Abstract
We report two cases of late occurring drug-eluting stent thrombosis (ST) where coronary angiography failed to identify the cause but intravascular ultrasound (IVUS) revealed underlying mechanical problems with the initial stent deployment. Mechanical factors such as stent underexpansion and residual edge stenoses may be more important in the pathogenesis of late drug-eluting ST than previously recognized. Intravascular ultrasound is required to reliably detect these problems and optimize subsequent reintervention.
1
Introduction
Recent data suggest patients suffering late stent thrombosis (LST) of drug-eluting stents (DES) are at high risk of recurrent ST, with an incidence of almost 20% at 3-year follow-up . As the etiological factors responsible for LST are not completely understood, the optimal treatment of these patients remains unclear. Delayed endothelialization, adverse vessel remodeling, and premature withdrawal of antiplatelet therapy are important, but technical issues related to suboptimal stent deployment may be more common than previously recognized .
We report a case of late and very late stent thrombosis (VLST), 4 and 30 months after successful DES implantation. In both instances, coronary angiography failed to identify the mechanism of ST, but intravascular ultrasound (IVUS) revealed significant residual stenoses.
1.1
Case 1
A 41-year-old male presented with unstable angina. Risk factors included hypercholesterolemia and smoking. Coronary angiography revealed a subtotal occlusion of the first marginal branch (OM1) of a dominant left circumflex artery ( Fig. 1 A ). There was minor coronary disease of the left anterior descending (LAD) artery and the right coronary (RCA) artery. Left ventricular systolic function was normal. Prior to intervention, he was preloaded with 300 mg of aspirin, 600 mg of clopidogrel, and 5000 U of heparin. The OM1 was predilated with a 2.0×8-mm balloon, and a 2.25×8-mm Taxus DES (Boston Scientific, Natick, MA, USA) was deployed at 12 atm. Final angiography revealed a well-deployed stent, no evidence of edge dissection but a moderate stenosis of the sidebranch. This required no intervention on the basis of preserved flow and no signs of ischemia ( Fig. 1 B). Medications at discharge included aspirin, clopidogrel, atenolol, and atorvastatin.
At routine 12-month review the patient was asymptomatic. Clopidogrel was ceased with the advice to continue aspirin and other medications indefinitely. Ten days later, he presented to a regional hospital with an inferolateral ST-elevation myocardial infarction complicated by in-hospital ventricular fibrillation. Thrombolysis (reteplase) was given with resolution of chest pain and electrocardiographic abnormalities. He was transferred to our institution for further management. Coronary angiography the following day showed the previously stented OM1 to be widely patent with minor progression of atheroma distal to the stent ( Fig. 1 C). The LAD and RCA were unchanged. He was discharged on indefinite dual antiplatelet therapy with aspirin and clopidogrel.
Eighteen months later, while continuing to take aspirin and clopidogrel he suffered an episode of chest pain accompanied by a minor elevation of cardiac enzymes. The patient was commenced on therapeutic intravenous unfractionated heparin. Repeat coronary angiography 24 h after presentation showed a hazy filling defect in the mid-OM1 stent suggestive of thrombus and an ostial stenosis in the sidebranch of OM1 ( Fig. 2 A ). Intravenous abciximab and low-pressure balloon angioplasty to 8 atm with a 2.0×8-mm balloon resulted in angiographic improvement. Visual assessment and subsequent quantitative coronary angiography (QCA) demonstrated minimal residual stenosis ( Fig. 2 , Table 1 ). IVUS was performed to define the mechanism of recurrent ST. There was significant focal underexpansion of the mid-stent (B) and a severe stenosis distal to the stent not readily apparent angiographically (D).
A | B | C | D | E | |
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QCA | |||||
MLD (mm) | – | 2.25 | – | 1.74 | 2.7 |
RVD (mm) | 2.5 | 2.38 | 2.8 | ||
Stenosis (%) | 10 | 27% | 4% | ||
EEM Area (mm 2 ) | 11.69 | 11.83 | 8.81 | 5.6 | 11.4 |
Vessel diameter (mm) | 3.6×4.1 | 3.7×4.0 | 3.1×3.5 | 2.4×3.0 | 3.8×3.9 |
Lumen area (mm 2 ) | 5.15 | 2.54 | 6.25 | 2.3 | 7.0 |
Lumen diameter (mm) | – | 1.6×1.9 | 2.62×2.97 | 1.5×1.9 | 2.8×3.0 |