Symbiot‚Ñ¢ Stent Delivery Via 8 Fr Guiding Catheter from the Right Radial Artery in an Acute Coronary Syndrome Due to a Degenerati

Recent studies have demonstrated that in the setting of acute coronary syndrome (ACS), with either intractable symptoms, acute left ventricular failure, acute mitral regurgitation, cardiac enzyme rise or electrocardiogram (ECG) change, percutaneous coronary intervention (PCI) is prognostically advantageous over conservative therapy.^1,2 The benefits of this treatment modality, both in the short term (in terms of procedural success) and in the longer term, is enhanced further by the use of aggressive anticoagulant strategies, including the use of aspirin, clopidogrel, heparin and glycoprotein IIb/IIIa inhibitors. However, the use of aggressive anticoagulation is associated with a higher incidence of access site complications, although several studies have shown that these can be reduced to nearly zero by the use of radial artery access. Thus, the use of direct stent placement via the radial artery,^3,4 which has a comparable stent implantation success rate to the femoral approach,⁵ provides an attractive technique for favorably altering the risk-to-benefit ratio in PCI requiring aggressive anticoagulation. Recent technological developments in the design of covered stents for use in degenerating saphenous vein grafts (SVGs) have been shown to improve outcomes in terms of major adverse cardiac events (MACE),⁶ and these may now be considered to be a preferred treatment option in this situation. The Symbiot stent by Boston Scientific (Maple Grove, Minnesota) is an example of such a stent and is designed to reduce the no-reflow phenomenon by confining friable material behind the cover of the self-expanding stent. Despite these advantages, an 8 Fr system is required to deliver the Symbiot stent and this is normally deployed from the femoral artery. Thus, in the setting of acute coronary syndrome due to SVG disease, deployment of the Symbiot stent normally exposes the patient to an increased risk of femoral access site bleeding due to the additional use of aggressive anticoagulation. In the following case, we describe the successful deployment of a Symbiot stent utilizing an 8 Fr system via the right radial artery in a patient who had developed ACS due to SVG disease. Case Report. A 72-year-old man presented to the accident and emergency department in February 2003 with chest pain at rest and evidence of left ventricular failure (LVF), characterized by dyspnoea, a gallop rhythm, basal crepitations on auscultation of the lung bases, and characteristic changes of LVF on chest x-ray. The patient had an extensive previous cardiac history. In 1989, he had had percutaneous transluminal coronary angioplasty (PTCA) of the first obtuse marginal, followed by a posterolateral infarct in 1989. In 1990, he underwent coronary bypass grafting, with two SVGs from the aorta to left anterior descending artery, and from the aorta to the first obtuse marginal. In 1990, he developed further angina and underwent PCI with stent deployment to the circumflex artery. The patient remained well until 2002 when he developed further angina. Coronary angiography at this time showed occlusion of the SVG to the obtuse marginal, but his symptoms settled with conservative treatment. The SVG to the left anterior descending artery was still patent and the circumflex stent was widely patent with no flow-limiting disease in the circumflex system. The right coronary artery was noted to be small and non-dominant. On admission, the patient was noted to be centrally obese (height 1 m 57 cm, weight 78 kg, and body mass index, 31.6) and had a significant abdominal fat apron. His ECG showed sinus rhythm and left bundle branch block (unchanged from out-patient status) and this remained unchanged throughout his admission. Renal function, inflammatory markers and haematological markers remained normal throughout admission, but he developed a troponin T peak of 1.86 u/l and a creatine kinase peak of 387 u/l. He was treated with intravenous diuretics, intravenous nitrates, low molecular weight heparin, oral clopidogrel and oral beta blockers. Aspirin was continued. Signs of LVF settled rapidly but despite the further addition of oral calcium antagonists, the patient continued to have episodes of chest pain at rest. Echocardiography showed good left ventricular function with no significant valve disease. Within 24, hours the patient underwent diagnostic coronary angiography that was performed using 5 Fr catheters from the right femoral artery. This revealed a new stenosis in the SVG to the LAD that had superimposed thrombus that were leading to a reduced distal blood flow. LV angiography showed good LV function. It was concluded that these were the culprits for the new ACS and that they should be treated with PCI during the patient’s current admission. However, in view of the thrombus load, he received pre-treatment for 24 hours with the glycoprotein IIb/IIIa inhibitor tirofiban, plus heparin, aspirin and clopidogrel. Over the next 24 hour, the patient remained cardiovascularly stable but developed a large right groin haematoma from the diagnostic angiography puncture site. Percutaneous interventional strategy. 1) Minimization of no-reflow and restenosis: it was proposed that aggressive anticoagulation, as outlined above, should be continued as above and that a Symbiot stent should be deployed. 2) Minimization of further access site complications: the right radial artery was proposed as the access site of choice to reduce the chance of further bleeding and to allow more rapid patient mobilization. Percutaneous intervention. Informed consent was obtained. The right radial artery was cannulated with a Terumo Radifocus II 8 Fr radial sheath which was flushed with a combination of 10,000 units of unfractionated heparin together with 5 mg of verapamil. An 8 Fr JR4 was used as a guide support. The lesion had TIMI 2 flow and QCA showed a 29 mm long lesion. A 4.0 mm diameter x 31 mm length Symbiot stent was deployed and post-dilated with a 4.0 mm diameter x 30 mm balloon to 18 atmospheres. There were no procedural complications. The patient continued on tirofiban for an additional 24 hours. The radial pulse was noted to be intact after the pressure bandage was removed. The procedure was straightforward and the patient had experienced no chest pain or untoward symptoms up to the time of discharge. Our standard practice, therefore, is not to check cardiac enzymes in these circumstances. The patient was discharged the following day and instructed to continue on aspirin and clopidogrel. When the patient was contacted one year later, he felt his own pulse and confirmed its presence, as well as his lack of complications with the procedure and the pulse. Conclusion. The case we have reported highlights several of the common dilemmas encountered by interventional cardiologists in patients with ACS due to degenerating SVGs. The patient described had an increased risk of thrombotic or embolic phenomena from PCI with an increased risk of “no reflow,” and given his previous acute presentation with left ventricular failure, this would have been likely to result in a grave outcome. Conversely, he was also at risk of access site complications from the femoral approach, aggravated by the necessity for aggressive anticoagulation. This was successfully overcome by the use of the radial artery for vascular access. Previous studies have documented the successful use of 8 Fr systems via the right radial artery with no adverse outcome in terms of radial artery damage in carefully selected cases. We suggest that in similar selected cases, the strategy described above could be successfully employed to minimize the complications of PCI to SVGs with a high risk of distal embolism and no-reflow while also minimizing the risk of access site complications.

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