Thrombus Aspiration for Restoring Flow: Stents for Scaffolding?

The majority of ST-elevation myocardial infarctions (STEMI) result from disruption of the fibrous cap of a preexisting atherosclerotic plaque, most times due to plaque rupture, but to a lesser extent from plaque erosion.¹ It has been postulated that these events occur from internal unstable metabolic abnormalities in the former and potentially from unstable circulating factors in the latter. However, regardless of the cause, multiple lines of evidence suggest that the initiating plaque is often nonobstructive and that the total flow cessation seen in STEMI is predominantly the result of a large thrombus burden attached to the injured plaque surface.² In the modern era of STEMI management, treatment focuses on early and complete reperfusion, most commonly by mechanical restoration of flow via primary percutaneous coronary intervention (PCI). Observational studies have demonstrated improved outcomes based on how rapidly reperfusion is achieved after hospital arrival, generally noted by door-to-balloon time (D2B).³ However, in addition to optimal D2B times, total ischemic time is important, and thus another factor is event (usually symptom) onset to hospital arrival. Both of these are important and are reasonably measurable, but other factors play a role. Advantages of PCI over earlier use of systemic fibrinolytics include more predictable success and greater completeness of reperfusion. More subtle forms of optimal reperfusion include avoiding distal microemboli that can contribute to gross no-reflow but disturbed microvascular flow, which is often graded angiographically by thrombolysis in myocardial infarction (TIMI) frame counts or myocardial blush scores, again both predictors of late outcome. Thrombus aspiration has been shown to improve outcomes in primary PCI for STEMI. Reasons for the benefits of thrombus aspiration may well be related to more effective clot removal without distal embolization of debris.^4,5 Furthermore, removing a large clot burden may limit multiple stent inflations caused by thrombus-mediated hazy angiographic results prompting multiple, often higher-pressure inflations, which create in the most dramatic form of distal microembolization, a no re-flow phenomenon. In the adjacent article by Talarico et al,⁶ the authors describe 4 patients who underwent thrombus aspiration for STEMI yielding non-significant residual culprit lesions which the operators chose to not stent. One of 3 patients re-studied during hospitalization subsequently underwent stenting due to intravascular ultrasaound documentation of a significant residual lesion. All patients did well out to 30 days. This report, while involving only 4 patients, reemphasizes the concept that clot, not plaque burden is often the major cause of coronary obstruction in STEMI. Thus, thrombus aspiration may be sufficient and even less injurious to the plaque/vessel site in selected cases, though longer-term follow up of larger populations is needed to reach a definitive conclusion. Conversely, stents serve an important purpose as a scaffold for those larger plaque-burden lesions, particularly those with disrupted segments of the vessel wall. However, future opportunities exist for “smarter” stents with more favorable polymer coatings and the ability to elute pharmaceutical therapies that may enhance healing of the vessel wall. Even more exciting is the potential for stents to elute from the luminal surface of the stent “timed” to deliver drugs into the distal myocardial bed to reduce local myocardial injury, apoptosis or to provide substrate for more favorable myocardial healing. In summary, the case series presented by Talarico et al⁶ supports current pathophysiological concepts of STEMI, but challenges the routine stenting of all STEMI lesions regardless of the extent of plaque burden or vessel disruption. This is an important challenge to assess as we continue to refine our approach to optimizing flow restoration while minimizing myocardial injury in patients presenting with STEMI.

References

1. Falk E. Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis. Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi. Br Heart J 1983;50:127–134. 2. Vetrovec GW, Cowley MJ, Richardson DW, et al. Intracoronary thrombus in unstable ischemic syndromes. Am Heart J 1981;102:1202–1208. 3. Nallamothu BK, Bradley EH, Krumholtz HM. Time to treatment in primary percutaneous coronary intervention. N Engl J Med 2007;357:1631–1638. 4. Silvaas T, Vlaar P, der Horst I, et al. Thrombus aspiration during percutaneous coronary intervention. N Engl J Med 2008;358:557–567. 5. Vetrovec G. Improving Perfusion in patients with myocardial infarction. N Engl J Med 2008;358:634–637. 6. Talarico GP, Burzotta F, Trani C, et al. Thrombus-aspiration without additional ballooning or stenting to treat selected patients with ST-elevation myocardial infarction. J Invasive Cardiol 2010;22:489–492.

——————————————————————————————————— From the Division of Cardiology, VCU Pauley Heart Center, VCU Medical Center, Richmond, Virginia. The author reports no conflicts of interest regarding the content herein. Address for correspondence: George W. Vetrovec, MD, Box 980036, Division of Cardiology,VCU Medical Center, Richmond, VA 23298-0036. E-mail: gvetrovec@mcvh-vcu.edu