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Case Report

Bilateral Coronary Ostial Stenoses Post-Bentall Procedure: Management Options in the DES Era

Matthew I. Worthley, MBBS, PhD, FRACP, John Burgess, MD, FRCS(C), Mouheiddin Traboulsi, MD, FRCP(C)
December 2005
The Bentall procedure for aortic root and valve replacement with coronary reimplantation was initially described in 1968.1 This procedure is considered the “gold standard” for treatment of combined valve and ascending aortic pathology. The procedure is performed most commonly in patients with degenerative aortic disease, including atherosclerotic disease, ectasia and poststenotic aortic dilatation.2,3 The complication of single coronary ostial stenosis following reimplantation is extremely rare in this procedure, occurring in less than 2% of patients.4,5 We describe the first case of bilateral coronary ostial stenoses following the Bentall procedure in a patient with documented heparin-induced thrombocytopenia (HIT) that was successfully treated with percutaneous coronary intervention (PCI). Case Report. A 67-year-old man presented to the emergency room late in the evening with sudden onset of chest pain. He was visiting his family following a recent complicated aortic valve replacement at another center. He was an ex-smoker, but had no other significant risk factors for coronary artery disease. The patient was on aspirin, ramipril, metoprolol and atorvastatin. On advice from his treating specialist, he had recently ceased furosemide and coumadin. Clinically, in the emergency department, he had both an ejection and pansystolic murmur on auscultation, suggesting some additional mitral regurgitation. The patient’s initial blood pressure was 92/60, with an elevated JVP and bibasal crackles. His admission electrocardiogram is shown in Figure 1. An echocardiogram showed a dilated left ventricle, with mild-to-moderate left ventricular dysfunction with an akinetic apex, hypokinetic septum and basal posterolateral wall, a dilated left atrium, moderate mitral regurgitation, and a small residual aortic bioprosthetic gradient. His blood work was unremarkable except for an elevated troponin T-value of 0.33 UG/L. The patient had a history of a complicated Bentall procedure for severe aortic stenosis and degenerative and heavily calcified disease in the ascending aorta 5 months previously. During this procedure, a #25 Medtronic Freestyle® Aortic Root Bioprosthesis (Medtronic, Inc., Minneapolis, Minnesota) was inserted into the aortic valve annulus. The left main coronary button sat to the left of the porcine coronary button, thus the porcine coronary button was oversewn and a new coronary ostium was created. Significant disease was observed in the ostium of the RCA during pre-operative coronary angiography which was thus bypassed with a saphenous vein graft. The right coronary button was, however, still successfully reanastomosed to the bioprosthesis. An aortic tube graft was anastomosed at that stage to the Freestyle bioprosthesis. As the patient was weaned from bypass, it was noted that the anterior wall was hypokinetic, which raised questions about the patency of the left main anastomosis. A Y saphenous vein graft was subsequently inserted to both the left anterior descending artery and a distal obtuse marginal branch of the circumflex system. A large amount of perioperative bleeding was then noted, requiring multiple blood product transfusions. In the evening following surgery, he had further hemodynamic compromise and had developed cardiac tamponade that required surgical reintervention. Other postoperative complications included pseudomonal infection, renal impairment and bilateral pleural effusions that ultimately required drainage. In addition, the patient had heparin-induced thrombocytopenia (HIT). He finally stabilized, however, and was ultimately discharged from the hospital on the 26th postoperative day. Due to the dramatic electrocardiographic changes, continuing ischemic symptoms and hemodynamic instability, the patient underwent urgent cardiac catheterization and coronary angiography. This was approximately 12 hours after admission, and at that stage, his ramipril was held, and the following medications were administered: Argatroban® (GlaxoSmithKline, Research Triangle, North Carolina), clopidogrel (Plavix®, Bristol-Myers Squibb/Sanofi-Synthelabo, New York, New York) and eptifibatide (Integrilin®, Key-Schering-Plough, Kenilworth, New Jersey). The cardiac catheterization showed that the left ventricle had anterior akinesis, with inferior hypokinesis with a left ventricular end-diastolic pressure of 17 mmHg. The peak-to-peak aortic gradient was 23 mmHg, and 1+ mitral regurgitation was observed. All saphenous vein grafts had occluded proximally. The native reimplanted coronary arteries had tight ostial stenoses, as seen in