Incremental Progress? The Roles of Direct Stenting and Routine Troponin Measurement After Percutaneous Coronary Intervention

Author(s): 

Stephen G. Ellis, MD

In this issue of the Journal, Timurkaynak et al. raises some important, but not easily resolvable, issues that deserve thought by practicing interventional cardiologists. In this small, observational study measuring cardiac enzymes after PCI, troponin T was found to be elevated somewhat more frequently in patients undergoing predilatation than those undergoing direct stenting. The authors call for further evaluation of the potential merit of the strategy of direct stenting and also suggest further study of the relevance of troponin elevations after PCI.

See Timurkaynak et al. on pages 167–170

The impetus for direct stenting without predilatation has arisen from several foci — lower profile and more flexible stents making this even possible, the concept suggested by Rogers1 that primary stenting may allow greater retention of coronary endothelium, thus allowing earlier re-endothelialization and less restenosis, by the idea that direct stenting might diminish trauma-related embolization and, of course, the hope that this would reduce procedure costs. Conversely, in a severe stenosis, direct stenting may lead to imperfect visualization of stent position and misplacement, as well as occasional failure to dilate after delivery of a stent, which might have been remedied had that problem been ascertained earlier during balloon predilatation. It is virtually impossible to conclusively demonstrate any of these potential benefits without a carefully controlled, appropriately sized randomized trial. Without this, operator choice favoring direct stenting for less challenging anatomy makes the comparison of outcomes problematic. In fact, such trials have been performed, although one must question whether or not results with one delivery system are generalizable to all available. In that study, Baim and colleagues2 randomized 399 patients undergoing stenting using the relatively low profile Medtronic AVE S670 stent to direct stenting or stenting after predilatation. When assessing the results, it is important to look at the inclusion and exclusion criteria and note that lesions in this study were relatively simple — they had to be de novo, < 15 mm in length, in vessels 3.0–4.0 mm in diameter, non-calcified, without significant proximal or distal disease and with no more than mild tortuosity. Patients with recent myocardial infarction were also excluded. Predilatation was generally accomplished with a balloon sized slightly smaller than the reference diameter; stents were implanted to a minimum of 12 and a maximum of 16 atmospheres. Patients were treated with aspirin and ticlopidine or clopidogrel, but generally did not receive glycoprotein IIb/IIIa inhibitors. Importantly, in-hospital outcomes were tracked in all patients and approximately 80% returned for a 6-month angiography. In this study, the direct approach was associated with slightly but not significantly reduced procedure time (33 vs. 36 minutes), significantly fewer balloons used (0.6 vs. 1.3) and there was no difference in the number of stents used (1.2 in each group). There was no difference in the incidence of non-Q wave infarction defined as CK-MB > 3 times the upper limit of the lab’s normal, although there was a weak trend for this to occur slightly less commonly in the direct group (5.6 vs. 7.5%; p = 0.57). There was one stent thrombosis in each group, and death and emergency bypass surgery were extremely uncommon. Importantly, the Rogers’ hypothesis was not confirmed at follow-up, with binary restenosis and late loss index being 20% and 21%, and 0.51 and 0.52 in the direct and predilatation groups, respectively. Thus, it would appear, at least for dilatation of simple native vessel coronary lesions, that one can save perhaps a little more than $150 per procedure on balloon costs with this approach, but there is little else to be gained. However, whether or not this would hold true for other types of lesions (such as more friable vein graft lesions, for instance) remains to be addressed. Given that nearly one million PCIs will be performed in the United States this year, efforts to save money on balloon costs are laudable, but will do little to defuse the upcoming crisis in medical care costs engendered by the costs of coated stents and other implantables.
A number of investigators have evaluated the incidence of troponin elevation following PCI in modest numbers of patients, and attempted to relate such elevations to long-term outcome, as has been previously described with creatine kinase by many authors.3,4 As expected, both troponin T and troponin I are more sensitive indicators than creatine kinase or creatine kinase MB isoforms. Their relevance in terms of affecting clinical outcome and therefore being an appropriate measure by which to judge different therapies remains unclear at best. There is no doubt that CKMB elevations 5–8 times or greater the upper limits of normal following PCI are strongly correlated with subsequent cardiac death.3–5 Whether lesser CKMB elevations are of clinical importance remains debated. Two recent studies have addressed this issue with larger patient numbers than were previously available. Stone and colleagues reported on a 7,147 patients followed for a mean of 1.4 years and could not demonstrate an increase in mortality until the CKMB fraction was 8 times or greater the upper limit of normal.3 The Cleveland Clinic reported data on 7,859 patients followed a mean of 3.2 years.6 In this series, the risk of subsequent death was clearly elevated with a CKMB of 5x or greater the upper limit of normal. There was also a modest increase in mortality for patients with CKMB elevations 1–5 times the upper limit, which was statistically significant but of questionable clinical importance (an absolute increase risk of death of 0.7% at 4 months and 2.5% at 4 years). Thus, it would appear that routine measurement of troponin levels following PCI is likely to be an overly sensitive measure of myocardial necrosis, which is more likely to pose concern for the patient and family than to provide useful clinical information. The same cannot be said for measurement of CKMB, which does have prognostic merit. It must be noted, however, that measurement of troponin may be useful to add sensitivity in the comparison of measures designed to reduce micro-embolism with PCI (as first described by Saber7), although judgment regarding the clinical relevance of these devices should probably rest on comparison of clinical outcomes and CKMB elevations of at least 3, if not 5, times the upper limit of normal.


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