Simultaneous Double-Vessel Acute Stent Thrombosis of Drug-Eluting Stents: Double Trouble

Abstract

Acute stent thrombosis is a catastrophe and may lead to death, if not managed promptly. We report a case of simultaneous acute stent thrombosis of drug-eluting stents in two vessels (the right coronary artery and left circumflex artery). The index case is learning in the era of interventional cardiology where multivessel percutaneous interventions are common. The end result was good and the patient was discharged in stable condition. To the best of our knowledge, such a case has not been previously described.

Case description 

A 65-year-old male, diabetic, hypertensive, and a smoker, was admitted with severe chest pain at rest with electrocardiographic (ECG) changes suggestive of non-ST elevation myocardial infarction. Troponin T was 0.6 ng/dl. The patient had stable angina for 4 years and was advised to undergo revascularization following a treadmill exercise test. Coronary angiography revealed triple-vessel disease (Figure 1A-B). He was considered for coronary revascularization with stenting of the culprit artery (left circumflex artery) and right coronary artery (RCA). 

A loading dose of 600 mg of clopidogrel and 325 mg of aspirin was given the night before the procedure. Right radial access was obtained and a Whisper ES guidewire (Abbott Vascular) was used to cross the lesion in the proximal left circumflex artery (LCX). The lesion was predilated successively with increasing sizes of semicompliant balloons (1.25 to 2.25 mm). A 3.0 x 24 mm drug-eluting stent (Metafor, Meril Life Sciences) was placed from the proximal LCX to the obtuse marginal. The stent was post dilated with a 3.5 x 10 mm non-compliant balloon at 14 atmospheres (atm). Post procedure angiography demonstrated TIMI-3 flow with no residual stenosis (Figure 1C). 

The RCA lesion was crossed with a Whisper ES guidewire with the intent of placing a stent proximally. Here, the lesion was dilated with a 2.25 x 12 mm compliant balloon at 10 atm. The predilation caused a long dissection extending to the distal RCA (Figure 1D) and required a total of 3 drug-eluting stents (3.0 x 38 mm, 3.0 x 20 mm, and 2.5 x 40 mm). Post procedure angiography showed TIMI-3 flow in RCA (Figure 1E). A loading dose of 180 µg/kg eptifibatide over 1 to 2 minutes was given immediately after the procedure, followed by an intravenous infusion of 2 µg/kg per minute. Post-procedure, the patient became hypertensive with a blood pressure of 220/130 mmHg. He was kept on an intravenous nitroglycerine (NTG) infusion starting at 5 μg/kg/minute, titrated up to 20 μg/kg/minute. Two hours later, the patient started sweating with mild chest discomfort. His blood pressure had dropped to 70 mmHg systolic.

Immediately, the NTG was stopped and an injection of atropine 0.6 mg was given. Intravenous dopamine was started at a dose of 10 μg/kg/minute. A 12-lead surface electrocardiogram showed ST segment elevation in leads II, III, aVF, and V1. An acute stent thrombosis was suspected and the patient was shifted to the cath lab on vasopressor support. In the cath lab, the patient developed complete heart block and temporary venous pacing was established. A right femoral access was obtained. An RCA angiogram showed complete occlusion starting from the ostia (Figure 2A). A floppy wire was passed and thrombosuction was done with a Thrombuster catheter (Kaneka Corporation). The RCA proximal stent was dilated with a 3.0 x 10 mm non-compliant balloon at 20 atm. TIMI-3 flow was achieved after thrombosuction (Figure 2B). Despite opening the acute occlusion in the RCA, the patient continued to have angina and his blood pressure was still 80 mmHg systolic on vasopressors. A left coronary angiogram showed the proximal LCX was totally occluded with thrombus (Figure 2C). The occlusion was again crossed with a Balance Middle Weight (BMW) guidewire (Abbott Vascular) and repeated thrombosuction was followed by dilation with a 3.0 x 10 mm non-compliant balloon at 20 atm, resulting in TIMI-3 flow (Figure 2D). Following the procedure, the patient’s chest pain subsided and his blood pressure increased. Vasopressors were discontinued after 3 hours. After 48 hours, the patient was discharged on aspirin 325 mg, prasugrel 10 mg, and atorvastatin 80 mg once daily.

Discussion

Acute stent thrombosis is a catastrophic event, carrying a very high mortality rate. The overall incidence of stent thrombosis is still 2.4%, despite the use of current drug-eluting stents and potent antiplatelet therapy. Acute stent thrombosis, i.e., within 24 hours of the procedure, has an incidence of 0.4%.¹ Various predictors have been identified related to stent thrombosis: both patient-related factors (antiplatelet drug discontinuation, diabetes, and smoking) and lesion-related factors (extent of coronary artery disease, thrombus-containing lesion, multiple stents, and smaller coronary artery diameter) are predictors of stent thrombosis. However, in an acute stent thrombosis procedure, those related factors that occur within 24 to 48 hours are of greater importance, such as residual dissection, stent under-expansion, and stent number/length. Due to its high mortality rate, every effort should be undertaken to reduce acute stent thrombosis. 

Simultaneous occlusion of two stents has been reported, occurring in bare metal stents² and drug-eluting stents^3-6,8-10, and cessation of antiplatelet agents has been an important factor.^2,4,8-10 Early^2,4-7 as well as late^3,8-10 simultaneous stent thrombosis in two vessels has also been documented. However, this case represents simultaneous stent thrombosis in two vessels within 3 hours, despite the patient being on triple antiplatelet therapy. Factors identified for simultaneous stent thrombosis include cessation of antiplatelet agents, antiplatelet resistance, a systemic inflammatory and thrombogenic milieu due to acute coronary syndromes, or secondary thrombosis due to systemic hypotension after one stent thrombosis.² 

This case brings various issues to question. Since both stents became thrombosed, it is possible the precipitating factor may be systemic rather than lesion-related. The patient developed hypotension that may have precipitated stasis in both stents, resulting in thrombosis. The reason for the thrombosis could also be vasodilation due to the NTG, given to the patient to control his sudden surge in blood pressure. Uncontrolled and unmonitored NTG is known to produce hypotension; however, the patient was in the intensive care unit and intra-arterial pressure was continuously being monitored. Another reason could be acute right ventricular dysfunction due to the dissection and stenting of the RCA. Right ventricular dysfunction along with intravenous NTG could produce a precipitous fall in systemic pressure. It may also be that acute stent thrombosis occurred in the RCA due to the multiple stents placed to cover the dissection. This, along with an acute occlusion of the right ventricular branch (with NTG on board), may have subsequently led to the LCX thrombosis. Aspirin resistance is present in 10-30% patients. Since the patient had been on aspirin when he suffered an acute coronary syndrome, a generalized cause of aspirin resistance can’t be ruled out as well. Of note, when a percutaneous intervention is contemplated in two different vessels, both should be considered for stent thrombosis if it is a suspected possibility. To the best of our knowledge, we report a first-of-its-kind case where two vessels simultaneously developed acute stent thrombosis.

References

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Disclosure: The authors report no conflicts of interest regarding the content herein.

Dr. Nirdesh Jain can be contacted at nirdeshjain8@gmail.com.