Changes in the left ventricular outflow tract after transcoronary ablation of septal hypertrophy (TASH) for hypertrophic obstructive cardiomyopathy as assessed by transoesophageal echocardiography and by measuring myocardial glucose utilization and perfusion.

AIMS AND METHODS: Transcoronary ablation of septal hypertrophy (TASH) leads to marked clinical and haemodynamic improvement in patients with hypertrophic obstructive cardiomyopathy. In order to obtain more detailed information about changes in the outflow tract after TASH, transoesophageal echocardiography and a repeat invasive investigation were conducted before as well as 2 weeks and 6 months after TASH (n=62). In a subset of patients (n=11), metabolism and perfusion of the myocardium ((18)F-FDG-PET and(99m)Tc-MIBI-SPET) were investigated.

RESULTS: After TASH there was a typical regional subaortic contraction disorder. It was quantified by a significant decrease in the fractional shortening of the left ventricular end-diastolic diameter, which declined from an average of 40.6% to 18.0%. The end-diastolic diameter increased from an average of 39.1 to 40.6 mm. There was also a significant reduction in septal thickness, which continued for up to 6 months after TASH, from an average of 20.0 mm to 11.1 mm in the region of ablation and from 23. 2 to 21.7 mm outside this region. The decrease in the gradient post TASH corresponded with a concomitant significant increase in the outflow tract area from a mean value of 1.04 cm(2)before the process to a value of 3.0 cm(2)after. In contrast to coronary heart disease, these changes were accompanied by non-diffuse, well demarcated subaortic-septal necrosis verified by(18)F-FDG-PET and(99m)Tc-MIBI-SPET. On average the TASH induced necrotic area comprised 6.6% of the left ventricle and correlated significantly with echocardiographic changes in the outflow tract.

CONCLUSIONS: Alterations post TASH indicated that this catheter interventional treatment for hypertrophic obstructive cardiomyopathy affects the specific region of obstruction. The changes reflect a 'therapeutic remodelling' of the outflow tract of the left ventricle. They were demonstrable over the entire 6 months investigation period and obviously constituted the basis of post TASH clinical and haemodynamic improvement. Progressive alterations post TASH (post TASH reduction of subaortic septal thickness and an increase in the end-diastolic diameter) need special consideration during long-term follow up.