© 2004 by European Society of Cardiology
Copyright © 2004, The European Society of Cardiology
Quantitative analysis of intraprocedural myocardial contrast echocardiography during percutaneous septal ablation for hypertrophic obstructive cardiomyopathy
Department of Cardiology, Heart Center North Rhine-Westphalia, Ruhr University, Georgstrasse 11, 32545 Bad Oeynhausen, Germany
Received 8 October 2003; received in revised form 31 March 2004; accepted after revision 2 April 2004.
* Corresponding author. Tel.: +49-5731-971258; fax: +49-5731-972194. akohlstaedt{at}hdz-nrw.de
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionNotesReferences |
|---|
Aims: We tested whether procedural success of percutaneous septal ablation for hypertrophic obstructive cardiomyopathy is related to quantitative measurements of intraprocedural myocardial contrast echocardiography.
Methods and results: In a study group of 34 patients, the mean area of the contrast depot was 8.5 ± 2.5 cm2, its length along the left ventricular endocardial border 3.0 ± 0.7 cm and its proximal edge 2.0 ± 0.6 cm upstream the point of mitral–septal contact. Clinical and hemodynamic success was achieved in all but one patient 3 months following percutaneous septal ablation. The proximal edge of the ablation lesion correlated weakly (r = 0.5) with the proximal edge of the contrast depot with respect to their distance from the mitral valve leaflet tips. No other correlations were found between the efficacy of percutaneous septal ablation and various quantitative measurements of intraprocedural contrast echocardiography.
Conclusions: The localization of the ablation lesion 3 months after percutaneous septal ablation is predicted by the localization of the contrast depot with respect to the point of mitral–septal contact. The final hemodynamic effect of the ablation lesion, however, does not correlate with quantitative parameters of intraprocedural contrast echocardiography, but appears to be the result of an individual remodeling process.
Keywords: Percutaneous septal ablation; Intraprocedural myocardial contrast echocardiography; Hypertrophic obstructive cardiomyopathy
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionNotesReferences |
|---|
Percutaneous septal ablation has been established as an alternative to surgical myectomy in patients with symptomatic hypertrophic obstructive cardiomyopathy.1–4 In our institution, intraprocedural myocardial contrast echocardiography is routinely employed to identify the correct septal branch for therapeutic occlusion.5–7 Results of intraprocedural contrast echocardiography are evaluated qualitatively by assessing the location of the contrast depot in relation to the outflow obstruction and the myocardial structures responsible for it (usually the bulging subaortic septum and the anterior mitral leaflet). Up to now, it is unclear whether quantitative echocardiographic measurements of the size and location of the myocardial territory opacified by the echo contrast agent can better predict long-term clinical and hemodynamic effects of percutaneous septal ablation.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionNotesReferences |
|---|
Theoretical rationale and practical application of intraprocedural myocardial contrast echocardiography during percutaneous septal ablation have been described in detail elsewhere.5–7 Briefly, 1–2 ml of the echo contrast agent (capillary-crossing, air-containing microspheres with a galactose-based shell stabilized by palmitine acid, mean diameter 7–8 µm, available as Levovist (Schering®, Germany), concentration 350 mg/ml) is injected into the suspected septal target vessel after probatory balloon occlusion. The opacified myocardial territory is assessed from the apical as well as from the parasternal or subcostal transducer positions in order to determine its spatial extension in the subaortic–apical and in the anterior–posterior direction. If the contrasted septal myocardium is adjacent to the zone of maximal acceleration of the obstructive outflow jet and includes the point of coaptation between septum and anterior mitral leaflet, and after exclusion of contrast deposition remote from the septal target area, percutaneous septal ablation is completed by ethanol injection.
Echocardiographic recordings of all percutaneous septal ablation procedures performed at our institution between September 1999 and July 2002 were reviewed retrospectively. Echocardiographic data had been acquired by commercially available ultrasound systems (Vingmed-GE, System Five or Vivid Five) with the tissue harmonic mode as default setting, a mean frame rate of 50–75 Hz and a 2.5 MHz probe. During the observational period, 73 patients underwent 75 consecutive interventions, 41 of which were unsuitable for the present analysis because follow-up data were not archived in a digital format allowing quantitative measurements (n = 18), inability to identify the exact border of the ablation lesion ("scar") induced by percutaneous septal ablation at follow-up examination (n = 16), or patient-related poor echocardiographic image quality (n = 7) that did not allow measurement of the quantitative parameters specified by the study protocol. The remaining 34 patients with 34 ablation procedures were selected for quantitative evaluation and formed the study population. Apical four and five chamber views at end systole were selected for analysis, with the patient placed in a supine position during intervention and in a left lateral position at follow-up examination. The apical views were chosen because they best allowed evaluation of the left ventricular outflow tract and the surrounding myocardial structures with acceptable image quality, and the transducer angles during the ablation procedure and at follow-up examination corresponded closely.
