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Acute myocardial infarction—A late complication of intracoronary stent placement
Author(s) -
Danenberg Haim D.,
Lotan Chaim,
Hasin Yonathan,
Gotsman Mervyn S.,
Rozenman Yoseph
Publication year - 2000
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960230514
Subject(s) - medicine , stent , restenosis , myocardial infarction , cardiology , angioplasty , stenosis , complication , lesion , dissection (medical) , angiography , ischemia , surgery , coronary stent , radiology
Background: Myocardial infarction (MI) as the first indication of postangioplasty restenosis is extremely rare, and it has been speculated that the fibroproliferative restenotic lesion is less likely to undergo plaque rupture than the lipid ‐laden native atherosclerotic lesion. Hypothesis: The present study was designed to examine whether intracoronary stent implantation affects this course. Methods: In all, 994 consecutive patients who underwent angioplasty and intracoronary stent implantation in our hospital were reviewed retrospectively for the occurrence of MI. Results: Eight patients (0.8%), all male and hypertensive, aged 33–83 years, presented with an MI due to stent occlusion more than 30 days following stenting (range: 35–398 days). In two patients, MI occurred 3 and 5 h, respectively, following completion of a maximal high‐level exercise test that was negative for ischemia. Angiography revealed complete occlusion or significant stenosis of the stent in all eight patients, with an obvious intimal dissection in either edge of the stent in six patients. Except for gender and hypertension, no correlation was found with other risk factors, vessel involved, initial angiographic results, or with stent design, diameter, or length. Conclusions: Myocardial infarction as a late complication of successful stent implantation occurred in 0.8% of our patients. This is only the lower bound of the estimated frequency for such an event. We hypothesize that the transition point between the relatively fixed stent and the normal artery is exposed to high deformation stress which makes it vulnerable to rupture and dissection. Strenuous exercise and hypertension may increase the deformation stress and the risk of intimal rupture.

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