Original Research MRI Evaluation of Microvascular Obstruction in Experimental Reperfused Acute Myocardial Infarction Using a T1 and T2 Preparation Pulse Sequence Yuesong Yang, MD, PhD, 1 * Warren D. Foltz, PhD, 2 John J. Graham, MBChB, 3 Jay S. Detsky, BSc, 1 Alexander J. Dick, MD, 3 and Graham A. Wright, PhD 1 Purpose: To investigate a T1 and T2 preparation pulse se- quence to evaluate microvascular obstruction (MO) in a por- cine model of reperfused acute myocardial infarction (AMI). Materials and Methods: A total of 14 pigs with reperfused AMI underwent MRI examinations at baseline and three to four hours after reperfusion. MRI scans included a left ventricular functional study, T1 and T2 measurement on a 1.5T MRI system. At reperfusion, first-pass myocardial per- fusion (FPMP) images were obtained after bolus injection of gadopentetate dimeglumine followed by an intravenous drip. Delayed contrast-enhanced MRI (DE-MRI) and T1 measurements were performed 30 and 45 minutes, respec- tively, after the bolus, during a constant infusion of gado- pentetate dimeglumine. Results: In 11 pigs MO was hypoenhanced in FPMP and DE-MRI. In later T1 preparation difference images postcon- trast, MO was hyperenhanced while delayed hyperenhanced (DHE) regions appeared dark. MO areas on DE-MRI and T1 images were comparable. T1 reduction (%) postcontrast in MO was small compared to measurements from DHE regions (P  0.0001) and similar to those from control segments (P = 0.66). Precontrast T1 and T2 values at reperfusion from MO and DHE regions were larger than in control regions. Conclusion: Using T1 preparation under a constant gado- pentetate dimeglumine (Gd-DTPA) infusion, delayed imag- ing at 30 to 45 minutes demonstrates MO as a positive contrast with larger T1 values. Elevated T1 and T2 values in MO precontrast may also help to differentiate them from both control and DHE regions. Key Words: microvascular obstruction; reperfused acute myocardial infarction; relaxometry; contrast-enhanced MRI; no-reflow J. Magn. Reson. Imaging 2007;26:1486 –1492. © 2007 Wiley-Liss, Inc. THE CONCEPT OF microvascular obstruction (MO), or the “no-reflow” phenomenon, was first proposed de- cades ago in various experimental animal studies fol- lowing reperfusion of severely ischemic myocardium, in which histology has validated intraluminal intrusion of endothelial cells plus blockage by activated neutrophils and stagnation of red blood cells (1–3). The incidence and extent of early MO have proven to be strong pre- dictors of negative left ventricular (LV) remodeling, LV systolic dysfunction, or congestive heart failure, and worse clinical outcome (4 – 8). Furthermore, long-term persistent MO predicts worse scar thinning and infarc- tion expansion (9). Thus, an early and accurate identi- fication of the presence of MO, and improved under- standing of its pathophysiology, should be beneficial to clinical management in patients with acute coronary syndrome. Microvascular obstruction in this popula- tion has a relatively high incidence and has emerged as a therapeutic target (10 –12). Noninvasive imaging techniques such as myocardial contrast echocardiography and positron emission tomog- raphy (PET) have been reported as effective methods to detect MO (13,14). First-pass myocardial perfusion MRI (FPMP) is the primary manner by which MO is identified (4,5,7). Delayed contrast-enhanced MRI (DE-MRI) is a widely used technique for the determination of myocar- dial viability and can also be used to delineate MO (5,11,15). Using contrast-enhanced MRI, infarcted myo- cardium is demonstrated accurately as a positive con- trast, or hyperenhanced area, while MO is depicted as a negative contrast, or hypoenhanced region (5,16,17). However, small areas of MO can be missed with this tech- nique (18) although the use of intravascular MR contrast agents may have the potential to quantify small MO in experimental studies (19). 1 Imaging Research, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, Ontario, Canada. 2 Department of Cardiology, St. Michael’s Hospital, Toronto, Ontario, Canada. 3 Department of Cardiology, Sunnybrook Health Sciences Centre, Uni- versity of Toronto, Toronto, Ontario, Canada. Contract grant sponsor: Canadian Institute of Health Research. *Address reprint requests to: Y.Y., MD, PhD, Imaging Research, Sun- nybrook Health Sciences Centre, S-605, 2075 Bayview Avenue, To- ronto, Ontario, M4N 3M5, Canada. E-mail: ysyang@sri.utoronto.ca Received July 10, 2006; Accepted May 30, 2007. DOI 10.1002/jmri.21063 Published online 26 October 2007 in Wiley InterScience (www. interscience.wiley.com). JOURNAL OF MAGNETIC RESONANCE IMAGING 26:1486 –1492 (2007) © 2007 Wiley-Liss, Inc. 1486