Changing the Standard of Care in STEMI PCI

Combining Mechanical Reperfusion and Pharmacologic Therapy to Improve Myocardial Perfusion

Case 2 of 5: Continuation of STEMI Case Series from September 2008 Cath Lab Digest

History of Present Illness A 57 year-old male was brought to the Harrisburg Hospital emergency room via ambulance for ongoing severe chest pain of 1 hour’s duration. He was determined to have acute inferior wall myocardial infarction by electrocardiographic (ECG) criteria. A Code STEMI protocol was initiated by the emergency room staff. The patient immediately after arrival to the ER went into ventricular fibrillation and was successfully cardioverted to a normal sinus rhythm. He received aspirin 325 mg, clopidogrel 600 mg, intravenous (IV) metoprolol, heparin, and IV amiodarone. He was immediately taken to the cardiac catheterization laboratory for primary percutaneous coronary intervention (PCI) of the infarct-related artery. Cardiac Catheterization Findings and Treatment On diagnostic angiography, the patient was found to have subtotal occlusion with large irregular thrombus burden of the proximal right coronary artery (RCA) with thrombolysis in myocardial infarction (TIMI) 1 flow and a myocardial blush grade of 0 (Figure 1). He also was found to have a 70% eccentric lesion of the mid left anterior descending artery (LAD). His left ventriculogram demonstrated inferior wall hypokenesis with a visually estimated ejection fraction of 45%. His activated clotting time was maintained between 200–250 seconds throughout the PCI procedure using IV heparin. A 7 Fr JR4 guide catheter was utilized to engage the RCA and the lesion was successfully crossed with 0.014 inch BMW wire (Abbott Vascular, Abbott Park, Illinois). Subsequently, aspiration thrombectomy was performed with a Fetch catheter (Possis Medical, Inc., Minneapolis, Minnesota) (Figure 2). Repeat angiography was now detected to have improved TIMI flow grade 2 to 3, with angiographic improvement in thrombus burden (Figure 3). At this point, ClearWay 2.0 x 20 mm Rx (Atrium Medical, Hudson, New Hampshire) therapeutic infusion catheter was placed across the lesion and intracoronary abciximab 0.25 mg/kg bolus was administered via the catheter to further address the thrombus (Figure 4). Next, a 3.5 x 30 mm Endeavor (Medtronic, Inc., Minneapolis, Minnesota) drug-eluting stent was deployed at 14 atm to treat the lesion (Figure 5). Repeat angiography demonstrated that TIMI 3 flow was restored. In addition, the patient became chest pain-free. Intravascular ultrasound examination of the stent was performed using an Eagle Eye Gold IVUS catheter (Volcano Corp., Rancho Cordova, California). The Endeavor stent was postdilated to 4.5 mm in diameter. This resulted in minor slow-flow of the RCA, which was treated with intracoronary 400 µg of sodium nitroprusside via the same ClearWay RX therapeutic infusion catheter used earlier in the procedure. Final angiography showed an excellent result at the site of intervention in the proximal RCA, with a TIMI flow of 3 and a myocardial perfusion grade of 3. The patient’s ST-segment elevation resolved at the end of the procedure (Figures 6 and 7). The patient had an uneventful hospital course post-PCI and was discharged three days later on aspirin, clopidogrel, metoprolol and atorvastatin. The patient was reevaluated four weeks later as an outpatient. At this time, his echocardiogram detected no wall motion abnormalities and a normal ejection fraction of 62%. His resting technetium myocardial perfusion scan detected normal perfusion of the inferior wall, with no evidence of residual infarction (Figure 8). He then underwent elective PCI of the LAD with 3.5 x 24 mm Endeavor stent, with an excellent result . Repeat angiography of the RCA at the time of the LAD PCI showed a continued excellent result of the prior PCI. Technical Tips During STEMI PCI, it is important to not stent thrombus. Address the thrombus first with mechanical and pharmacologic therapies instead. Typically in a STEMI PCI, I will perform aspiration thrombectomy first, allowing better angiographic evaluation of the lesion and the extent of thrombus burden. This helps determine the size of the ClearWay RX therapeutic perfusion catheter needed for the vessel. In most cases, I choose a 1.5 or 2.0 mm ClearWay RX catheter based on the severity of the lesion. Do not attempt to use a large ClearWay RX catheter (i.e., larger than 2.0 in native coronary cases) without first assessing the lesion severity or vessel size. As a rule of thumb, always downsize the ClearWay Catheter by 1 mm to improve trackability, and allow placement within the thrombus burden. To optimize stent implantation, imaging technologies such as intravascular ultrasound (IVUS) or vessel measurement technology using devices such as the Gemini catheter (Neovasc, Canada) can be extremely useful. For vasodilator administration, use the same ClearWay catheter and inject selectively inside the vessel. We prefer prophylactic use of sodium nitroprusside or adenosine prior to stent placement to prepare the distal microcirculatory bed, which inevitably will be subject to some degree of distal embolization during stent deployment. Always assess the MBG upon completion of the procedure. Discussion As shown in this case, aspiration thrombectomy and intracoronary abciximab delivered via a ClearWay RX substantially improved the likelihood of