Coronary stents reduce restenosis and repeat revascularizations and may also improve survival

Dundar et al. (1) present a comprehensive meta-analysis of randomized studies comparing coronary stents with balloon angioplasty.The main message fromthisanalysis is that routine use of stents reduces angiographic restenosis and the need for repeat revascularizations, but according to their analysis does not improve survival or the risk of acute myocardial infarction. The authors conclude that the widespread use of stents has become routine despite limited evidence of long-term clinical benefit or even benefit in real clinical outcomes. The introduction of coronary stents is considered the most important breakthrough in interventional cardiology since the start of balloon angioplasty by Andreas Gruentzig and co-workers in 1977. Stenting was introduced 10 years later, mainly as a method for the treatment of the acute complications of balloon angioplasty (2), and has improved the safety of angioplasty by providing a reliable treatment for acute or threatened occlusion and has thereby almost abolished the need for same-day emergency bypass surgery (3). The elective stenting era began in 1994 with the publication of two pivotal randomized clinical studies, Benestent (4) and STRESS (5) trials, showing a substantial reduction of restenosis by stenting compared with balloon angioplasty. At the same time the antithrombotic treatment was simplified by the change from warfarin to ticlopidine or clopidogrel (6), and the use of coronary stents increased exponentially. At present, stents are used in 80–90% of patients and in 70–80% of lesions in most hospitals. The meta-analysis presented by Dundar et al. from the University of Liverpool (1) included a total of 50 trials published in the period 1994–2002. This is a more complete meta-analysis than earlier presented (7, 8), including also 11 studies appearing only as abstracts. In interpreting the results of this meta-analysis, it is important to bear in mind that the trials did not compare the use of stents with no use of stents, instead they compared two different strategies for using stents – routine elective stenting and a more restrained (or provisional) approach using stents only for the treatment of complications and suboptimal results after balloon angioplasty. Not surprisingly the restenosis rate after 6 months is substantially reduced by stenting in non-specific coronary heart disease, acute myocardial infarction, small coronary arteries and chronic total occlusions, in agreement with most of the individual studies. The average absolute reduction was 12 fewer angiographic restenoses resulting in eight less events, mostly repeat angioplasties, per 100 patients treated by stenting compared with balloon angioplasty. As the authors correctly argue, the increased number of revascularizations in patients treated with balloon angioplasty alone might partly have been driven by protocol-required coronary angiograms (8), and thus the true difference between the two treatment strategies might have been less. On the other hand, several other factors might have influenced the results in the other direction. The crossover rate from balloon angioplasty to stent varied from 0 to 57%, and many of the larger studies had a crossover rate of more than 30%. The reduction in repeat revascularizations by stenting is found to be closely dependent on the crossover rate (8), and diminishes with increasing use of stents in the balloon angioplasty group. Once a 20–40% rate of stenting is achieved, the number of repeat angioplasties avoided is about five per 100 patients treated (8), in accordance with findings in this meta-analysis. Given that stenting was introduced to reduce the acute complications during the angioplasty procedure, it is somewhat surprising that this analysis, including Department of Cardiology, St Olav University Hospital, Trondheim, Norway. Correspondence to Harald Vik-Mo, MD, PhD, Department of Cardiology, St Olav University Hospital, NO-7006 Trondheim, Norway. E-mail: harald.vik-mo@ medisin.ntnu. no Scand Cardiovasc J 38; 195–196, 2004