Stenting Temporarily Unprotected by Platelet Inhibitor Drugs (an unplanned case study)

Disclosure: James Tyson and Dr. Jack Chen report no conflicts of interest regarding the content herein.

This article received a double-blind peer review from members of the Cath Lab Digest editorial board.

The authors can be contacted via Dr. Jack Chen at chenjackapollo@yahoo.com.

Case presentation

A 64-year-old gentleman presented to the emergency department with 6 hours of intermittent substernal chest pressure associated with mild diaphoresis and dyspnea. His vital signs included blood pressure of 123/73mmHg and heart rate of 62, normal sinus rhythm. Electrocardiogram revealed subtle ST-elevation in lead aVL (Figure 1). Aspirin (ASA) 325 mg was administered orally by the emergency room staff.

Emergent transradial cardiac catheterization revealed the culprit vessel to be a totally occluded left-sided saphenous vein graft, which appeared to supply the obtuse marginal (OM) circulation (Figure 2). There was also a chronic totally occluded saphenous vein graft (SVG) “stump.” Two other saphenous vein grafts to the left anterior descending and right coronary arteries were widely patent. 

Intravenous bolus and infusion of bivalrudin were initiated. A 6-French Amplatz left-1 guiding catheter was used to engage the SVG ostium, and a Whisper Extra Support guide wire (Abbott Vascular) was advanced easily through the occlusion and the distal native OM. Gentle predilatation was performed with serial inflations using a 2.0 x 20mm Trek balloon (Abbott Vascular) at 8 atmospheres. Subsequent gentle manual aspiration with an Export catheter (Medtronic) restored TIMI-3 flow, with retrieval of copious amounts of thrombotic material. Finally, two overlapping drug-eluting stents (DES) [2.5 x 22mm and 2.5 x 18mm Resolute stents (Medtronic)] were deployed at 16 atmospheres with an excellent result, less than 0% residual stenosis, and TIMI-3 flow (Figure 3). No slow- or no-reflow occurred during the procedure.  Post-procedure, bivalrudin infusion was discontinued and ticagrelor 180mg was administered.

Thereafter, the patient had no further angina, with improvement of his electrocardiographic findings (Figure 4). Vital signs remained essentially unchanged throughout and after the procedure. However, after admission to the coronary care unit, his blood pressure began to gradually elevate into the 160-170/80-90mmHg ranges, as he had initially informed us of erroneously lower dosages of his home antihypertensive medications. The patient complained of a headache, which was initially attributed to his elevated blood pressure. Over the next few hours, his antihypertensive therapy was aggressively titrated. Subsequent computerized tomography (CT) revealed a left-sided intracerebellar hemorrhage, with edema (Figure 5). Fortunately, his neurologic examination was entirely within normal limits. All antiplatelet and anticoagulant therapies were immediately discontinued. Neurosurgical consultation emphatically agreed with the necessity of cessation of all anticoagulant/antiplatelet therapy and recommended conservative observation, along with analgesics and dexamethasone for cerebellar edema reduction. His cardiac and neurologic status remained uneventful throughout the remainder of his two-week hospitalization, with improvement of his headache. On day 14 post procedure, repeat transradial angiography revealed widely patent stents, identical to the final interventional images (Figure 6).  The following day, he had no further headache and was subsequently discharged on a steroid taper regimen without antiplatelet therapy, according to neurosurgical recommendations.

On day 25 post-procedure, repeat outpatient head CT revealed total hemorrhage resolution, with minimal edema, and no underlying vascular pathology (Figure 7). With neurosurgery clearance for initiation of antiplatelet therapy, the patient was begun on ASA 81mg; clopidogrel 75mg was then added to his regimen 32 days post procedure. He has done well since then, headache-free and without any cardiac or neurologic sequelae.

Discussion

Dual antiplatelet therapy (DAPT) is mandatory therapy after stent implantation. While encouraging recent data have suggested the safety and feasibility of curtailed DAPT; it nonetheless appears that the initial month post-implantation remains critical.^1,2 A study published in 2012 evaluated the efficacy of 3-month DAPT compared to 1 year of DAPT in patients following DES implantation. Of the 2,117 patients observed, no difference in the two DAPT groups was observed (4.7%) with regards to occurrence of cardiovascular death, myocardial infarction, stent thrombosis, target vessel revascularization, or bleeding, after 1 year post-implantation. Although the recommended duration of DAPT for DES in Europe is shorter, domestic FDA recommendation remains at 1 year.^3,4 The absolute contraindication to DAPT in our case was particularly concerning due to unfavorable anatomic features. Although an SVG, the vessel diameter was small. Additionally, the occlusion was quite long, requiring long overlapping DESs, another potential predictor for stent thrombosis.⁵ Moreover, clinically, the thrombogenic milieu associated with the ST-elevation myocardial infarction (STEMI) setting further amplified the acute risk.  

Some technical considerations may have contributed to the success of this case. While conflicting data exist regarding the long-term benefits of pre-stent manual aspiration thrombectomy during STEMI, failure to remove the large thrombotic burden in this case may have resulted in no-reflow or at least slow-reflow after stent deployment. While intracoronary vasodilator administration frequently improves this scenario, it is unclear whether potential residual microcirculatory compromise would have impacted stent patency thereafter, especially in the absence of DAPT. Furthermore, while intravascular ultrasound was not utilized, the stents were deployed at high pressure (16 atmospheres), with excellent angiographic results. The patient did receive 1 dose of ASA, as well as ticagrelor, perhaps the most efficacious of the three available antiplatelet agents. Additionally, the dexamethasone ordered by the neurosurgeons may have interfered with the ticagrelor hepatic metabolism, thereby prolonging its bioavailability.  

Although “cleared” by neurosurgery for DAPT at day 25, we were encouraged by the pristine stent appearance during repeat angiography and elected to start conservatively with ASA 81mg daily, with addition of clopidogrel a week later. The latter thienopyridine was chosen, as it may be the least potent. Despite American College of Cardiology/American Heart Association recommendations for ASA 325mg daily initially after acute coronary syndrome stent implantation, we elected the lower dose due to the complex nature of this case. 

Obviously, only the most serious, life-threatening circumstances should prompt even consideration of DAPT cessation post-stenting. While this extremely unusual, isolated case is by no means an endorsement for withholding DAPT, especially in the initial timeframe, we were quite fortunate to have the availability of the third-generation DES, which is possibly less thrombogenic than its predecessors. The Swedish Coronary Angiography and Angioplasty Registry reported on 34,147 patients with STEMI from January 2007 to January 2013, and found superior DES thrombosis rates of third-generation devices over those of earlier generations. Additionally, all DESs demonstrated lower thrombosis rates than bare metal stents.⁶

The neurosurgeons found no predisposing anatomic anomaly for the hemorrhage, which was likely triggered by the powerful antithrombotic/antiplatelet regimen. As illustrated by this case, headache following antithrombotic or antiplatelet therapy should prompt immediate suspicion for intracranial bleeding and aggressive blood pressure lowering, if elevated. Our case was clearly a major therapeutic dilemma; given our treatment limitations, we observed the patient in the hospital for 2 weeks and performed repeat angiography at the end of that time. During repeated discussions with both the patient/family and neurosurgical consultants, all were in agreement that in the worst-case scenario, perhaps stent thrombosis, serious as it is, may still be the lesser of two evils when compared to a second, potentially fatal, intracranial bleed. This case is a sobering reminder of potentially catastrophic non-cardiac and non-procedure-related complications from PCI which resulted, in our case, in an unfortunate and ironic acronym. 

References

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