Figure 2. A discussion was then had between interventionist, cardiac surgeon and patient, and ultimately the decision was made to proceed with PCI. At this stage, a 6 French (Fr) arterial sheath and venous sheath were inserted in the left groin. The 6 Fr right femoral sheath was exchanged for an 8 Fr sheath and a Fidelity™ 40 cc intra-aortic balloon pump (Datascope, Fairfield, New Jersey) was inserted for hemodynamic support. The left main lesion was wired “at a distance” through a JL4 6 Fr guiding catheter with a Wizdom™ “soft J tip” wire (Cordis Corporation Miami, Florida), as the guide was damping if the ostium was fully cannulated. The lesion was initially dilated with a 2.5 x 15 mm Maverick™ balloon (Boston Scientific Corporation, Natick,Massachusetts), stented with a 3.5 x 16 mm Taxus™ stent (Boston Scientific), and then postinflated with a 4.0 x 15 mm Quantum™ balloon (Boston Scientific). The right coronary artery was likewise wired “at a distance” through a JR4 6 Fr guiding catheter using a Wizdom “soft J tip” wire, with the ostial stenosis directly stented with a 3.5 x 12 mm Taxus stent and postinflated with a 4.5 x 12 mm Quantum balloon. The right ostial stent was undersized for its diameter, yet we opted to deploy a smaller drug-eluting stent and aggressively postdilate, rather than use a larger bare metal stent. Both coronary ostia were “flared” during postdilation, yet despite this, it was still difficult to pass these balloons into the left main artery. We thus opted not to interrogate the stent deployment with intravascular ultrasound postprocedure. The final results are shown in Figure 3. The patient had an uneventful recovery, and was ultimately discharged on day 5 postprocedure. His peak creatine kinase was 1,037 U/L, which had peaked prior to the procedure. He had his intra-aortic balloon pump in situ for a further 2 hours, at which stage this and all femoral sheaths were removed. Postprocedure, the patient had his argatroban stopped, but continued taking eptifibatide for another 12 hours. Discussion A single coronary ostial stenosis has been reported to occur post-Bentall procedure at an incidence of less than 2%.4 A number of other large registries have not reported it as a complication,2,3,6–9 however, ostial coronary stenosis may be responsible for sudden cardiac death in some of these reports.6 Coronary ostial disease, particularly pseudoaneurysms, have been reported, particularly in patients with Marfan’s disease following a Bentall procedure.10 Successful stenting of coronary ostial stenosis has been reported twice to date, once following a reimplanted left main coronary artery for an anomalous origin11 and once following a Bentall procedure.12 This case, however, is the first to report successful ostial stenting of both reimplanted coronary arteries following a Bentall procedure. A complicating factor of this procedure was the patient’s previous HIT. The direct thrombin inhibitor Argatroban is a synthetic arginine derivative, predominantly hepatically cleared, with a half-life of between 39–51 minutes.13 It is considered a first-line option for anticoagulation in patients with HIT, and previous reports confirm its effectiveness in PCI as a substitute for heparin in these patients14,15 and its safety in combination with glycoprotein IIb/IIIa antagonists.16 Serology confirmed post-PCI that our patient remained HIT antibody-positive, thus further supporting a high risk of developing HIT on rechallenge, particularly with cardiopulmonary bypass.17 The effectiveness of Argatroban during cardiopulmonary bypass remains uncertain,17,18 with evidence to support altered pharmacokinetics in the critically ill post-bypass patient.19 Our decision to opt for PCI revascularization was based on the uncertain effect of Argatroban during cardiopulmonary bypass, knowledge of a friable and heavily calcified aortic root and a previous complicated postoperative course. Our initial plan was to proceed with angioplasty of the left main artery and perform the right coronary procedure at a later date. However, the first procedure went smoothly and with ECG evidence of global ischemia, it was reasonable to proceed with intervention on the second vessel. The patient will be followed up by our department (by phone) in two months, as he is returning to his home province and will ultimately be under the long-term care of his initial treating cardiology team. In patients who are not attractive surgical candidates, this case demonstrates the acute effectiveness of PCI for the treatment of bilateral ostial stenoses following the Bentall procedure. However, long-term follow-up will determine the durability of our approach. Figure 1. Admission electrocardiograph suggestive of diffuse myocardial ischemia. Figure 2. Bilateral coronary ostial stenoses. Figure 3. Successful bilateral coronary ostial stenting.
