Cardiac MRI Evaluation of Infarct Size with Thrombus Aspiration During ST-Segment Elevation Myocardial Infarction

The clinical importance of thrombus-driven microvascular obstruction (MVO) during acute myocardial infarction (MI) has been increasingly recognized in the last decade.¹ Indeed, several studies have documented a failure to achieve Thrombolysis In Myocardial Infarction (TIMI) 3 flow in up to 30% of patients presenting with MI with initial balloon angioplasty.² Angiographic no-reflow occurs more frequently in patients presenting with ST-segment elevation myocardial infarction (STEMI),³ attributed most commonly to MVO from embolized thrombotic and plaque debris. Distal embolization has been associated with larger infarct size and lower left ventricular (LV) systolic function.³ However, it is important to indicate that angiographic no-reflow in the setting of STEMI may be multifactorial and not exclusively determined by intracoronary thrombus burden.⁴

Multiple studies have investigated pharmacological and mechanical strategies for the management of no-reflow. Pharmacologic strategies include the use of glycoprotein IIb/IIIa inhibitors⁵ and/or vasodilators, like nitroprusside⁶ and adenosine,⁷ albeit with only modest success. Mechanical management of no-reflow includes distal protection and thrombectomy strategies. While distal protection has failed to show a clear benefit,³ aspiration thrombectomy has emerged as an effective strategy and has been included as a Class IIa recommendation during percutaneous coronary intervention (PCI) for STEMI.⁸

This recommendation is mainly based on the findings from the Thrombus Aspiration during Percutaneous Coronary Intervention in Acute Myocardial Infarction (TAPAS) trial, which randomized 1,071 patients presenting with STEMI, to PCI with or without thrombus aspiration (TA).⁹ The study results indicate a significant improvement in myocardial blush grades (primary endpoint) and electrocardiographic reperfusion measures. There was a favorable trend for the reduction of major adverse cardiac events (MACE), but the study was not powered to detect differences in clinical endpoints. There was no significant difference in levels of the MB fraction of creatinine kinase (CK-MB) after PCI between the two strategies. This observation is often interpreted as a lack of infarct size reduction with TA.

In this issue of the Journal of Invasive Cardiology, An and colleagues utilize cardiac magnetic resonance imaging (cMRI) as an objective method for evaluation of infarct size following PCI with TA in patients presenting with STEMI. The authors conclude that successful TA prior to balloon angioplasty and coronary stenting significantly reduces infarct size and preserves myocardial viability by cMRI, along with a trend toward improvement in left ventricular ejection fraction (LVEF).¹⁰

The investigators did not use randomized assignment of TA to patients presenting with STEMI. By including all-comers during a given time period, the investigators can be credited for minimizing selection bias. In terms of the methodology, the angiographic description of a successful TA is acceptable; the histologic confirmation seems arbitrary in the absence of a described method or reference. Evaluation of atheroembolic material in the aspirate has been described in previous studies.⁹ Another limitation is the lack of information regarding prior MI, which may have allowed assessment of TA on myocardial damage in patients with pre-existing infarcts using cMRI.

The authors use well-validated infarct indices to adjudicate parameters of myocardial perfusion and contractile function in patients with MI.¹¹ These include LV volume and function, absolute infarct volume, infarct volume ratio and transmurality index. Also, myocardial viability is known to be well-assessed by cMRI, as it can distinguish between reversible and irreversible injury independent of wall motion, infarct age, and reperfusion status.

Consistent with some studies,⁹ the current analysis shows a lack of correlation between success of TA and peak CK level, traditionally considered to be a marker of infarct size. In contrast, other studies report a strong association between infarct size, by cMRI and peak cardiac enzyme released post MI.¹² Therefore, this issue remains controversial and further investigations are clearly needed.

Overall, the weight of the evidence seems to indicate successful TA reduces infarct size and correlates with greater myocardial viability, as measured by cMRI. These results need to be validated by clinical outcome studies. This study strengthens the evidence for routine TA during primary PCI of patients presenting with STEMI as endorsed by the American College of Cardiology/American Heart Association guidelines.

References

1. Weaver WD, Simes RJ, Betrin A, et al. Comparison of primary coronary angioplasty and intravenous thrombolytic therapy for acute myocardial infarction: A quantitative review. A meta analysis. JAMA 1997;278:2093–2098.
2. Piana RN, Paik GY, Moscucci M, et al. Incidence and treatment of “no-reflow” after percutaneous coronary intervention. Circulation 1994;89:2514–2518.
3. Stone GW, Webb J, Cox DA, et al. Distal microcirculatory protection during percutaneous coronary intervention in acute ST-segment elevation myocardial infarction: A randomized controlled trial. JAMA 2005;293:1063–1072.
4. Niccoli G, Burzotta F, Galiuto L, et al. Myocardial no-reflow in humans. J Am Coll Cardiol 2009;54:281–292.
5. Danzi GB, Sesana M, Capuano C, et al. Comparison in patients having primary coronary angioplasty of abciximab versus tirofiban on recovery of left ventricular function. Am J Cardiol 2004;94:35–39.
6. Amit G, Cafri C, Yaroslavtsev S, et al. Intracoronary nitroprusside for the prevention of the no-reflow phenomenon after primary percutaneous coronary intervention in acute myocardial infarction. A randomized, double-blind, placebo-controlled clinical trial. Am Heart J 2006;152:887.E9–E14.
7. Ross AM, Gibbons RJ, Stone GW, et al. AMISTAD-II Investigators. A randomized, double-blinded, placebo-controlled multicenter trial of adenosine as an adjunct to reperfusion in the treatment of acute myocardial infarction (AMISTAD-II). J Am Coll Cardiol 2005;45:1775–1780.
8. Kushner FG, Hand M, Smith SC, et al. 2009 Focused Updates: ACC/AHA Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction (Updating the 2004 Guideline and 2007 Focused Update) and ACC/AHA/SCAI Guidelines on PCI (Updating the 2005 Guideline and 2007 Focused Update). J Am Coll Cardiol 2009;54:2205–2241.
9. Svilaas T, Vlaar PJ, van der Horst IC, et al. Thrombus aspiration during primary percutaneous coronary intervention. N Engl J Med 2008;358:557–567.
10. An Y, Kaji S, Kim K, et al. Successful thrombus aspiration during primary percutaneous coronary intervention reduces infarct size and preserves myocardial viability: A cardiac magnetic resonance imaging study. J Invasive Cardiol 2011;23:172–176.
11. Kim HW, Farzaneh-Far A, Kim RJ. Cardiovascular magnetic resonance in patients with myocardial infarction: Current and emerging applications. J Am Coll Cardiol 2009;55:1–16. 
12. Ingkanisorn WP, Rhoads KL, Aletras AH, et al. Gadolinium delayed enhancement cardiovascular magnetic resonance correlates with clinical measures of myocardial infarction. J Am Coll Cardiol 2004;43:2253–2259.

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From the ^†University of Texas Southwestern Medical Center at Dallas, Texas and the ^‡VA North Texas Health Care System, Dallas, Texas.
Dr. Brilakis discloses the receipt of speaker honoraria from St. Jude Medical and Terumo Corporation, research support from Abbott Vascular and Infraredx; spouse is an employee of Medtronic Corporation. Dr. Banerjee has served on the Speaker’s Bureau for St. Jude Medical Center, Medtronic Corporation, and Johnson & Johnson and has received a research grant from Boston Scientific.
Address for correspondence: Subhash Banerjee, MD, Division of Cardiology (111A), 4500 S. Lancaster Rd, Dallas, TX 75216. Email: subhash.banerjee@utsouthwestern.edu