Changes in the left ventricular outflow tract after transcoronary ablationof septal hypertrophy (TASH) for hypertrophic obstructive cardiomyopathy as assessed by transoesophageal echocardiography and by measuring myocardialglucose utilization and perfusion

Aims and Methods Transcoronary ablation of septal hypertrophy (TASK) leads to marked clinical and haemodynamic improvement in patients with hypertroph ic obstructive cardiomyopathy. In order to obtain more detailed information about changes in the outflow tract after TASH, transoesophageal echocardio graphy 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), me tabolism and perfusion of the myocardium (F-18-FDG-PET and Tc-99m-MIBI-SPET ) were investigated. Results After TASH there was a typical regional subaortic contraction disor der. It was quantified by a significant decrease in the fractional shorteni ng of the left ventricular end-diastolic diameter, which declined from an a verage of 40.6% to 18.0%. The end-diastolic diameter increased from an aver age of 39.1 to 40.6 mm. There was also a significant reduction in septal th ickness, 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 outsi de this region. The decrease in the gradient post TASH corresponded with a concomitant significant increase in the outflow tract area from a mean valu e of 1.04 cm(2) before the process to a value of 3.0 cm(2) after. In contra st to coronary heart disease, these changes were accompanied by nondiffuse, well demarcated subaortic-septal necrosis verified by F-18-FDG-PET and Tc- 99m-MIBI-SPET. On average the TASH induced necrotic area comprised 6.6% of the left ventricle and correlated significantly with echocardiographic chan ges in the outflow tract. Conclusions Alterations post TASH indicated that this catheter intervention al treatment for hypertrophic obstructive cardiomyopathy affects the specif ic region of obstruction. The changes reflect a 'therapeutic remodelling' o f 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 p ost TASH (post TASH reduction of subaortic septal thickness and an increase in the end-diastolic diameter) need special consideration during long-term follow up. (EUF Heart J 1999; 20: 1808-1817) (C) 1999 The European Society of Cardiology.