1. Bentall H, De Bono A. A technique for complete replacement of the ascending aorta. Thorax 1968;23:338–339. 2. Gelsomino S, Morocutti G, Frassani R, et al. Long-term results of Bentall composite aortic root replacement for ascending aortic aneurysms and dissections. Chest 2003;124:984–988. 3. Hagl C, Strauch JT, Spielvogel D, et al. Is the Bentall procedure for ascending aorta or aortic valve replacement the best approach for long-term event-free survival? Ann Thorac Surg 2003;76:698–703. 4. Guilmet D, Bonnet N, Saal JP, et al. Long term survival with the Bentall button operation in 150 patients. Arch Mal Coeur Vaiss 2004;97:83–91. 5. Aomi S, Nakajima M, Nonoyama M, et al. Aortic root replacement using composite valve graft in patients with aortic valve disease and aneurysm of the ascending aorta: Twenty Years’ experience of late results. Artif Organs 2002;26:467–473. 6. Sioris, T, David TE, Ivanov J, et al. Clinical outcomes after separate and composite replacement of the aortic valve and ascending aorta. J Thorac Cardiovasc Surg 2004;128:260–265. 7. Prifti E, Bonacchi M, Frati G, et al. Early and long-term outcome in patients undergoing aortic root replacement with composite graft according to the Bentall’s technique. Eur J Cardiothorac Surg 2002;21:15–21. 8. Gelsomino S, Masullo G, Morocutti G, et al. Sixteen-year results of composite aortic root replacement for non-dissecting chronic aortic aneurysms. Ital Heart J 2003;4:454–459. 9. Bachet J, Termignon JL, Goudot B, et al.Aortic root replacement with a composite graft. Factors influencing immediate and long-term results. Eur J Cardiothorac Surg 1996;10:207–213. 10. Milano AD, Pratali S, Mecozzi G, et al. Fate of coronary ostial anastomoses after the modified Bentall procedure. Ann Thorac Surg 2003;75:1797–1801. 11. Ohmoto Y, Hara K, Kuroda Y, et al. Stent placement in surgically reimplanted left main coronary artery in patient with anomalous origin of left main coronary artery from pulmonary artery. Cathet Cardiovasc Diagn 1997;42:48–50. 12. Franck H, Weber K, Frese W, et al. Stent-supported angioplasty of an ostial left main stenosis following replacement of the ascending aorta with reimplantation of the coronary arteries. J Invasive Cardiol 1999;11:571–574. 13. Weitz JI, Bates ER. Direct thrombin inhibitors in cardiac disease. Cardiovasc Toxicol 2003;3:13–25. 14. Lewis BE, Iaffaldano R, McKiernan TL, et al. Report of successful use of argatroban as an alternative anticoagulant during coronary stent implantation in a patient with heparin-induced thrombocytopenia and thrombosis syndrome. Cathet Cardiovasc Diagn 1996;38:206–209. 15. Lewis BE, Matthai WH Jr, Cohen M, et al. Argatroban anticoagulation during percutaneous coronary intervention in patients with heparin-induced thrombocytopenia. Catheter Cardiovasc Interv 2002;57:177–184. 16. Cox DS, Kleiman NS, Boyle DA, et al. Pharmacokinetics and pharmacodynamics of argatroban in combination with a platelet glycoprotein IIB/IIIA receptor antagonist in patients undergoing percutaneous coronary intervention. J Clin Pharmacol 2004;44:981–990. 17. Warkentin TE, Greinacher A. Heparin-induced thrombocytopenia: Recognition, treatment, and prevention. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126(Suppl 3):311S–337S. 18. Cannon MA, Butterworth J, Riley RD, et al. Failure of argatroban anticoagulation during off-pump coronary artery bypass surgery. Ann Thorac Surg 2004;77:711–713. 19. Reichert MG, MacGregor DA, Kincaid EH, et al. Excessive argatroban anticoagulation for heparin-induced thrombocytopenia. Ann Pharmacother 2003;37:652–654.

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