Direct Stenting: Good for the Patient, Good for All?

Conventional stenting techniques initially incorporated routine target lesion predilatation with a balloon catheter to permit easy, uncomplicated stent passage prior to stent deployment. With extensive experience in stenting, cardiac interventionalists have simplified and economized the procedure. Direct stenting, or stenting without balloon predilation is the next step in approaching percutaneous revascularization.1 This technique results from technologic advancements that include premounted stents (well-secured), low crossing profiles (0.035´´ or less) and enhanced flexibility. Direct stenting in vessels without severe angulation or calcification is feasible and safe, and procedural success rates are 90% or greater.2–3 These are as good or better than as with a “balloon-first” approach. Even though direct stenting reduces resource utilization, questions remain. In this issue of the Journal of Invasive Cardiology, Thuraia contributes another positive perspective: direct stenting lowered both post-procedural troponin levels and major adverse events compared to traditional stenting techniques. Direct stenting should result in less myocardial damage, because more effective trapping of friable plaque and thrombus occurs between the stent and vessel. Indeed, higher risk patients suffering acute myocardial infarction have less angiographic embolization when stented directly.4 Assuming less vascular disruption, lower intimal dissection and propagation risk by direct stenting, vascular injury should be reduced. This nevertheless may not translate into lower restenosis rates, as in the TRENDS study. This prospective, randomized trial evaluated multiple 30-day and 6-month clinical and angiographic endpoints. Six-month instent binary restenosis for predilatation and direct stenting groups was 11.4% and 11.6% respectively (p = ns). Further, although this trial excluded acute MI patients, six-month MACE was 7.1% in the predilatation group and 8.8% in the direct stenting group (p = ns).5 Ischemic myocardial injury remains the most common acute complication associated with percutaneous coronary intervention.6–7 Lower procedural ischemic complications may be asociated with better longterm outcomes,6,8 but in direct stenting little comparable information exists. Atmaca showed that direct stenting reduces cardiac troponin post-procedure,9 although troponins rises after PCI have uncertain impact on long term prognosis. While the present study has limitations (small, non randomized, more diabetic patients in the conventional group) it suggests that direct stenting creates less postprocedural tronponin elevation, and (possibly) lower long-term event rates. Direct stenting is associated with uncommon complications that must be borne in mind. Stent loss occurs rarely, but more frequently when trying to cross or withdraw from tight stenoses. Specific lesion subsets may also present problems for stent placement, including total and subtotal occlusions that prevent distal vessel opacification with the delivery system positioned across them. Moreover, poor lesion visualization may cuase additional stent utilization. It is also possible that aggressive stent deployment resulting from inaccurate referencing the distal vessel diameter may increase distal edge dissections. These disadvantages are typically avoided by operator experience and appropriate lesion selection. Undoubtedly improved stent and delivery technology will enhance the already high proportion of patients who might successfully undergo direct stenting. The only clear advantage of direct stenting demonstrated to date is decreased resource utilization and perhaps lower periprocedural myocardial injury measured by troponin elevation. Whether or not this yields improved long-term patient benefit is less certain. Thus far existing data do not support decreased restenosis rates. The role of direct stenting must be re-evaluated in the new era of drug-eluting stents.

1. Chevalier B, et al. Is direct stent implantation feasible? Eur Heart J 1997;18(Suppl P):386. 2. Briguori C, Sheiban I, De Gregorio J, et al. Direct coronary stenting without predilation. J Am Coll Cardiol 1999;34:1910–1915. 3. Herz I, Assali A, Solodky A, et al. Effectiveness of coronary stent deployment without predilation. Am J Cardiol 1999;84:89–91. 4. Loubeyre C, Morice MC, Lefevre T, et al. A randomized comparison of direct stenting with conventional stent implantation in selected patients with acute myocardial infarction. J Am Coll Cardiol 2002;39:15–21. 5. TRENDS study data. Presented at the American College of Cardiology, March 17, 2002. 6. Abdelmeguid AE, Topol EJ, Whitlow PL, et al. Significance of mild transient release of creatine kinase-MB fraction after percutaneous coronary interventions. Circulation 1996;94:1528–1536. 7. Savage MP, Douglas JS, Fischman DL, et al. Stent placement compared with balloon angioplasty for obstructed coronary bypass grafts. N Engl J Med 1997;337:740–747. 8. Califf RM, Abdelmeguid AE, Kuntz RE, et al. Myonecrosis after revascularization procedures. J Am Coll Cardiol 1998;31:241–251. 9. Atmaca Y, Ertas F, Gulec S, et al. Effect of direct stent implantation on minor myocardial injury. J Invas Cardiol 2002;14:443–446.