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