Case presentation

A 69-year-old man with a history of coronary artery disease presented for a left nephroureterectomy for transitional cell carcinoma. Two years prior to presentation, he underwent percutaneous coronary intervention with placement of a 3.0 mm diameter by 18 mm long sirolimus-eluting stent in the proximal circumflex and a 2.5 mm diameter by 18 mm long sirolimus-eluting stent in the mid-left anterior descending artery. He was treated for 6 months with dual antiplatelet therapy consisting of aspirin and clopidogrel, after which he was continued on low-dose aspirin. Aspirin was discontinued 3 weeks prior to surgery. The nephroureterectomy was performed laparoscopically under general anesthesia and the patient tolerated the procedure with no complications. Following transfer to the postanesthesia care unit, the patient developed marked ST depressions in leads V2 through V5, followed by ventricular fibrillation requiring multiple defibrillations with subsequent intubation. One dose of amiodarone was given and a lidocaine drip was started. After consultation with the surgeons, a heparin bolus was given and he was transferred to the cardiac catheterization laboratory for emergent angiography.

Cardiac catheterization

The right coronary artery was small and nondominant, with luminal irregularities (Figure 41-1). The left anterior descending artery (LAD) was patent with a long tubular stenosis of mild severity just prior to the previously placed stent. The stent itself was widely patent. The circumflex artery was occluded at the ostium within the previously placed stent, consistent with late stent thrombosis (Figure 41-2 and Video 41-1). Anticoagulation was achieved with heparin and abciximab, and a 0.014 inch guidewire was advanced easily through the thrombosed stent and into the distal circumflex. The lesion was dilated with a 3.0 mm diameter by 15 mm long compliant balloon with return of flow to the artery, but with residual thrombus (Figure 41-3 and Video 41-2). The operator felt there was residual stenosis and attempted to dilate the lesion with a 3.0 mm diameter by 15 mm long noncompliant balloon. However, the balloon would not advance into the stented segment. A 2.5 mm diameter by 15 mm long noncompliant balloon was advanced easily into the lesion and inflated to high pressure. Subsequently, the 3.0 mm diameter noncompliant balloon passed easily and the lesion was dilated multiple times with high-pressure inflations. The final angiogram revealed minimal thrombus within the stented segment and the artery had TIMI-3 flow (Figure 41-4 and Video 41-3).

FIGURE 41-1 Right coronary angiography revealed a small, nondominant right coronary artery with luminal irregularities.

FIGURE 41-2 There was occlusion of the left circumflex artery within the previously placed stent (arrow).

FIGURE 41-3 This is the angiogram of the left circumflex artery after balloon dilation, demonstrating return of flow to the artery but significant residual thrombus (arrow).

FIGURE 41-4 This is the final angiogram of the left circumflex artery, demonstrating a patent artery with minimal residual thrombus.

Postprocedural course

The patient was treated for mild heart failure with diuretics and was easily extubated the day following the procedure. His postoperative course was complicated by aspiration pneumonia, and he was discharged 9 days after admission with mild fatigue but no cardiac symptoms. He suffered no increase in surgical bleeding from the procedural anticoagulation. Five months after discharge, the patient had no angina or heart failure symptoms and had no evidence of residual cancer.

Discussion

The frequency of stent thrombosis after placement of bare-metal or drug-eluting stents is rare if there is no interruption in antiplatelet therapy. Although the proper duration of dual antiplatelet therapy following bare-metal stents is fairly well defined, this is not the case for drug-eluting stents. Late stent thrombosis has been seen as far as 2 years post drug-eluting stent implantation and often occurs when antiplatelet therapy is discontinued, particularly in the setting of noncardiac surgery. Perioperative stent thrombosis generally presents as an ST-elevation myocardial infarction and can be a devastating event. The recent surgery greatly complicates management of stent thrombosis, since anticoagulants needed for the procedure may cause dangerous perioperative bleeding complications.

Approximately 5% of patients undergoing stent placement require noncardiac surgery within the following year.¹ The current guidelines recommend postponement of noncardiac surgery for at least 6 months following bare-metal stent placement and for at least 1 year following drug-eluting stent placement.^2,3 However, there appears to be some degree of later risk with cessation of antiplatelet therapy and/or with surgery that has not been well defined. Several retrospective studies have now addressed the risk of stent thrombosis at several time points after stent implantation. With increasing time from implantation, risk of thrombosis decreases; however, the incidence of stent thrombosis was still significant beyond 3 months for bare-metal stents and beyond 12 months for drug-eluting stents. Over half of the patients experiencing an event were on single or dual antiplatelet therapy up to the time of the procedure, demonstrating that many events may not be preventable even with continuation of antiplatelet therapy.^4,5 Several factors have been found to correlate with adverse events, including stent thrombosis, in the perioperative period, including: myocardial infarction within 30 days of surgery, preoperative heparin use, emergency surgery, longer treated lesion length, lower preoperative ejection fraction, shorter time following stenting, and use of aspirin or clopidogrel 24 hours prior to surgery.

Stent thrombosis in the perioperative period also presents challenges in terms of anticoagulation strategies.⁶ Use of antithrombotic agents during the procedure in combination with antiplatelet agents following the procedure significantly increases the risk of major bleeding.

Due to the devastating implications of stent thrombosis, the possible need for surgery in the upcoming year should be clearly ascertained by the operator when determining the type of stent to be implanted, or whether revascularization is even necessary prior to surgery. In the absence of high-risk features, such as left main disease, unstable angina, or severe cardiomyopathy, the incidence of perioperative myocardial infarction is not changed by preoperative revascularization. Thus, in stable patients, revascularization can generally be safely delayed until after the perioperative period.⁷

Fortunately, in the case presented here, the patient was successfully resuscitated and flow was restored to the stented artery. Also, it was fortunate that the patient did not also thrombose the stent in the LAD. Despite the use of heparin, abciximab, aspirin, and clopidogrel, the patient had no significant surgical site bleeding. Following this event, it was recommended that the patient remain indefinitely on clopidogrel and low-dose aspirin in order to help prevent future episodes of stent thrombosis.