The technical goal of coronary stenting should be to eliminate or lessen ischemic symptoms in the short/intermediate term and possibly reduce the risk of death or myocardial infarction, while not exposing the patient to excess short- or long-term risk. Yet major adverse cardiac events (MACE) occur in 4% to 20% of stented sites within a year,1,2 and stent underexpansion3,4 and axial misalignment (“geographic miss”)5 account for nearly half of these. Although a discussion of choosing percutaneous intervention instead of bypass surgery or optimal medical therapy alone is beyond the scope of this chapter, we will address various issues to be considered to provide the patient with an optimal technical result.
CHOICE OF VASCULAR ACCESS
Improvements in guide catheter and wire support, as well as balloon and stent deliverability, have facilitated small-caliber device intervention and, in particular, radial access–based intervention. The result has been a dramatic reduction in bleeding complications and red cell transfusion–induced inflammation and perhaps even a reduction in patient mortality under some circumstances (especially primary percutaneous coronary intervention [PCI] for ST-segment elevation myocardial infarction [STEMI]).6 Except when anatomy precludes it, radial access should be the preferred route of vascular access. Femoral, brachial, and axillary access can at times be reasonable alternatives.
Both antiplatelet and antithrombin therapies are required for safe stent implantation and healing. Aspirin and clopidogrel are usually sufficient antiplatelet therapy for patients with stable ischemic symptoms. Second-generation P2Y12 inhibitors have been shown to be superior to clopidogrel in unstable angina patients but not, in general, in stable patients.7,8
Although direct thrombin inhibitors have several potential advantages over unfractionated heparin as the requisite antithrombin agent to accompany coronary stenting, with good dual antiplatelet therapy, heparin alone is almost always adequate to prevent complications9 and is cost effective.10 The situation with STEMI patients is perhaps less clear, with a recent post HEAT-PPCI (Unfractionated Heparin Versus Bivalirudin in Primary Percutaneous Coronary Intervention) meta-analysis showing no difference between bivalirudin and heparin for the end points of death or myocardial infarction, but more stent thrombosis and less bleeding with bivalirudin.11 Although disputed by some,12 most operators use activated clotting time monitoring to assure satisfactory antithrombin effect (200-250 seconds for the commonly used HemoTec) (Medtronic, Dublin, Ireland system) (the Hemochron [Accriva, Piscataway, NJ] system measures 50 seconds longer),13 with higher levels for complex interventions (eg, acute coronary syndrome)14 or those requiring multiple guide wires in the same coronary artery.
In general, stents should be chosen to cover the lesion, from (angiographic) “normal to normal” vessel. Assessing where “normal” begins and ends is sometimes challenging, and intravascular imaging can often be helpful. Stent ends should not be deployed in areas of obvious plaque buildup, ...