Case Report and Brief Review

Percutaneous Treatment of Catheter-Induced Dissection of the
Right Coronary Artery and Adjacent Aortic Wall

Bahram Sohrabi, MD, Babak Kazemi, MD, Naser Aslanabadi, MD
Bahram Sohrabi, MD, Babak Kazemi, MD, Naser Aslanabadi, MD

Acute aortic dissection during coronary arteriography or percutaneous coronary intervention is quite rare,1,2 but is a feared complication. Patients in this clinical setting may have a potential risk for acute myocardial infarction (MI) requiring emergency surgery.3 Awareness of the problem and its prompt recognition are essential and the possibility of such a complication should be kept in mind when the patient develops severe chest pain during angioplasty. Still, there remains a paucity of data regarding the risk factors and management of aorto-coronary dissection.

In recent years, some reports have shown that stenting the ostium of the coronary artery (right coronary or left main artery) can be a valid, possibly life-saving therapeutic option.3–6 We describe a case in which a right coronary artery (RCA) dissection occurred during diagnostic coronary arteriography and extended beyond the coronary ostium into the ascending aorta. Sealing of the aortic dissection and rescue of the RCA with stabilization of the patient was possible with rapid stenting of the right coronary ostium.

Case Report. A 50-year-old hypertensive male with a history of anterior MI and primary ventricular fibrillation with successful resuscitation (2 months prior) was referred to our institution for coronary angiography because of unstable angina.

 

Left coronary system injection showed a significant ostial lesion of the left anterior descending (LAD) artery, with no significant lesion elsewhere (Figure 1). Using a 6 Fr Judkins Right 4 (JR4) diagnostic catheter (Cordis Corp., Miami, Florida), the ostium of the RCA was easily cannulated and contrast medium was manually injected. This revealed a normal RCA (Figure 2), but subsequent vigorous injection of contrast medium caused a spiral dissection in the proximal RCA with rapid forward extension distally and acute occlusion of the posterior descending artery (PDA) branch (Figure 3).

 

The patient experienced an abrupt onset of severe chest pain and ST-segment elevation in the inferior leads followed by hypotension (systolic blood pressure of 60 mmHg) and bradycardia with complete heart block. A temporary pacemaker lead was immediately introduced into the right ventricular apex via femoral vein puncture and clopidogrel (600 mg p.o.) and heparin (8000 IU intravenous) were administered. Using a 6 Fr Launcher (JR 4) guiding catheter (Medtronic Inc., Minneapolis, Minnesota), the ostium of the RCA was cannulated and a 0.014 inch floppy Balanced Middle Weight guidewire (Guidant Corp., Indianapolis, Indiana) was advanced into the true lumen. A 2.5 x 20 mm Lekton Motion (Biotronik, Inc., Lake Oswego, Oregon) stent was implanted in the distal RCA, achieving restoration of the PDA flow. Sinus rhythm returned shortly after, with no evidence of atrioventricular block. Further contrast injection into the RCA retrogradely escaped into the ascending aorta through the dissected lumen beyond the coronary ostium, and showed clear involvement of the right coronary sinus of Valsalva (CSV) (Figure 4). Extension to the ascending aorta occurred during injections done for stent positioning in the proximal RCA. There was retention of contrast in the ascending aorta. An aortogram was not performed due to the patient’s unstable condition. Altogether, 6 stents were successfully implanted in the RCA, with the last stent in the ostium (from the distal to proximal RCA: 2.5 x 20 mm and 3 x 30 mm and 3 x 20 mm and 3 x 13 mm Lekton Motion stents [Biotronik], 3 x 23 mm Bx Sonic [Cordis] stent, and stent 3 x 18 mm Driver [Medtronic] stent, respectively).

After successful coronary stenting, TIMI-3 flow was achieved, persistent dye-staining of the ascending aorta diminished, and the patient’s condition stabilized (Figure 5). Aortic root angiography was not performed at this stage either because of nearly complete dye clearance of the ascending aorta after stenting of the RCA ostium. Transesophageal echocardiography revealed an intact ascending aorta without evidence of an intimal flap, pericardial effusion or aortic regurgitation. Twenty-four hours later, a second control echocardiography revealed no abnormality. Thepatient’s hospital course was uneventful, and the patient was discharged the following day with clopidogrel (75 mg daily) and aspirin (325 mg daily).

Discussion. Iatrogenic aorto-coronary dissection is quite rare.1,2 The overall incidence of catheter-induced coronary dissection remains unknown, but aorto-coronary dissection has been estimated to occur in approximately 0.008–0.02% of diagnostic catheterizations and 0.04–0.06% of PCIs.1,7–9 Of the type-A dissections in the International Registry of Aortic Dissection (IRAD), 27% were caused by coronary angiography or interventions.2 This event is a devastating complication of PCI, with a mortality rate up to 32%, similar to that of spontaneous type-A aortic dissection (35%).2

The exact mechanism responsible for the propagation of coronary dissection and the occurrence of aortic dissection remains to be established. However, it appears that the entry point originates within the coronary dissection and subsequently leads to progressive retrograde extension of the subintimal space into the aortic root. It occurs following a trauma caused by the tip of the guiding or diagnostic catheter (due to unintended deep intubation), subintimal passage of therigid guidewire, or because of balloon dilatation. With the advent of complex interventions such as revascularization of chronic total occlusions, left main stenting, ostial and bifurcation lesions and saphenous vein graft lesions, this complication may become more prevalent.

