Copyright © 1999 by the European Society of Cardiology.
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
a Department of Internal Medicine and Division of Cardiology, The Bielefeld Hospital, Academic Teaching Hospital of the University of Müster, Bielefeld, Germany
b Department of Nuclear Medicine, University of Müster, Müster, Germany
revised May 7, 1999; accepted May 12, 1999
Abstract
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 (18F-FDG-PET and99mTc-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 40·6mm. There was also a significant reduction in septal thickness, which continued for up to 6 months after TASH, from an average of 20·0mm to 11·1mm in the region of ablation and from 23·2 to 21·7mm 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 1·04cm2before the process to a value of 3·0cm2after. In contrast to coronary heart disease, these changes were accompanied by non-diffuse, well demarcated subaortic–septal necrosis verified by18F-FDG-PET and99mTc-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.
Key Words: Hypertrophic obstructive cardiomyopathy, catheter therapy, perfusion and glucose metabolism, TASH
f1 Correspondence: H. Kuhn, MD, FESC, Professor of Internal Medicine/Cardiology, The Bielefeld Hospital, Teutoburgerstraße 50, D-33604 Bielefeld, Germany.
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