SPECIAL SECTIONS: LETTERS TO THE EDITOR
Nonocclusive coronary dissections: to stent or not to stent?
Fernando Alfonso, MD, PhD, FESCa
a Interventional Cardiology Department, San Carlos University Hospital, Madrid, Spain
Cappelletti et al. (1) reviewed the outcome of 129 consecutive patients treated with conventional angioplasty (PTCA) at a time when coronary stents were not available. Patients (45; 35%) presenting nonocclusive dissections post-PTCA had a significantly lower restenosis rate than patients without dissections (12% vs. 44%; p < 0.001). The restenosis rate in another group of patients undergoing stenting for nonocclusive dissection (clinically and angiographically matched), later on in their experience, was 25% (1). At a time when coronary stenting is experiencing an exponential increase, these results would appear rather provocative. Some classical studies, however, also suggested that most dissections are not only benign but also predict a lower restenosis rate (2,3). Nevertheless, no previous study was able to demonstrate such a low restenosis rate in this cohort of patients.
Furthermore, to demonstrate convincingly that a conservative approach—namely a "watchful waiting" strategy—may even be superior in the long run to coronary stenting is much more challenging. Given the potential clinical implications of this study, some methodological clarifications appear warranted.
First, it is not clear why two patients with vessel closure were excluded. Keeping in mind that this is a retrospective study, it will be important to know whether these dissections were flow-limiting immediately after PTCA or flow deterioration occurred later on. Second, 67% (33/49) of the nontreated dissections were type A versus none (0/60) of the stented dissections (chi-square p < 0.0001). Therefore, it is difficult to assume that these two populations were similar, and thus direct comparison of results may not be appropriate. Further details on whether the restenosis rate tended to cluster around patients with type C-D dissections (untreated/stented groups) will be helpful.
Finally, the methodology of quantitative coronary analysis was not specified. This is relevant because the analysis of dissected coronary segments is technically demanding. In fact, at first glance it appears difficult to explain a mean lumen diameter post-PTCA of 3.23 ± 0.65 mm (reference 3.20 ± 0.54 mm) yielding a 20 ± 7% diameter stenosis. The large lumen diameter of the dissected segments indicates that the dissection image was fully included into the lumen measurements. This is in contradistinction with some prior studies using careful edge-detection quantitative angiography (4,5). We previously demonstrated (5) that residual coronary dissections after stenting had a benign outcome when they were stable, were not associated with significant lumen narrowing, and did not compromise coronary flow.
Our data (5) also concur with the current study, suggesting that most residual dissections disappear at follow-up. Moreover, these dissected coronary segments may promote a unique pattern of vessel remodeling that could explain a lower restenosis rate (1) or even a significant lumen improvement on late angiography (5). We fully agree with the idea that conservative management of coronary dissections is attractive in selected cases (adverse anatomy, small vessels, type A-B dissections). However, we believe that only properly designed studies will be able to determine whether this strategy is superior to stenting in most patients experiencing nonocclusive dissections. In the interim, accepting the potential risk of vessel closure and the logistic implications (prolonged observation or even repeat angiography) inherently associated with the conservative strategy should be weighted against the results of coronary stenting using currently available stent designs. Although we sympathize with the words of caution against the indiscriminate use of stents, it would appear more reasonable to challenge first the systematic use of "elective" stenting in clinical/angiographic settings where its efficacy—as compared with PTCA—remains largely unsettled.
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References
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- Cappelletti A, Margonato A, Rosano G, et al. Short- and long-term evolution of unstented nonocclusive coronary dissection after coronary angioplasty. J Am Coll Cardiol. 1999;34:1484–1488[Abstract/Free Full Text]
- Leingruber PP, Roubin GS, Anderson HV, et al. Influence of intimal dissections on restenosis after successful coronary angioplasty. Circulation. 1985;72:530–550[Abstract/Free Full Text]
- Ellis SG, Roubin GS, King SB, Douglas JS, Cox WR. Importance of stenosis morphology in the estimation of restenosis risk after elective percutaneous transluminal coronary angioplasty. Am J Cardiol. 1989;63:30–34[CrossRef][Medline]
- Ozaki Y, Violaris AG, Kobayashi T, et al. Comparison of coronary luminal quantification obtained from intracoronary ultrasound and both geometric and videodensitometric quantitative angiography before and after balloon angioplasty and atherectomy. Circulation. 1997;96:491–499[Abstract/Free Full Text]
- Alfonso F, Hernandez R, Goicolea J, et al. Coronary stenting for acute coronary dissection after coronary angioplasty: implications of residual dissection. J Am Coll Cardiol. 1994;24:989–995[Abstract]
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F. Alfonso
Residual coronary dissections after drug-eluting stenting: the good, the bad, and the ugly
Eur. Heart J.,
March 1, 2006;
27(5):
503 - 505.
[Full Text]
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