Serial Evaluations of Myocardial Infarct Size After Alcohol Septal Ablation in Hypertrophic Cardiomyopathy and Effects of the Changes on Clinical Status and Left Ventricular Outflow Pressure Gradients Raed A. Aqel, MD*, Fadi G. Hage, MD, Gilbert J. Zohgbi, MD, Paul B. Tabereaux, MD, MPH, David Lawson, PA, Jaekyeong Heo, MD, Gilbert Perry, MD, Andrew E. Epstein, MD, Louis J. Dell’ Italia, MD, and Ami E. Iskandrian, MD Alcohol septal ablation (ASA) as a treatment for obstructive hypertrophic cardiomyopathy produces septal infarction. There is a concern that such infarcts could be detrimental. Changes in the size of these infarcts by serial perfusion testing have not been studied. We performed resting serial-gated single-photon emission computed tomographic myocardial perfusion imaging in 30 patients (age 51 17 years, 57% were women) who had ASA between September 2003 and March 2007 before, 2 0.8 days (early), and 8.4 6.9 months (late) after ASA. Patients were also followed clinically and with serial 2-dimensional echocardiography. New York Heart Association class decreased from 3.50 0.51 before to 1.14 0.36 (p <0.0001) 3 months after ASA. The left ventricular (LV) outflow gradient (by Doppler echocardiography) decreased from 63 32 mm Hg before to 28 23 mm Hg after ASA (p <0.005). None of the patients had perfusion defects at rest before ASA. After ASA, perfusion defect size, involving the basal septum, decreased from 9.4 5.8% early to 5.2 4.2% of LV myocardium late after ASA (p <0.001). There were no changes in LV size and ejection fraction after ASA. In conclusion, ASA produces small basal ventricular septal infarcts (resting perfusion abnormality) involving <10% of the LV myocardium (including ventricular septum). There is a significant reduction in the perfusion abnormality late after ASA without an increase in LV outflow obstruction or recurrence of symptoms. © 2008 Elsevier Inc. All rights reserved. (Am J Cardiol 2008;101:1328 –1333) Alcohol septal ablation (ASA) therapy, with the infusion of alcohol into the major septal perforator branch of the left anterior descending artery, is reported to relieve left ven- tricular (LV) outflow obstruction and improve symptoms in a subset of patients with obstructive hypertrophic cardio- myopathy (HCM). 1,2 Long-term follow-up studies are only now beginning to be reported showing that the benefit of ASA extends beyond 5 years. 3 ASA produces localized myocardial necrosis that has been documented by myocar- dial perfusion imaging (MPI) with single-photon emission computed tomography, contrast echocardiography, and magnetic resonance imaging. 2,4–6 The hypothesis being tested is that infarct size affects LV remodeling; a decrease in infarct size on serial imaging should predict a benign long-term outcome. This study provides, for the first time, information on serial changes in infarct size and correlates the changes to clinical status and pressure gradients. Methods Patients with HCM who underwent ASA at the hospital of the University of Alabama at Birmingham between Septem- ber 2003 and January 2007 were considered for this study. All patients gave informed consent for their procedure after understanding the available alternatives. Chart review was approved by the local institution review board. Patients with HCM underwent ASA at our institution if they had severe symptoms that were unresponsive to max- imally tolerated medical therapy and had an LV outflow gradient 30 mm Hg at rest or 50 mm Hg with provo- cation. These patients underwent clinical evaluation, rest MPI, and Doppler 2-dimensional echocardiography before and after ASA. Rest MPI was done 4.0 10.0 days before ASA as well as 2 0.8 days (early) and 8.4 6.9 months (late) after ASA. The timing of the follow-up studies was flexible to accommodate the patients, who often lived long distances away from our medical center. Rest gated single-photon emission computed tomogra- phy MPI studies with Tc-99m sestamibi were acquired with a dual-head detector (ADAC, Miltipas, California), accord- ing to previously described methods, 60 minutes after in- travenous injection of 20-40 mCi of the radiotracer. 7 The images were acquired with and without attenuation correc- tion using emission line source. Images were obtained in 32 projections (30s/projection) using 180° anterior elliptical Division of Cardiovascular Disease, Department of Medicine, Univer- sity of Alabama at Birmingham and the Birmingham Veterans Affairs Medical Center, Birmingham, Alabama. Manuscript received October 17, 2007; revised manuscript received and accepted December 27, 2007. *Corresponding author: Tel: 205-558-7018; fax: 205-558-4714. E-mail address: raed.aqel@med.va.gov (R.A. Aqel). 0002-9149/08/$ – see front matter © 2008 Elsevier Inc. All rights reserved. www.AJConline.org doi:10.1016/j.amjcard.2007.12.042