Abstract
Myocardial infarction secondary to stent thrombosis has high mortality and recurrence rate. Emergency PCI has high risk of no-reflow. We used a 2-step approach of early recanalization with minimal mechanical intervention followed by delayed PCI 1–2 days later guided by Optical Coherence Tomography (OCT). From October 2011 to December 2013, we treated 5 patients with this approach. Time from early recanalization to the delayed definitive PCI was 1 day (median, range 1–3 days). All the OCT images were diagnostic with a clear view of the underlying structures.
Summary
A 2-step approach to treat stent thrombosis appears beneficial with low incidence of peri-procedural thrombosis or no-reflow phenomena during the second step, and superb OCT imaging.
1
Introduction
Stent thrombosis often presents as acute myocardial infarction (MI), and this condition has high mortality and recurrence rate . Early angiography typically shows occlusion of the involved stented segment with absent or sluggish flow and large clot burden. Re-establishment of antegrade flow can usually be achieved by passing a guide-wire, aspiration thrombectomy, or dilation with a small (≤ 2 mm) angioplasty balloon. Understanding of the underlying mechanism is important, as targeted treatment may reduce the likelihood of recurrence . Reported predisposing factors include stent under-expansion, mal-apposition, fracture, uncovered struts, residual inflow/outflow disease, neointimal hyperplasia, and neoatherosclerosis. Angiography only provides a longitudinal image of the lumen, and does not provide details of the 3-dimensional vessel. Optical coherence tomography (OCT) has high resolution and can provide a clear view of the affected vessel and stent structure. In general, OCT is superior to intravascular ultrasound (IVUS) in demonstrating the above abnormality with better definition .
During the acute phase of stent thrombosis, large amount of thrombus is usually present, and this can obscure visualization of the underlying structures by OCT due to dorsal shadowing. Further treatment with mechanical devices in this pro-thrombotic environment may lead to distal embolization and micro-vascular obstruction. Thus, we hypothesize that a 2-step delayed approach may help to circumvent the above problems.
Step 1: Early non-aggressive mechanical reperfusion.
Stent thrombosis often presents with acute ST elevation MI. We typically treat such patients with aspirin, a P2Y 12 inhibitor (ticagrelor, prasugrel or clopidogrel), and unfractionated heparin in the emergency room. If angiography shows absent antegrade flow (TIMI flow grade 0 or 1), we recanalize the occlusion with a guide-wire, aspiration thrombectomy, or a small balloon (≤ 2 mm), as appropriate. We also consider adding an intravenous glycoprotein IIb/IIIa inhibitor therapy (e.g. eptifibatide, tirofiban or abciximab). If TIMI 2–3 flow can be restored, then we assess the amount of thrombus burden. If significant amount of thrombus is present (TIMI thrombus grade ≥ 3, i.e. filling defect ≥ ½ of vessel diameter), then no further mechanical intervention will be done. Additional imaging at this step was left to the discretion of the treating physician. We continue to infuse intravenous anti-thrombin and anti-platelet therapy as appropriate. We pay careful attention to hemostasis (e.g. use vascular closure device for femoral, and manual compression for radial access). We usually transfer patients to the coronary care unit (CCU) for monitoring. If only small amount of thrombus is seen, then we skip the 2-step approach and proceed with immediate OCT guided treatment.
Step 2: Repeat angiography and definitive treatment 1–2 days later.
We expect significant dissolution of thrombus. If so, we shall proceed with OCT examination to understand the underlying mechanism for the stent thrombosis. It is common to see multiple types of abnormalities. We shall treat with balloon dilation, stenting or surgical revascularization as appropriate.
In this report, we present 5 cases of stent thrombosis treated at the Vancouver General Hospital (BC, Canada) using this 2-step approach ( Table 1 ).
| Case # | MI | Prior stent | shock | Initial TIMI | Post TIMI | Defer | OCT findings of stent | Treatment | Final TIMI |
|---|---|---|---|---|---|---|---|---|---|
| 1 | Ant STEMI | 4y | yes | 0 | 3 | 1 day | Malapposition | PTCA | 3 |
| 2 | Ant STEMI | 8y | no | 0 | 3 | 1 day | Residual inflow disease | DES | 3 |
| 3 | Ant NSTEMI | 8d | no | 0 | 3 | 2 day | Under-expansion | PTCA | 3 |
| 4 | Ant STEMI | 3y | no | 0 | 3 | 2 days | Under-expansion | PTCA & CABG | 3 |
| 5 | Ant STEMI | 9y | no | 0 | 3 | 2 days | Focal aneurysm and Neoatherosclerosis | Drug eluting balloon | 3 |
1.1
Case 1
A 67-year old diabetic male patient presented to our hospital with acute anterior ST segment elevation MI (STEMI) and cardiogenic shock in October 2011. He had prior percutaneous coronary intervention (PCI) in 2007 at another institution. Proximal left anterior descending artery (LAD), mid right coronary artery (RCA) and right posterolateral branch (RPLB) were treated with drug-eluting stents (DES). He was taking aspirin but not clopidogrel at the time of admission. An intra-aortic balloon pump was inserted for hemodynamic support. Angiography showed thrombotic occlusion of the proximal LAD stent (TIMI-0 flow). This was treated with aspiration thrombectomy, which restored TIMI-3 flow. OCT examination showed a large amount of residual thrombus obscuring the underlying structures. He was treated with heparin and eptifibatide infusion, and was monitored in CCU. Repeat angiography and OCT the next day showed dissolution of thrombus. The LAD stented segment showed multiple malapposed struts with evagination of the vessel wall. Dilation with larger balloons at high pressure (18 atm) failed to eliminate the mal-apposition. OCT performed 4 months later showed persistent mal-apposition at the proximal LAD stent edge. This was treated with a single bare metal stent (BMS) with good immediate results. Reassessment 7 months later with OCT showed complete stent coverage with tissue. ( Fig. 1 ).
