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European Heart Journal Advance Access originally published online on October 10, 2006
European Heart Journal 2006 27(23):2901-2902; doi:10.1093/eurheartj/ehl297
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Improvement of left ventricular diastolic function after alcohol septal ablation for obstructive hypertrophic cardiomyopathy? Yes, of course, but...

Josef Veselka

Department of Cardiology
CardioVascular Center
V úvalu 84
Prague 5
Czech Republic 15000
Tel: +420 224434901
Fax: +420 224434920
E-mail address: veselka.josef{at}seznam.cz

Recently, I have read with a great interest a very important paper by Jassal et al.1 The authors reported their results of non-invasive evaluation of left ventricular (LV) diastolic function in 30 selected patients with a highly symptomatic obstructive hypertrophic cardiomyopathy (HCM) treated by alcohol septal ablation (ASA). The authors concluded that positive changes in Doppler variables are likely to be due to the improvement of LV relaxation following ASA. Similarly, we have shown the improvement of isovolumic relaxation time after ASA and, moreover, the improvement of Tei index which incorporates both systolic and diastolic time intervals for expressing global ventricular performance.2 However, in fact, the observation by Jassal et al. is the first study to provide a comprehensive evidence that ASA leads to sustained improvement in LV diastolic function.

I would like to mention a few issues with the report.

  1. Several regression equations have been proposed to assess LV filling pressures. The authors used the equation proposed by Nagueh et al.3 (PCWP=1.25 [E/Ea]+1.9). Unfortunately, the formula based on E/Ea had the 95% confidence interval (2 SD) 7.6 mmHg in original paper by Nagueh et al., which is even more than significant difference between presented measurements at baseline and follow-up (20±6 vs. 15±3 mmHg; P<0.0001). Moreover, as far as I know, this equation has not been validated for patients with obstructive HCM (patients with HCM have not been included in this study by Nagueh et al.—ref. no. 20 in Jassal's paper). Hence, the utility of this method of left atrial pressure calculation in population of HCM patients is unknown.
  2. The authors demonstrated that with the exception of deceleration time (E) and isovolumic relaxation time, no other conventional parameter improved following ASA. Both parameters have already been improved at a 1-year follow-up and these favourable changes have been sustained for up to 2 years. Recently, we have also shown the improvement of isovolumic relaxation time early after ASA,4 and both in a 12-month2 and in a 24-month follow-up.5 The improvement in LV relaxation is likely to be determined by LV remodelling (LV dimension increase and basal septum thickness reduction) and elimination of LV obstruction, which is a relatively fast process in the early postprocedural period. Of course, continuous regression of LV hypertrophy and some other factors may also contribute to the improvement of diastolic function. However, majority of echocardiographic variables describing LV diastolic function has changed up to 6 months after ASA. Hence, I feel that the crucial period for important functional changes after ASA seems to be first 3 weeks (months).
  3. There is a key methodological issue in this study. The authors treated 57 consecutive patients with HOCM by ASA. They excluded 27 patients because of inability to deliver ethanol (six patients) or incompleteness of diastolic echocardiographic parameters (21 patients). The final cohort included 30 patients. One of the major complications of ASA is a complete heart block, which may require permanent pacemaker implantation. Unfortunately, the authors did not describe how many patients required new permanent pacing after ASA. I would expect that three to six patients (10–20%) from this cohort had to be paced following ASA. It is of note that permanent pacing could markedly change Doppler variables describing diastolic function.
  4. The authors stated that the present study is the first to demonstrate sustained reduction in left atrial dimensions in patients 2 years after ASA. However, several studies and also the German registry have convincingly demonstrated reduction in left atrial size following ASA during a long-term follow-up.

References

  1. Jassal DS, Neilan TG, Fifer MA, Palacios IF, Lowry PA, Vlahakes GJ, Picard MH, 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]
  2. Veselka J, Procházková S, Duchonová R, Bolomová-Homolová I, Tesar D. (2005) Effects of alcohol septal ablation for hypertrophic obstructive cardiomyopathy on Doppler Tei index: a mid-term follow-up. Echocardiography 22:105–110.[CrossRef][Web of Science][Medline]
  3. Nagueh SF, Middleton KJ, Kopelen HA, Zoghbi WA, Quinones MA. (1997) Doppler tissue imaging: a noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol 30:1527–1533.[Abstract]
  4. Veselka J, Tesar D, Honek T. (2002) Left ventricular remodeling and improvement of left ventricular relaxation after alcohol septal ablation for hypertrophic obstructive cardiomyopathy. Am J Cardiol 90:Suppl. 6A, 140H.
  5. Veselka J. (2005) Alcohol septal ablation for hypertrophic obstructive cardiomyopathy improves myocardial performance: a 24-month follow-up. Prog Coron Artery Dis 6:363–366.

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This Article
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