The first descriptions of alcohol septal ablation (ASA) arose around 1994–1995. Based on the findings of a gradient reduction during temporary balloon occlusion of the first septal branch, combined with the long-lasting experience of transcoronary injection of ethanol for cardiac arrhythmia, this method was further developed.

During the first procedures, an inflated balloon was temporarily placed in the first septal branch to induce ischaemia. Simultaneous pressure recordings with a catheter in the left ventricle and the aorta were used to observe a reduction of at least 30% of the gradient. When a pressure drop was observed, 96% of ethanol (average 4–6 mL) was injected through the balloon catheter in order to induce a sustained reduction of the gradient.

The first reported periprocedural mortality rate in 62 patients was 4%, and permanent pacemaker (PM) implantation was necessary in 38% of all patients. The potential risk of ventricular rhythm disturbances was recognised from the inception of the ASA procedure. An extensive study was published in 1999 by Gietzen et al, including electrophysiological testing and a pathoanatomical study. Surprisingly, electrophysiological induction of sustained ventricular tachycardia (VT) occurred only in 2.6% of patients after the ASA procedure. This was much lower than the 20%–34% reported inducible sustained VT after myocardial infarction. The histological pattern of the alcohol-induced scar showed a different pattern as compared with the one known after myocardial infarction. ‘A well-defined area, characterized by a homogeneous necrosis with contracted fibers encircled by a sharply demarcated scar’ was thus seen in deceased ASA patients.1 This was thought to be the reason why patients after ASA …