Background: Debulking and ablative techniques are sometimes used for the treatment of in-stent restenosis (ISR) secondary to resistant stent under-expansion (SU). The safety and effectiveness of orbital atherectomy (OA) in this cohort of patients has not been reported. Methods: We retrospectively evaluated consecutive patients treated with OA for ISR secondary to balloon undilatable SU at two academic tertiary care centers between October 2016 and June 2019. Angiographic or intravascular imaging identified SU. Technical success was defined as residual 0% stenosis with TIMI III flow. Results: A total of 41 patients were included in the study. Patients had an average age of 65 ± 12 years; 73% male, 61% diabetic, 41% with prior coronary artery bypass grafting, 61% with a prior incident of ISR, 51% presented with stable angina, 17% unstable angina, and 32% non-ST elevation myocardial infarction (MI). Implantation of the under-expanded stents occurred between 2 months and 22 years prior to the index procedure. A total of 27% of patients had multiple layers of stents in the target lesion and 32% of patients had in-stent chronic total occlusion. Technical success was achieved in 40 (98%) patients. There were 2 (5%) major adverse cardiovascular events; both of them were periprocedural MI from the no-reflow phenomenon. There were 2 (5%) Ellis type II coronary perforations that required no intervention. Conclusions: OA can be effectively performed as an adjunctive tool in the treatment of ISR with balloon undilatable SU. The use of OA for SU is not approved by the U.S. Food and Drug Administration and is "off label" and caution must be used to limit any device/stent interaction.
BackgroundCollagen is a major determinant of atherosclerotic plaque stability. Thus, identification of differences in enzymes that regulate collagen integrity could be useful for predicting susceptibility to atherothrombosis or for diagnosing plaque rupture. In this study, we sought to determine whether prolidase, the rate-limiting enzyme of collagen turnover, differs in human subjects with acute myocardial infarction (MI) versus those with stable coronary artery disease (CAD).MethodsWe measured serum prolidase activity in 15 patients with stable CAD and 49 patients with acute MI, of which a subset had clearly defined thrombotic MI (n = 22) or non-thrombotic MI (n = 12). Prolidase activity was compared across study time points (at cardiac catheterization, T0; 6 h after presentation, T6; and at a quiescent follow-up, Tf/u) in acute MI and stable CAD subjects. We performed subgroup analyses to evaluate prolidase activity in subjects presenting with acute thrombotic versus non-thrombotic MI.ResultsAlthough prolidase activity was lower at T0 and T6 versus the quiescent phase in acute MI and stable CAD subjects (p < 0.0001), it was not significantly different between acute MI and stable CAD subjects at any time point (T0, T6, and Tf/u) or between thrombotic and non-thrombotic MI groups. Preliminary data from stratified analyses of a small number of diabetic subjects (n = 8) suggested lower prolidase activity in diabetic acute MI subjects compared with non-diabetic acute MI subjects (p = 0.02).ConclusionCirculating prolidase is not significantly different between patients with acute MI and stable CAD or between patients with thrombotic and non-thrombotic MI. Further studies are required to determine if diabetes significantly affects prolidase activity and how this might relate to the risk of MI.
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