European Heart Journal Advance Access originally published online on April 26, 2007
European Heart Journal 2007 28(10):1270-1271; doi:10.1093/eurheartj/ehm103
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Septal alcohol ablation in hypertrophic obstructive cardiomyopathy: improving cardiac function by generating a myocardial scar
Cardiology Department
AHEPA General Hospital
Stilp. Kiriakidi 1, 54 637
Aristotle University of Thessaloniki
Thessaloniki
Greece
Saint Lukes Hospital
Thessaloniki
Greece
Cardiology Department
AHEPA General Hospital
Stilp. Kiriakidi 1, 54 637
Aristotle University of Thessaloniki
Thessaloniki
Greece
Cardiology Department
AHEPA General Hospital
Stilp. Kiriakidi 1, 54 637
Aristotle University of Thessaloniki
Thessaloniki
Greece
Tel: +30 2310994830 Fax: +30 2310994673 E-mail address: efthymos{at}med.auth.gr
We read with great interest the article by van Dockum et al.1 on the improvement of systolic myocardial function of the left ventricular (LV) lateral (free) wall in patients with hypertrophic cardiomyopathy (HCM) after alcohol septal ablation (ASA). Using cardiac magnetic resonance (CMR) tissue tagging and three-dimensional strain analysis, the authors found that both maximum end-systolic strain index and systolic strain index rate improved significantly in remote myocardium.
This report shows for the first time that the reduction of the LV outflow tract gradient in symptomatic patients with obstructive HCM treated with ASA is associated with the improvement in intramural systolic function in the lateral wall remote from the ablated area. Although this is an interesting finding, there is a main point to be addressed in relation with the procedure. In Figure 1, there is a clear demonstration of a gross gadolinium late myocardial hyperenhancement in the interventricular septum attributable to the procedure, although there is no report of direct comparison with pre-procedural gadolinium myocardial enhancement in the same patient. It would be very interesting if myocardial hyperenhancement data derived by CMR before and after ASA could be provided by the authors. Such data would be very helpful to estimate the impact of ASA on the development of new fibrosis superimposed on an already existing one.
The most dramatic event in HCM is sudden death attributable to arrhythmogenic substrate owing to cardiac fibrosis. Cell death with subsequent healing and replacement fibrosis induced by ASA eventually leads to an increase in the already existing myocardial fibrosis, creating a substrate more prone to arrhythmic events. In other words, we are trying to improve patient's symptoms by generating a scar tissue that may be deleterious long life, especially for young subjects. Data on sudden death after ASA are lacking. Therefore, as stated by Maron,2 avoidance of septal ablation in young patients is probably prudent, especially if the surgical option is feasible.
References
- van Dockum WG, Kuijer JPA, Götte MJW, ten Cate FJ, ten Berg JM, Beek AM, Twisk JWR, Marcus JT, Visser CA, van Rossum AC. Septal ablation in hypertrophic obstructive cardiomyopathy improves systolic myocardial function in the lateral (free) wall: a follow-up study using CMR tissue tagging and 3D strain analysis. Eur Heart J (2006) 27:2833–2839.
[Abstract/Free Full Text] - Maron BJ. Role of alcohol septal ablation in treatment of obstructive hypertrophic cardiomyopathy. Lancet (2000) 355:425–426.[Web of Science][Medline]
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