye injection may then have caused retrograde propagation of the dissection toward the ascending aorta.3 Thus, from a technical point of view, optimal coaxial alignment of the guiding catheter and gentle injection of the contrast material are recommended, as well as careful manipulation of guidewires,1 to prevent this complication. If aortic dissection occurs, there are two different responses.1 First, if the dissection involves the ascending aorta or extends more distally to the entire aorta,3 or is due to an inherently weakened aorta caused by cystic medial necrosis,4 emergency surgical repair should be considered, particularly if there are other lethal complications.4,5 Second, if the dissection remains just a few centimeters beyond the aortic valve,1 which occurs in most cases, a careful patient monitoring strategy is recommended because it is usually self-limiting.1,6 In our case, we made careful course observation because the dissection did not seem to progress and abnormal staining of the false lumen disappeared within an hour. As a result, the dissection repaired itself spontaneously in a day. Sealing the entry port of the coronary dissection with a stent can also be effective in preventing the dissection from progressing.7,8 We implanted a NIR stent in the ostium of the right coronary artery, but we do not know whether it covered the entry port exactly because the abnormal dye-staining of the false lumen remained after implantation. Moreover, the stent did not prevent the dissection from progressing into the ascending aorta. Coronary stents have become more flexible with a lower profile and better crossability. In this case, however, we could not pass these new-generation stents through a calcified curvature with minimum stenosis. It should be emphasized, therefore, that there are still types of lesions for which coronary stents are not useful.

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