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.

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.