European Heart Journal Advance Access originally published online on April 26, 2007
European Heart Journal 2007 28(10):1271; doi:10.1093/eurheartj/ehm104
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Septal alcohol ablation in hypertrophic obstructive cardiomyopathy: improving cardiac function by generating a myocardial scar
Department of Cardiology
VU University Medical Center
De Boelelaan 1117
PO Box 7057
1081 HV Amsterdam
The Netherlands
Department of Cardiology
VU University Medical Center
De Boelelaan 1117
PO Box 7057
1081 HV Amsterdam
The Netherlands
Department of Cardiology
VU University Medical Center
De Boelelaan 1117
PO Box 7057
1081 HV Amsterdam
The Netherlands
Department of Cardiology
VU University Medical Center
De Boelelaan 1117
PO Box 7057
1081 HV Amsterdam
The Netherlands
Tel: +31 204442244 Fax: +31 204442446 E-mail address: wg.vandockum{at}vumc.nl
We thank Efthimiadis et al. for their comments on our article concerning the improvement of systolic myocardial function in the lateral (free) wall in hypertrophic obstructive cardiomyopathy (HOCM) after alcohol septal ablation (ASA), which was studied using CMR tissue tagging and 3D strain analysis.1 In a previous work, we have demonstrated that in symptomatic patients with HOCM, left ventricular remodelling after ASA occurs early and progresses on mid-term follow-up, and total left ventricular mass reduction exceeded septal mass reduction.2 The remote mass reduction was correlated with the LVOT pressure gradient reduction, and thus we concluded that myocardial hypertrophy in HOCM is, at least in part, afterload-dependent and reversible and is not exclusively caused by the genetic disorder.
In this article, we have studied in a subgroup of patients the regional changes in septal, adjacent, and remote systolic myocardial function by calculating the shortening index, a combined strain parameter reflecting myocardial contraction. We have demonstrated for the first time that reduction in symptomatic HOCM patients achieved by ASA not only was associated with a significant reduction in myocardial mass, but also with an improvement of intramural systolic myocardial function in the lateral (remote) wall, supporting the concept of reversed LV remodelling.
Previously, our group had demonstrated that contrast-enhanced CMR allowed detailed evaluation of size and location of septal myocardial infarction induced by ASA, and that the infarction size was correlated with clinical indexes of infarct size.3 In this study, we have demonstrated that contrast-enhanced imaging data derived in 
60% of the study-group pre-ASA after administration of gadolinium-DTPA contained only small pre-existing foci of delayed myocardial hyperenhancement, representing myocardial fibrosis and other pathological changes in the myocardial wall (e.g. disarray, inflammation, oedema, myolysis, and necrosis).4 Compared with these hyperenhanced area-size-assessed pre-ablation, the infarct-size induced by ASA was 10-fold larger. In this respect, the induced myocardial infarct after septal ablation therapy enlarges the already existing arrhythmogenic substrate in HOCM patients. However, an electrophysiology report in high-risk patients after ASA has not indicated an increased arrhythmic substrate necessitating higher rates of implanting defibrillators.5 Although ventricular tachycardia and sudden death have been reported after ASA, these clinical features characterize the natural course hypertrophic cardiomyopathy irrespective of therapeutic LVOT gradient reduction. Further studies are necessary to evaluate the long-term effects of ASA with respect to ventricular arrhythmias and sudden cardiac death. Our goal in the near future must be developing additional tools to identify the high-risk HOCM patients, regardless of a potential intervention for LVOT obstruction, in whom defibrillator implantation is justified.
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] - van Dockum WG, Beek AM, ten Cate FJ, ten Berg JM, Bondarenko O, Götte MJW, Twisk JWR, Hofman MBM, Visser CA, van Rossum AC. Early onset and progression of left ventricular remodeling after alcohol septal ablation in hypertrophic obstructive cardiomyopathy. Circulation (2005) 111:2503–2508.
[Abstract/Free Full Text] - van Dockum WG, ten Cate FJ, ten Berg JM, Beek AM, Twisk JWR, Vos J, Hofman MBM, Visser CA, van Rossum AC. Myocardial infarction after percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: evaluation by contrast-enhanced magnetic resonance imaging. J Am Coll Cardiol (2004) 43:27–34.
[Abstract/Free Full Text] - Knaapen P, van Dockum WG, Bondarenko O, Kok WE, Götte MJW, Boellaard R, Beek AM, Visser CA, van Rossum AC, Lammertsma AA, Visser FC. Delayed contrast enhancement and perfusable tissue index in hypertrophic cardiomyopathy: comparison between cardiac MRI and PET. J Nucl Med (2005) 46:923–929.
[Abstract/Free Full Text] - Lawrenz T, Obergassel L, Lieder F, Leuner C, Strunk-Mueller C, Meyer Zu Vilsendorf D, Beer G, Kuhn H. Transcoronary ablation of septal hypertrophy does not alter ICD intervention rates in high risk patients with hypertrophic obstructive cardiomyopathy. Pacing Clin Electrophysiol (2005) 28:295–300.[CrossRef][Medline]
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