Risk factors for aorto-coronary dissection include hypertension, older age,1 extensive atherosclerosis10 and underlying structural weakness of the media (e.g., cystic medial necrosis). Pande et al11 reported a case of iatrogenic aortic dissection during angioplasty of the RCA in a patient with cystic medial necrosis. Our patient was hypertensive without aortic root dilation, and had neither clinical evidence nor family history of Marfan’s syndrome or other causes of medial necrosis, although there is no histopathologic specimen.

A history of MI has been proposed as a risk factor for aorto-coronary dissection. Dunning et al1 described 2 patients with an extensive aorto-coronary dissection. Both of these patients underwent coronary angiography due to acute MI. Our patient also had a history of recent MI.

In a previously published report exclusively on RCA, the left Amplatz guiding catheters were involved in a disproportionate number of catheter-induced right coronary dissections.1 The choice of guiding catheter is a risk-benefit tradeoff between extra backup and the possibility of coronary dissection.12 Other reported risk factors include variant anatomy of the coronary ostia (e.g., downward sloping origin of the left main coronary artery),13 vigorous hand injection of contrast material9 (as in our case), and even vigorous inspiration during contrast injection (respiratory-induced changes in Amplatzshaped catheter position).14 The size of the diagnostic catheters may also be important. We routinely use 6 Fr catheters for this purpose, but with smaller 4 or 5 Fr diagnostic catheters, the incidence of iatrogenic coronary dissections might be reduced.9

Cautious techniques that can minimize the occurrence of iatrogenic dissection include: (1) checking pressure before every coronary injection; (2) avoiding deep engagement of guiding catheters and maintaining a steady tension on the guiding catheter while the angioplasty balloon is withdrawn; (3) prompt and timely recognition of this complication; and (4) minimizing futile efforts to halt the progression of the dissection.12

Many of the cases of aorto-coronary dissections described in the literature have involved the RCA.1,3,6,7,11,12Currently, it is unknown why the RCA is more susceptible to retrograde dissection into the CSV than the left main coronary artery (LMCA). Furthermore, it is interesting to note that when dissecting aortic aneurysms involve the coronary arteries, the RCA is also the one usually affected.4 The inherent properties of the RCA, which defers from the LMCA, may predispose the patient to aorto-coronary dissection.3

Still, there remains a paucity of data regarding the management of aorto-coronary dissections and wide variety of potential clinical outcomes hampers attempts to standardize treatment.12 Despite the lack of evidence-based guidelines for the optimal treatment of aorto-coronary dissection, some reports have shown that stenting the ostium of the coronary artery (RCA or left main) can be a valid and life-saving therapeutic option for the patient.3–6 It is reasonable to attempt to seal the entry site of the dissection with PCI and stenting first, then the extent of dissection can be assessed. From the technical viewpoint, soft-tip wires should be used when attempting to access the true lumen,5,15 and if the initial wire enters the false lumen, another soft-tip wire should be carefully manipulated into the true lumen (double-wire technique).15 If conventional methods have resulted in dissection, the use of a ball-tipped guidewire, such as the Magnum wire, proves very useful to localize the true lumen in cases of spiral dissection.16 Stenting should be performed as soon as possible, as saving time is mandatory in this setting, and implantation should be started distally and finally to the RCA ostium.3

The evolution of the aorto-coronary dissection can be monitored by means of transesophageal echocardiography. This conservative management (the “watchful waiting” strategy, suggested by Alfonso et al4) is a reasonable option only in the hemodynamically stable patient with localized aortic dissection. On the other hand, the progression of an aortic dissection with unstable hemodynamics, acute severe aortic regurgitation, hemopericardium and intractable chest pain are clear indications for intervention.17 The sinus of Valsalva dissections that remain localized during catheterization tend to resolve spontaneously in the first month.7 Localized dissections of coronary arteries have also been successfully treated conservatively,9 although Mulvihil et al18 have described intense healing of these localized coronary dissections, resulting in scar formation with coronary flow obstruction.

To guide the choice for the best therapeutic strategy, a classification of iatrogenic dissection of the ascending aorta has been proposed.1 This classification is based on the extent of dissection to the aortic root. A focal dissection limited to the coronary cusp (Class 1) and a dissection extending to the ascending aorta but 40 mm in length (Class 3) is still controversial, and ostial stenting may be life-saving,6 (as in our case).

