European Heart Journal Advance Access originally published online on November 10, 2006
European Heart Journal 2006 27(23):2746-2747; doi:10.1093/eurheartj/ehl324
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Can alcohol septal ablation normalize systolic function in HOCM?
Department of Medicine, Section of Cardiology, Baylor College of Medicine, Houston, TX, USA
* Corresponding author. Tel: +1 713 873 2083; fax: +1 713 873 4903. E-mail address: nlakkis{at}bcm.tmc.edu
This editorial refers to ‘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’
by W.G. van Dockum et al., on page 2833
Patients with hypertrophic obstructive cardiomyopathy (HOCM) and significant left ventricular outflow tract (LVOT) obstruction are prone to dyspnoea, angina, syncope, and sudden cardiac death.1 These clinical features are primarily due to intrinsic myocardial dysfunction, impaired systolic and diastolic function, myocardial ischaemia, and arrhythmias. The management of this condition has attracted molecular, clinical, and interventional cardiologists, cardiac surgeons, and epidemiologists. Alcohol septal ablation (ASA) has been shown, in multiple reports, to successfully relieve the LVOT obstruction with subsequent relief of symptoms.2,3 However, the effect of ASA on sudden cardiac death and arrhythmias has not been well studied.
Multiple reports have suggested that the early haemodynamic benefits from ASA are associated with significant, measurable, and sustained improvement in myocardial relaxation up to 2 years after the procedure.4 To date, there is a paucity of data evaluating potential changes in systolic function after ASA, likely owing to the hitherto sub-optimal methods by which to accurately assess the complex nature of LV systolic function.5 Cardiac magnetic resonance (CMR), using cine imaging and myocardial tagging, lends itself to the evaluation of both structural and functional systolic changes in HOCM patients after ASA.
CMR has provided some insights into myocardial changes after ASA. van Dockum et al.6 have previously demonstrated that patients undergoing ASA had no evidence of infarction remote to the area of the septum ablated. The mean size of septal infarction was 20 g, corresponding to about 10% of the left ventricular (LV) mass and 30% of the septal mass. They also showed that total LV mass was reduced by an amount that exceeded septal mass reduction. These findings are similar to those reported by our group and others using echocardiographic methods.7,8
In this issue, van Dockum et al.9 employed CMR with cine imaging and tissue tagging to shed light on the changes in septal, adjacent, and remote myocardial systolic function after ASA. They calculated 3D strain values for the radial, circumferential, and longitudinal directions, averaged from base to apex. From each strain parameter, peak values were determined and expressed as maximum strain patterns. Systolic strain rate reflecting the rate of myocardial deformation, and shortening index (SI) reflecting myocardial contraction, were calculated.
This report shows for the first time that reduction in the LVOT obstruction in nine symptomatic HOCM patients treated with ASA is associated with a significant reduction in myocardial mass at all regions of the heart, along with improvement in intramural systolic function in LV myocardium remote from the ablated area. The implications of this report, if confirmed and reproduced, are tremendous. First, reduction of non-septal LV mass suggests that myocardial hypertrophy in HOCM is at least partially due to LV obstruction, that is afterload dependent, and potentially reversible. It would have been very interesting to correlate these changes with reduced angiotensin or aldosterone levels. These findings also suggest that there is some independence of this putatively haemodynamic effect from the genetic coding—i.e. modifiability of the genetic predisposition to hypertrophy and obstruct. Secondly, ASA appears to improve regional and intramural myocardial systolic function in the adjacent and remote myocardium leading to reversed LV remodelling. Thirdly, overall septal systolic function is unchanged after ASA, most likely due to improvement in the non-ablated septal tissue systolic function which may counterbalance the reduced or absent myocardial systolic function in the ablated septal tissue. Finally, the improvement in SI in adjacent and remote myocardium seems to correlate with the reduction in myocardial mass in these areas.
In conclusion, despite the small number of patients studied, the results of this study are provocative and promising for patients with symptomatic HOCM. Now, improvements in systolic function can be added to the previously demonstrated amelioration of diastolic function post-ASA. One would hope that future investigations employing CMR or echocardiographic speckle imaging will validate these findings. Further studies assessing the impact of ASA on survival of patients with HOCM, and the relationship to non-invasively assessed systolic and diastolic parameters, are also needed.
Conflict of interest: none declared.
Footnotes
The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
doi:10.1093/eurheartj/ehl358 
References
- Sigwart U. (1995) Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet 346:211–214.[CrossRef][ISI][Medline]
- Lakkis N, Nagueh SF, Kleiman NS, Killip D, He ZX, Verani MS, Roberts R, Spencer WH III. (1998) Echocardiography-guided ethanol septal ablation for hypertrophic obstructive cardiomyopathy. Circulation 98:1750–1755.
- Knight C. (2006) Alcohol septal ablation for obstructive hypertrophic cardiomyopathy. Heart 92:1339–1344.
[Free Full Text] - Nagueh SF, Lakkis NM, Middleton KJ, Killip D, Zoghbi WA, Quiñones MA, Spencer WH III. (1999) Changes in left ventricular diastolic function 6 months after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. Circulation 99:344–347.
- Jassal DS, Neilan TG, Palacios IF, Lowry PA, Vlahakes GJ, Picard MH, Fifer MA, Yoerger DM. (2006) Sustained improvement in left ventricular diastolic function after alcohol septal ablation for hypertrophic obstructive cardiomyopathy. Eur Heart J 27:1805–1810.
[Abstract/Free Full Text] - Abraham T, Nishimura R, Holmes D, Belohlavek M, Seward J. (2002) Strain rate imaging for assessment of regional myocardial function. Circulation 105:1403–1406.
- van Dockum WG, Beek AM, ten Cate FJ, ten Berg JM, Bondarenko O, Götte MJW, Twisk JWR, Hofman MBM, Visser CA, van Rossum AC. (2005) Early onset and progression of left ventricular remodeling after alcohol septal ablation in hypertrophic obstructive cardiomyopathy. Circulation 111:2503–2508.
- Mazur W, Nagueh SF, Lakkis NM, Middleton KJ, Killip D, Roberts R, Spencer WH III. (2001) Regression of left ventricular hypertrophy after nonsurgical septal reduction therapy for hypertrophic obstructive cardiomyopathy. Circulation 103:1492–1496.
- van Dockum WG, Kuijer JPA, Götte MJW, ten Cate FJ, ten Berg JM, Beek AM, Twisk JWR, Marcus JT, Visser CA, van Rossum AC. (2006) 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 27:2833–2839 First published on November 10, 2006, doi:10.1093/eurheartj/ehl358.
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EHJ 2006 27: 2833-2839.[Abstract] [Full Text]
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