Case presentation. An 83 year-old woman with chronic exertional angina presented to an outside hospital with new rest symptoms and was diagnosed with a non-ST segment elevation myocardial infarction (MI). Five years earlier, coronary angiography had documented an occluded mid-left anterior descending (LAD) artery with well-developed collaterals, and normal left ventricular function. She was referred for repeat angiography, which demonstrated a new 90% stenosis in the proximal LAD, the previously seen mid-LAD occlusion, and a new 90% lesion in the distal right coronary artery (RCA). A two-vessel intervention was performed, with placement of a 3.0 x 8 mm stent in the proximal LAD, and a 3.0 x 23 mm stent in the distal RCA. The RCA stent appeared undersized when initially deployed, and was therefore post-dilated with a 3.5 mm balloon. Intravascular ultrasound (IVUS) was not performed. She received unfractionated heparin during the intervention to maintain an ACT >250 seconds, but glycoprotein (GP) IIb/IIIa antagonists were withheld due to a prior history of retinal hemorrhage. After the procedure, she was treated with aspirin, 325 mg daily, and clopidogrel, 300 mg loading dose followed by 75 mg daily. The next day, an echocardiogram showed severe anterior and anteroseptal hypokinesis, mild inferolateral hypokinesis and an LV ejection fraction of 30%. She was discharged home two days later in good condition. Ten days later she returned with the acute onset of severe chest pain. She had discontinued her aspirin 4 days earlier due to stomach upset, and had forgotten her dose of clopidogrel for the previous few days. ECGs revealed inferior ST-segment elevations, and she was taken emergently to the catheterization laboratory for repeat angiography, which demonstrated thrombotic occlusion of the RCA stent. Normal flow was restored following rheolytic thrombectomy using the 5 French AngioJet catheter (Possis, Minneapolis, MN). A residual filling defect was seen at the proximal stent margin, prompting concern for an edge dissection. IVUS demonstrated that the proximal portion of the 3.0 stent occupied an ectatic vessel segment with a diameter of over 4.0 mm. No dissection was seen. The original stent was therefore dilated with a 4.0 x 15 mm balloon, and a new 4.0 x 16 mm stent was deployed in overlapping fashion at the proximal edge of the stented segment. GPIIb/IIIa inhibitors were again withheld. Following repeat intervention, the serum creatine kinase peaked at 1073 IU/L with an MB fraction of 224 ng/ml. Compared with the earlier study, repeat echocardiography showed improved function in the anterior wall, worsened inferior hypokinesis, and no change in the estimated LV ejection fraction. She was again treated with daily aspirin and clopidogrel. After one day in intensive care and three days on the telemetry unit, she was ambulating independently without overt congestive symptoms and was discharged home. Discussion. The potential for thrombus to form inside a newly placed coronary stent, leading to vessel occlusion, myocardial infarction and associated sequelae, has been recognized since the earliest use of coronary stents. With refinements in interventional equipment and techniques and the use of effective post-procedure antiplatelet regimens, this complication occurs following <1% of stent procedures, but still leads to serious consequences.1 Identified predictors of SAT include longer total stent length, smaller minimum luminal diameter, persistent coronary dissection, stent underexpansion or undersizing, and possibly multi-vessel interventions, though the latter may simply be due to the longer total lengths of stent used. 1-3 Recent data have also suggested that SAT is more likely to occur following intervention for acute coronary syndromes than in more elective settings. 4,5 Since combined treatment with aspirin and a thienopyridine has been shown to be the most effective post-procedure prophylaxis against SAT, 6 patient adherence (or lack thereof) to the prescribed regimen may be a critical issue in selected cases. Several of these factors may have been important in the case described above. Episodes of SAT are costly, both for the patient and the health care system. This patient suffered a moderate-sized infarction clinically without further complication, but 30-day mortality rates of 7% or higher following SAT have been reported. 1 Most patients with SAT undergo repeat angiography and intervention, and have hospital stays typical for that of an acute MI patient. Estimated direct hospital costs for this patient were $13,250, including $7200 from her catheterization laboratory procedure. Careful attention to interventional technique and strict adherence to post-procedure prophylaxis are essential in minimizing the risk of SAT. The efficacy of other measures at preventing SAT remains unclear. In the case of GPIIb/IIIa inhibitors, specific reduction in the rate of SAT had not been reported until the recent CADILLAC trial involving acute MI patients randomized to PTCA or stenting with or without abciximab. 7 Nonetheless, these agents are frequently used in high-risk interventions based on trials demonstrating reduced post-procedural MI and target vessel revascularization rates following PCI procedures. Heparin coating was developed to decrease the thrombogenicity of stents, as demonstrated in various animal models. 8,9 In large human trials, reported rates of SAT with heparin coated stents in both acute MI (0.9%)10 and stable/unstable angina (0.2%)11 populations have been lower than historical controls. Although heparin coated stents have not been proven to yield lower rates of SAT than conventional stents in a randomized trial, it may be reasonable to consider using them in high-risk cases such as acute MI or when bleeding risk or patient compliance may be an issue. SAT remains an uncommon but costly both in clinical and economic terms event following stent procedures. Given that clinical and procedural risk factors for its occurrence have been recognized, specific efforts at reducing its likelihood in high-risk patients are warranted.
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