The patient remained hypotensive (83/49 mm Hg) despite isotonic fluid administration (about 1.5-2.0 liters of 0.9 normal saline at 999 mL/h). A dopamine drip for persistent hypotension was started, and he was taken emergently to the catheterization laboratory for primary PCI. Coronary angiography showed no significant left CAD and a 100% mid-RCA occlusion with faint left-to-right collaterals. After aspiration thrombectomy, bare metal RCA stenting was performed. Transient no-reflow was treated with intracoronary nicardipine and nitroglycerin. The patient continued to be in shock, and an intra-aortic balloon pump was inserted and 1:1 counterpulsation was initiated.
Following admission to the coronary care unit, the patient’s mean arterial pressure improved. Inotropes were weaned off 2 days after PCI, and the intra-aortic balloon pump was removed. During his stay, the post-MI course was uneventful except for an episode of asymptomatic paroxysmal atrial flutter and nonspecific back dermatitis attributed to a prolonged recumbent position.
The patient was transferred to the internal medicine ward for medical therapy optimization and the initiation of low-intensity cardiac rehabilitation. After 2 days on the ward, discharge planning was initiated. However, he developed an episode of atrial fibrillation with fast ventricular response. Metoprolol 5 mg IV bolus was given, and the ventricular rate was controlled. At that point, the dose of long-acting beta-blocker (metoprolol succinate) was optimized, he was started on full-dose anticoagulation (warfarin), and clopidogrel was discontinued. Two days later, the patient reported back pruritus, and an erythematous raised rash on his back spreading to the torso was noticed. An aspirin allergy was suspected as the trigger for the rash, thus aspirin was also discontinued.
Three days later, the patient developed recurrent neck pain (angina) with radiation to his shoulders and left arm. The ECG revealed re-elevation of the ST segment (inferior, posterior, and lateral leads). He received reloading of clopidogrel 600 mg and aspirin 325 mg. Also, an eptifibatide IV bolus followed by an infusion was given for immediate antiplatelet action. He was transferred for emergent coronary angiography with suspected subacute stent thrombosis.
Upon arrival to the catheterization lab, the patient was awake and alert but in mild respiratory distress. Intravenous dopamine was started due to hypotension (systolic blood pressure was about 85 mm Hg). Limited RCA angiography showed a large clot burden with a partially thrombosed stent and TIMI grade 3 flow. After intracoronary eptifibatide and nicardipine were given, successful aspiration thrombectomy was performed twice with partial removal of thrombus. In-stent high-pressure balloon angioplasty was performed and optimal stenting was confirmed by intravascular ultrasound (IVUS) criteria. However, a residual layered thrombus along the distal stent edge was noticed. The patient tolerated the procedure without complications.
Dual antiplatelet therapy with aspirin and clopidogrel for 12 months was recommended. The eptifibatide infusion was continued for 48 hours. The jaw pain, shortness of breath, and ECG changes disappeared, but the patient remained on vasopressors for the following 7 days.
Around 1 week after the stent thrombosis event, the patient was found pulseless. Advanced cardiopulmonary resuscitation was started. ST segment elevation in lead II was noted on the cardiac monitor. There was no return of spontaneous circulation after 20 minutes, and the patient was pronounced dead. The autopsy revealed a patent RCA stent without evidence of occlusion, a large transmural inferior MI, left ventricular rupture, and hemopericardium.
Discussion
Stent thrombosis is an uncommon complication after coronary stent implantation. Based on the Academic Research Consortium criteria, definite stent thrombosis is defined as a clinical event with symptoms suggestive of an acute coronary syndrome (ACS) with angiography or pathology that confirms the presence of stent thrombosis.2 Probable stent thrombosis is defined as an unexplained death within 30 days or MI involving the territory of the target vessel without angiographic confirmation of stent thrombosis.2 Finally, possible stent thrombosis is any unexplained death after 30 days.2
Based on timing, stent thrombosis is divided by acute (< 24 hours post stent implantation), subacute (24 hours to 30 days post stent implantation), late (> 30 days post stent implantation), and very late (> 12 months post stent implantation).3 However, most cases (up to 60%) occur within the first 30 days after placement, irrespective of stent type.4
The incidence of subacute stent thrombosis is reported to approach 1% during the first 30 days postprocedure but may be as high as 5% or 10% depending on associated clinical and angiographic variables (Table 1).5 The strongest clinical predictors of stent thrombosis are premature cessation of antiplatelet therapy, renal insufficiency, diabetes mellitus, and ACS.2,6 Lesion and procedural characteristics associated with increased risk of stent thrombosis include bifurcation lesions, longer stent length, multiple implanted stents, stent underexpansion, and/or stent malapposition.6-9 Stent type (drug or non–drug-eluting) has no impact on the risk of stent thrombosis during the first 30 days postprocedure.10,11
