Author + information
- Gianmarco Iannopollo, MD,
- Marco Ferlini, MD,
- Marek Koziński, MD,
- Maurizio Ferrario Ormezzano, MD,
- Gabriele Crimi, MD,
- Ludovico Lanfranchi, MD,
- Rita Camporotondo, MD,
- Luigi Oltrona Visconti, MD,
- Gaetano Maria De Ferrari, MD∗ ( and )
- Stefano De Servi, MD
- ↵∗Department of Molecular Medicine, University of Pavia, Coronary Care Unit and Laboratory of Clinical and Experimental Cardiology, Fondazione IRCCS Policlinico San Matteo, Viale Golgi 19, 27100 Pavia, Italy
Primary percutaneous coronary intervention (PPCI) is the preferred approach to ST-segment elevation myocardial infarction (STEMI) patients. PPCI involving coronary artery aneurysms (CAAs) is challenging because of difficulties in “wiring” the distal part of the lesion, the presence of extensive thrombus burden, and increased risk of distal embolization and no reflow (1). Moreover, CAA is a risk factor for stent thrombosis after stenting for acute coronary syndromes (2). Given the paucity of data in the STEMI setting, we assessed 1-year outcomes of STEMI patients treated with PPCI of the culprit lesion (CL) involving CAA, using our prospective single-center 2005–14 STEMI registry.
Two interventional cardiologists (M.F. and G.I.), blinded to patient outcome, reviewed PPCI-treated STEMI patients, selecting cases with CL within the CAA (defined as localized or diffused >1.5-fold coronary artery dilation). They were compared with a non-CAA PPCI group; the primary endpoint was a composite of all-cause death and recurrent MI.
Follow-up visits were performed in our post-MI clinic. Definite stent thrombosis was diagnosed according to the Academic Research Consortium (3). Categorical variables were compared with the chi-square test; continuous variables were compared with Student or Mann-Whitney tests. Event rates were derived as Kaplan-Meier estimates and compared with log-rank test. A multivariable Cox regression model evaluated variables associated with endpoints.
Overall 32 of 2,312 patients (1.4%) had a CL involving CAA. In 28 cases, proximal or distal lesions to the CAA were found, whereas 4 patients had isolated CAA. CAA involved more than 1 coronary segment in 28 cases. Coronary stents were less frequently used in the CAA group although, when used, number, total length, and diameter were higher. Stenting was not performed in 6 patients (4 had isolated CAA): 2 patients had aspiration, 2 patients had balloon dilation only, and 2 patients had both. Intravascular imaging was performed at operator’s discretion; overall, in 10 CAA patients (8 with intravascular ultrasound, 2 with optimal coherence tomography). Dual-antiplatelet therapy was prescribed in all patients for 1 year, and CAA patients more frequently received ticagrelor as second antiplatelet drug. Of the 20 CAA patients who received glycoprotein IIb/IIIa receptor inhibitors in the catheter laboratory, 18 had the drug continued for 12 hours after PPCI.
The primary endpoint occurred more frequently in CAA patients (Table 1) because of more recurrent MIs, caused by more definite stent thrombosis, mostly occurring within 30 days. Stent thrombosis rates in the CAA group were high, irrespective of aspiration, GPI use, ticagrelor or clopidogrel administration, and implantation of bare-metal or drug-eluting stent. However, no stent thrombosis was observed in 6 patients who received an everolimus-eluting stent.
CAA as CL was independently associated with death + recurrent MI (hazard ratio: 2.24; 95% confidence interval: 1.02 to 5.39; p = 0.04) and with stent thrombosis (hazard ratio: 6.29; 95% confidence interval: 2.32 to 17.05; p < 0.001). Our study indicates high 1-year risk of MI primarily driven by stent thrombosis, mostly occurring within 30 days in patients undergoing PPCI of CL involving CAA. The high definite stent thrombosis rate observed in CAA patients (16.5% at 1 year) might have been secondary to stent malapposition, residual thrombus, or disturbed flow through a metallic-jailed CAA. Self-apposing stents, new-generation stent grafts, or micro-mesh stents and intravascular imaging guidance (4) reduce stent malapposition, improve lesion coverage, and may be useful in this setting. The absence of stent thrombosis in the small number of everolimus-eluting stents is interesting but needs confirmation in larger series. We found that aggressive dual antiplatelet therapy with ticagrelor did not effectively prevent stent thrombosis; therefore, the possibility of adding an oral anticoagulant should be considered, possibly limited to a short period after PPCI.
The low prevalence of CAA is likely caused by inclusion of only cases with CL within the CAA. The lack of standardized anticoagulant, antiplatelet therapy and of routine intravascular imaging is a potential limitation, but reflects real life. Additional limitations include the retrospective nature of this observational study and the small number of observed events.
In conclusion, PPCI-treated patients with STEMI caused by CAA show unacceptable rates of early stent thrombosis causing recurrent MIs. Tailored strategies, including self-apposing stents, intravascular imaging and additional short-term anticoagulation should be considered.
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2017 American College of Cardiology Foundation
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