Management of Thrombotic Lesions









Introduction


Acute myocardial infarction is caused by thrombotic occlusion of a native coronary artery. While partial occlusion usually presents as a non ST-elevation myocardial infarction (NSTEMI), it is expected that complete occlusion will result in ST-elevation myocardial infarction (STEMI). Acute myocardial infarction can also occur as a result of thrombotic occlusion of a saphenous vein graft. Saphenous vein graft occlusion may be associated with larger thrombus burden than native coronary artery occlusion and therefore may require different strategies for management. Stent thrombosis is becoming increasingly recognized as a distinct cause of acute myocardial infarction.


Primary percutaneous coronary intervention (PCI) is effective at reperfusing or recanalizing the infarct related artery with a success rate that exceeds 90%. Traditionally this has been accomplished by passing an uninflated coronary balloon “back and forth” across the thrombus, possibly coupled with serial balloon inflations at the site of occlusion. This established the term “door-to-balloon time” that is currently used as a quality metric for catheterization laboratories that offer primary PCI. Unfortunately, such disruption of thrombus likely results in macro- and micro-embolization into the downstream coronary bed. Impaired myocardial perfusion can be observed by failure of electrocardiographic ST-segments to return to baseline. This can also be observed during coronary angiography by assessment of myocardial blush grade, which represents flow in the micro-circulation (0 = no blush, 1 = minimal blush, 2 = moderate blush, and 3 = normal blush). Despite successful epicardial coronary flow, impaired myocardial flow (blush grade 0 to 2) has been observed in over 70% of patients. Impaired myocardial perfusion has been associated with poor prognosis. For example, after coronary flow is re-established in acute myocardial infarction, no ST-segment resolution is associated with 29% long-term mortality compared with 4% for complete resolution. Similarly, poor myocardial blush (grade 0/1) is associated with 23% long-term mortality compared with 3% for normal blush (grade 3).


Accordingly, different strategies have been developed to manage thrombus during primary PCI in order to mitigate the adverse effects associated with embolization. This review will principally center on the current pharmacological and mechanical approaches to manage thrombotic lesions.




Stent Thrombosis


An important etiology of acute myocardial infarction is stent thrombosis. In fact, in a relatively large registry, the proportion of STEMI cases due to stent thrombosis increased from 6% in 2003 to 2004, to approximately 11% in 2009 to 2010. This is important since primary PCI for stent thrombosis is less effective (76% to 80% successful reperfusion) than primary PCI for native artery occlusion. STEMI due to stent thrombosis is also associated with an increased risk for long-term myocardial infarction (~23%) and repeat stent thrombosis (~15%) compared with STEMI due to native artery occlusion.


With current generation drug-eluting stents (everolimus and zotarolimus-eluting), late and very late stent thrombosis is exceedingly rare; however, this complication is still seen during periods of inadequate antiplatelet therapy. Inadequate antiplatelet therapy might be the result of poor patient compliance, but is also seen among patients undergoing noncardiac surgical procedures who have been instructed to minimize or stop their antiplatelet therapy.




Pharmacological Strategies to Improve Myocardial Perfusion


Facilitated PCI has been studied as a potential mechanism to improve outcomes during acute myocardial infarction. With this approach it was hoped that improvement in preprocedure coronary flow could reduce infarct size and improve survival. PCI can be facilitated by potent antiplatelet agents (i.e., glycoprotein IIb/IIIa inhibitors) or by thrombolytic agents. Dong et al. performed a metaanalysis on nearly 3000 STEMI patients who received upstream eptifibatide or tirofiban versus in-lab eptifibatide or tirofiban. Although upstream glycoprotein inhibitor use was associated with improved preprocedure coronary flow, it did not reduce recurrent myocardial infarction or mortality. Glycoprotein IIb/IIIa inhibitors can also be administered intra-coronary, rather than intravenous; however, recent randomized trial data did not find a benefit in regard to survival or recurrent myocardial infarction from this approach.


The Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events (FINESSE) trial randomized nearly 2500 patients who presented within 6 hours of a STEMI to one of the following study drug strategies: upstream abciximab versus upstream abciximab with half-dose reteplase versus upstream placebo. Efficacy was similar between all treatment arms; however, major bleeding was increased from a facilitated approach, especially with thrombolytic therapy. Major bleeding was 10.1% with upstream abciximab versus 14.5% with upstream abciximab with half-dose reteplase versus 6.9% with upstream placebo. Eitel et al. also conducted a metaanalysis to examine the association between facilitated PCI and mortality. Compared with primary PCI, the odds ratio (OR) for mortality from glycoprotein IIb/IIIa inhibitor–facilitated PCI was 0.88, 95% confidence interval (CI), 0.59 to 1.33; for thrombolytic-facilitated PCI, OR = 1.47; 95% CI, 0.96 to 2.25; and for combination glycoprotein IIb/IIIa inhibitor/half-dose thrombolytic–facilitated PCI, OR = 1.22; 95% CI, 0.55 to 2.67. Therefore, facilitated PCI does not appear to improve survival and, in the case of thrombolytics, may even be associated with harm.




Mechanical Strategies to Improve Myocardial Perfusion


Currently Approved Devices


The simplest way to retrieve coronary thrombus is with the use of a manual aspiration thrombectomy catheter. A variety of catheters are commercially available ( Table 14-1, Figure 14-1 ). The catheter is attached to a stopcock and syringe that is prepped with negative pressure and advanced over a 0.014-inch wire proximal to the site of occlusion. When the stopcock is turned, the catheter aspirates blood/thrombotic debris from the catheter tip. The catheter is slowly advanced through the site of occlusion and returned to the guide catheter when the syringe is filled with blood and thus no longer aspirating. Normally one to two or more passes with the aspiration catheter are performed to restore epicardial blood flow. One can continue passes until there is no more debris noted in the aspirate when run through a mesh filter or gauze. Many catheters now come preloaded with a stylet that can facilitate deliverability of the device to the site of occlusion. There is no clear advantage of one device over another; however, most of the clinical trial data support the Export device. Table 14-2 provides pearls to consider for optimal use.



TABLE 14-1

Commercially Available Aspiration Thrombectomy Catheters






















































MANUFACTURER DEVICE PRELOADED WITH STYLET GUIDE CATHETER (Fr)
Medtronic Export AP No 6, 7
Export Advance Yes 6, 7
Terumo PriorityOne Yes 6, 7
Vascular solutions Pronto V3 No 6
Pronto V4 No 6, 7, 8
Pronto LP Yes 6
Maquet ExpressWay Yes 6
Spectranetics QuickCat No 6
Bayer Fetch 2 No 6

Fr, French.

The Pronto V4 has an embedded wire for additional deliverability and kink resistance. The Pronto LP is intended for small vessels (~1.5 mm).



FIGURE 14-1


Composite of commercially available aspiration thrombectomy catheters.


TABLE 14-2

Pearls for Optimal Use of Aspiration Thrombectomy Catheters

























PEARL REASON/EXPLANATION
Activate suction proximal to lesion Prevent systemic embolism of thrombus
Keep suction activated until device is completely removed from body Firm thrombus might be trapped at catheter tip and prematurely stopping suction could liberate thrombus into guide catheter/systemic circulation
Once device is removed from body, back bleed from hemostatic valve The device can entrain air. This is also to potentially discharge retained thrombus as above
Caution if the guide catheter pressure is severely damped, since opening the hemostatic valve can entrain air rather than bleed back
Aspiration thrombectomy catheters can also be used to infuse medications into the myocardial bed With poor coronary flow, intracoronary administration of medications through the guide catheter may end up in the systemic rather than coronary circulation
Aspiration thrombectomy catheter can be difficult to advance to the target. In this scenario, consider a catheter that comes loaded with a stylet or delivers through a guide extender The sylet stiffens the catheter and enhances deliverability
Similarly, a guide extender may provide enough support to allow the thrombectomy catheter to track into position
Despite being designed to be “kink-resistant,” all catheters are relatively easy to kink Slow down during advancement of catheter into the body

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Mar 21, 2019 | Posted by in CARDIAC SURGERY | Comments Off on Management of Thrombotic Lesions

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