obtaining TIMI 3 and a MBG of 3 in a very high-risk lesion. A recent meta-analysis of primary angioplasty STEMI trials utilizing abciximab (11 trials; 27,115 patients) showed a significant reduction in mortality. These data from randomized, controlled trials confirm improved epicardial flow, better tissue perfusion, with a reduced no-reflow phenomenon, and improved clinical outcomes with abciximab use in STEMI, and therefore, make a compelling case for the use of abciximab as a standard of care in patients undergoing primary PCI.4 The PCI strategy used in this case, i.e., aspiration and intracoronary abciximab via the ClearWay RX, in my opinion, substantially reduces the likelihood of no-reflow and reduces the severity of myocardial infarction. The follow-up of this patient’s sestamibi scan and the echocardiogram demonstrate full preservation of the myocardial infarct-related territory and good left ventricular function. Kotani et al demonstrated that patients with no-reflow after PCI for STEMI are often found to have a significantly greater amount of embolic debris from platelet/fibrin- rich complexes as well as cholesterol crystals and macrophages in distal protection devices compared to patients who do not experience no-reflow.3 It is extremely important to address thrombus first before delivery of the stent to prevent the dreaded no-reflow phenomenon. No-reflow is traditionally defined as TIMI grade 0 or 1, and slow-flow is defined as TIMI grade 2. If there is a lack of ST-segment resolution after PCI, no-reflow must be suspected. Moreover, it is important to not stent the thrombus-containing lesion. Sainos et al showed that placement of a drug-eluting stent in a large thrombus-burden lesion is associated with a 9.6% higher rate of major adverse cardiovascular events (MACE) than with small thrombus-containing lesions at 24 months post STEMI PCI. In addition, placement of a drug-eluting stent in a large thrombus burden lesion is associated with an 8.2% higher rate of infarct-related artery stent thrombosis event than small thrombus-containing lesions at 24 months post STEMI PCI.1 The Large thrombus-burden lesion is an independent predictor of MACE and infarct-related artery stent thrombosis.1 It is rational that the larger the thrombotic burden, the higher will be the incidence of incomplete stent apposition that might account for the higher rates of late stent thrombosis in LTB patients in the long term. Thrombus compression/displacement by the stent struts in the acute phase with abluminal thrombus resolution in the long term has been proposed as a potential mechanism. However, its incidence with drug-eluting stents was 31.8%, or three times higher than compared with bare-metal stents (11.5%) in this retrospective analysis.1 Further, the largest study published to date did not demonstrate that the type of stent, i.e., drug-eluting or bare-metal, is a predictor of stent thrombosis.2 As I discussed in the September edition of Cath Lab Digest, intracoronary administration of vasodilators such as adenosine or sodium nitroprusside is critically important to address the inevitable downstream debris released during PCI to allow quick dispersion from the distal microcirculatory bed. It is my routine practice to place drug-eluting stents in STEMI PCI procedures if thrombus removal is adequate during the PCI procedure, and the patient can withstand prolonged dual antiplatelet therapy. In most cases, I also utilize intravascular ultrasound to optimize stent deployment results. I see no advantage in routinely placing bare-metal stents during STEMI PCI if thrombus is addressed appropriately. This case demonstrates the clinical challenge of a large thrombus-containing lesion that interventionists routinely face during STEMI PCI. Earlier studies have suggested that a large thrombus burden is associated with a very high likelihood of no-reflow during PCI and poor outcomes.5 Many interventionists, in the excitement of STEMI PCI, are tempted to either stent or balloon these thrombotic occlusions to achieve a successful PCI. In my opinion, such a large thrombus-containing lesion needs the utmost care and diligence during the PCI procedure to achieve successful long term outcomes and preserve the infarct-related territory. Dr. Rajesh Dave can be contacted at: rdintervention@yahoo.com

1. Sianos, G, Papafaklis MI, Daemen J, et al. Angiographic stent thrombosis after routine use of drug-eluting stents in ST-segment elevation myocardial infarction. J Am Coll Cardiol 2007;50:573–583. 2. Van Werkum, JW, et al. High recurrence rates after a first episode of stent thrombosis: Results from the Dutch Stent Thrombosis Study. American College of Cardiology Scientific Sessions/i2 Summit-SCAI Annual Meeting; March 29, 2008, Chicago, Illinois. 3. Kotani J, Nanto S, Mintz GS, et al. Plaque gruel of atheromatous coronary lesion may contribute to the no-reflow phenomenon in patients with acute coronary syndrome. Circulation 2002;106:1672–1677. 4. De Luca G, Suryapranata H, Stone GW, et al. Abciximab as adjunctive therapy to reperfusion in acute ST elevation myocardial infarction: A metaanalysis of randomized trials. JAMA 2005;293:1759–1765. 5. Yip H-K, Chen M-C, CHANG H-W, et al. Angiographic morphologic features of infarct related arteries and timely reperfusion in acute myocardial infarction. Predictors of slow-flow or no-reflow phe?.,m,;lkjhn nomenon. Chest 2002:122;1322–1332.