Moles et al19 reported the first cases of aortic dissection as a complication of PCI. Their 2 cases had different evolutions. In their first case, the dissection of the aorta was limited to the left CSV, and surgical intervention was not necessary. In their second case, on the other hand, surgical management was necessary because the entry was in the aortic intima adjacent to the conal artery, leading to dissection of the ascending aorta. A patient reported by Varma et al16 with RCA dissection during PCI extending into the aortic root died within 48 hours with conservative treatment. Dunning et al1 described 2 patients with a Class 3 dissection who were submitted to surgery, and who died before discharge. In Maiello’s report,6 a case of extensive dissection (Class 3) of the ascending aorta that occurred during angioplasty of the RCA was successfully treated by means of coronary stent implantation. Sutton et al20 described a case in which retrograde dissection of the aorta necessitating urgent surgical repair occurred during an attempt to open a chronically occluded RCA. Initially localized, the dissection extended during an attempt to seal the right coronary ostium. They suggested that if localized retrograde aortic dissection occurred, the management would depend on the stability of the distal coronary vessel. If stable, a conservative approach would be preferable to an attempt to seal the dissection.

In the present case, an extensive iatrogenic aortic dissection that was limited to the ascending aorta was successfully managed by stenting the ostium of the RCA and monitoring the aortic dissection by transesophageal echocardiography.

References

References

1. Dunning DW, Kahn JK, Hawkins ET, O’ Neill WW. Iatrogenic coronary artery dissections extending into and involving the aortic root. Catheter Cardiovasc Interv 2000; 51: 387– 393.

2. Januzzi JL, Sabatine MS, Eagle KA, et al. For the International Registry of aortic dissection investigators. Iatrogenic aortic dissection. Am J Cardiol 2002; 89: 623– 626.

3. Yip HK, Wu CJ, Yeh KH, et al. Unusual complication of retrograde dissection to the coronary sinus of valsalva during percutaneous revascularization. A single- center experience and literature review. Chest 2001;119:493–501.

4. Alfonso F, Almeria C, Fernandez-Ortiz A, et al. Aortic dissection occurring during coronary angioplasty: Angiographic and transesophageal echocardiographic findings. Cathet Cardiovasc Diagn 1997; 42: 412– 415.

5. Al-Saif SM, Liu MW, Al-Mubarak N, et al. Percutaneous treatment of catheterinduced dissection of the left main coronary artery and adjacent aortic wall: A case report. Catheter Cardiovasc Interv 2000; 49: 86– 89.

6. Maiello L, La Marchesina U, Presbitero P, Faletra F. Iatrogenic aortic dissection during coronary intervention. Ital Heart J 2003;4:419–422.

7. Perez-Castellano N, Garcia-Fernandez MA, Garcia EJ, et al. Dissection of the aortic sinus of Valsalva complicating coronary catheterization: Cause, mechanism, evolution, and management. Cathet Cardiovasc Diagn 1998;43:273–279.

8. Carter AJ, Brinker JA. Dissection of the ascending aorta associated with coronary angiography. Am J Cardiol 1994; 73: 922– 923.

9. Awadalla H, Sabet S, El Sebaie A, et al. Catheter-induced left main dissection incidence, predisposition and therapeutic strategies: Experience from two sides of the hemisphere. J Invasive Cardiol 2005; 17: 233– 236.

10. Wilson SK, Hutchins GM. Aortic dissecting aneurysms: Causative factors in 204 subjects. Arch Pathol Lab Med 1982; 106: 195– 214.

11. Pande AD, Gosselin G, Leclerc Y, Leung TK. Aortic dissection complicating coronary angioplasty in cystic medial necrosis. Am Heart J 1996; 131: 1221– 1223.

12. Boyle AJ, Chan M, Dib J, et al. Catheter-Induced coronary artery dissection: Risk factors, prevention and management. J Invasive Cardiol 2006; 18: 500– 503.

13. Curtis MJ, Traboulsi M, Knudtson ML, Lester WM. Left main coronary artery dissection during cardiac catheterization. Can J Cardiol 1992; 8: 725– 728.

14 . Biel SI, Lrone RJ. Left coronary artery dissection with an Amplatz-shaped catheter. The role of vigorous inspiration during contrast injection. Chest 1984; 86: 640– 641.

15. Chai H-T, Yang C-H, Wu C-J, et al. Utilization of a double-wire technique to treat long extended spiral dissection of the right coronary artery. Evaluation of incidence and mechanisms. Int Heart J 2005; 46: 35– 44.

16. IAGS 1996 Proceedings: Panel discussion: Cardiovascular (Part I) From the 4th Biennial International Andreas Grüntzig Society meeting held in Aruba February 4–7, 1996. J Invasive Cardiol 1997; 9: 78– 82.

17. Varma V, Nanda NC, Soto B, et al. Transesophageal echocardiographic demonstration of proximal right coronary artery dissection extending into the aortic root. Am J Cardiol 1992;123:1055–1057.

18. Mulvihill NT, Boccalatte M, Fajadet J, Marco J. Catheter-induced left main dissection: A treatment dilemma. Cathet Cardiovasc Intervent 2003;59:214–216.

19. Moles VP, Chappuis F, Simonet F, et al. Aortic dissection as a complication of percutaneous transluminal coronary angioplasty. Cathet Cardiovasc Diagn 1992; 26: 8– 11.

20. Sutton AG, Aggarwal RK, de Belder MA. Type A dissection of the ascending thoracic aorta during percutaneous coronary intervention. J Invasive Cardiol 2000; 12: 147– 15