Our patient, a 40-year-old physician, was diagnosed to have hypertrophic cardiomyopathy in 1999 after an episode of exertional syncope. Thereafter, he had two more episodes of syncope at rest, in 2001 and 2008 respectively. He was also having exertional angina of a variable threshold despite being on maximally tolerated doses of beta blockers. On physical examination, there was grade 3/6 systolic ejection murmur along the left and upper right sternal border and a grade 3/6 pan-systolic murmur at the apex that radiated to the axilla.

The electrocardiogram (ECG) of this patient revealed normal sinus rhythm, left ventricular hypertrophy with strain pattern and QRS duration of 120 msec. The echocardiogram showed an asymmetrical septal hypertrophy (ASH) with maximal septal thickness of 34 mm. Systolic anterior motion of AML was present along with moderate mitral regurgitation (MR). Peak instantaneous left ventricular outflow tract (LVOT) gradient was 68 mm Hg. Cardiac catheterisation revealed a peak LVOT gradient of 40 mm Hg. Selective coronary angiography showed a large septal artery from proximal LAD supplying the basal septum. A large septal branch from RPDA also supplied the same area. A simultaneous angiogram of both right and left coronary arteries confirmed the common area of perfusion by these two septal arteries (Figure 1). In view of these two large septal arteries, one each from LAD and RPDA supplying the basal septum, it was decided to target both septal arteries for treating ASA.

A 6 Fr temporary pacing catheter was placed at right ventricular apex via the left femoral vein. The right coronary artery was selectively cannulated with 6 Fr Judkins right coronary guiding catheter via the right femoral artery. Three thousand units of unfractionated heparin were given. A floppy tip 0.014 guidewire was placed in the large septal artery arising from the RPDA. A 2 x 12 over-the-wire (OTW) balloon was tracked over this wire and up into the septal branch. This septal branch was occluded after inflating the balloon and the area of perfusion of this artery was delineated by injecting contrast agent through the balloon lumen. The perfused area corresponded with the SAM septal contact area. Following this, 2 ml of absolute alcohol was slowly injected over five minutes, through the distal port of the OTW balloon. Repeat angiogram confirmed the occlusion of septal artery (Figure 2). Echocardiography showed no decrease in the LVOT gradient. Subsequently, the septal artery from the LAD was treated in a similar fashion. Angiography of the left coronary artery revealed occlusion of this septal artery (Figure 3). There was an immediate fall in the LVOT gradient to 26 mm Hg. On day two, the patient developed a right bundle branch block with QRS duration of 150 msec and normal PR interval. Measurements of creatine kinase (CK) and creatine kinase myocardial band fraction (CK-MB) on the day following the procedure revealed peak levels of 1613 and 79 U/L, respectively. A pre-discharge echocardiogram showed peak instantaneous LVOT gradient of 40 mm Hg and mild mitral regurgitation. The patient was discharged on aspirin three days after the ASA. On a follow-up visit three months after ASA the patient had improved dramatically. He did not complain of any exertional angina or dyspnea. On echocardiography, there was no resting LVOT gradient and the provoked LVOT gradient was only 20 mm Hg. Mild MR was present and basal septal thickness was 25 mm.