All echocardiographic studies were reviewed by a single experienced echocardiographer (D. H.), who was blinded to the clinical and hemodynamic outcome of the intervention. Clinical and echocardiographic data were obtained at the time of intervention and after a 3-month follow-up period. Quantitative echocardiographic parameters are defined in Table 1 and illustrated in Fig. 1. Several indices using a combination of parameters were computed to characterize the location of the myocardial contrast depot in relation to the adjacent myocardium and the ablation lesion visible at follow-up (Table 2). Clinical success of percutaneous septal ablation was characterized by an improvement in symptomatic status of at least one functional class of the New York Heart Association classification to class I or class II symptoms at follow-up. Hemodynamic success was defined as a complete abolition or >50% reduction of the left ventricular outflow tract gradient at rest below a threshold of 30 mmHg, with the gradient under provocation (Valsalva's maneuver or postextrasystolic augmentation) not exceeding 60 mmHg.3,5,7
|
|
|
Patient data were collected in a relational database (Filemaker 3.0, Claris Corp.) and analyzed with the Statview 5 (SAS Inc.) statistical software package. All continuous data are expressed as mean ± standard deviation. Student's t-test for paired and unpaired samples, or their non-parametric analogues (Wilcoxon and Mann–Whitney-test), were used for group comparisons. Frequency distributions were assessed with the chi2 test. Linear correlations (Pearson) were calculated for selected variables. A p value of <0.05 by the two-tailed test was considered to indicate statistical significance.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionNotesReferences |
|---|
Application of a mean ethanol dose of 1.9 ± 0.3 ml was followed by a creatin kinase rise up to 529 ± 197 U/l. Two patients (6%) required permanent pacemaker implantation because of persistent atrioventricular conduction defects. Clinical and hemodynamic success was achieved in all but 1 of the 34 patients: symptomatic status improved from New York Heart Association class 2.9 ± 0.4 to class 1.5 ± 0.6, and left ventricular outflow tract gradient at rest decreased from 61 ± 26 to 8 ± 16 mmHg (p both <0.001). Left atrial size was reduced from 50 ± 7 to 45 ± 7 mm (p<0.01).
The mean area of the contrast depot was 8.5 ± 2.5 cm2 (range: 2.5–14.4 cm2), its length along the endocardial border of the left ventricle 3.0 ± 0.7 cm (1.5–4.5 cm) and its proximal border 2.0 ± 0.6 cm (1.0–3.7 cm) upstream the point of mitral–septal contact (Table 1). The anterior mitral leaflet contacted the septum within the proximal and distal endocardial border of the contrast depot in 33 of the 34 patients. In the remaining patient, the distal border of the contrast depot was slightly proximal to the point of mitral–septal contact, resulting in a negative value of the index (b–c)/b (Table 2). This patient did not benefit from percutaneous septal ablation and underwent a second ablation procedure 4 months later. Endsystolic septal thickness measured in the apical four-chamber view decreased from 2.8 ± 0.4 cm before percutaneous septal ablation to 1.9 ± 0.4 cm at follow-up (p < 0.001). Additional results of the quantitative echocardiographic measurements are listed in Tables 1 and 2
.
There was a negative correlation between septal thickness at follow-up (d2) and the distance between the mitral leaflet tips and the left ventricular endocardial border at follow-up (f; r = –0.50). A similar correlation could be established between the proximal edge of the contrast depot (c) and the proximal edge of the ablation lesion (e) with respect to their distance from the mitral valve leaflet tips (Fig. 2). No correlations were found between the various quantitative echocardiographic variables and clinical or hemodynamic results after percutaneous septal ablation.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionNotesReferences |
|---|
Selection of the correct septal branch is crucial to obtain optimal clinical and hemodynamic results after percutaneous septal ablation. The initial reports on this procedure described probatory balloon occlusion of the assumed septal target vessel as a diagnostic tool: the hemodynamic effect of the ethanol-induced therapeutic infarction was thought to be predicted by the gradient reduction following balloon-induced acute ischemia.3–5,7–9 In our patient population, however, probatory balloon occlusion did not allow precise estimation of the late clinical and hemodynamic response following percutaneous septal ablation.5–7 Therefore, intraprocedural contrast echocardiography was introduced to improve identification of the culprit septal vessel, especially if it originated atypically from diagonal or intermediate branches of the left coronary artery. In addition, exclusion of contrast deposition in remote myocardial regions like the apical septum or papillary muscles served to prevent potentially severe complications after ethanol application. At our institution, intraprocedural contrast echocardiography has been routinely incorporated into the septal ablation procedure in late 1996. This has resulted in a significant increase of acute and mid-term procedural success rate and a consistent decrease of complication rate.5,7 It appeared thus logical that not only qualitative, but also quantitative echocardiographic analysis of the contrast depot with respect to size and location could further increase the diagnostic utility of intraprocedural contrast echocardiography and offer additional insight into the complex myocardial remodeling process following percutaneous septal ablation. To test this hypothesis, we performed the present study in a limited number of patients treated during a 3-year observational period.
We were able to demonstrate that the proximal edge of the ablation lesion 3 months after percutaneous septal ablation is predicted by the proximal border of the contrast depot with respect to the point of mitral–septal contact. If the contrast depot is located upstream, i.e. proximal to the point of mitral–septal contact, results of percutaneous septal ablation are likely to be unsatisfactory. This observation is in concordance with the results of qualitative assessment of intraprocedural contrast echocardiography published earlier.5,7 In general, however, clinical and hemodynamic effects following percutaneous septal ablation were not related to quantitative echocardiographic measurements of the contrast depot during the ablation procedure or of the ablation lesion after 3 months. Several reasons might explain this result. The number of patients analyzed in this study is small. A considerable number of interventions during the observational period had to be excluded because of missing digital echo data or poor echocardiographic image quality not allowing quantitative analysis according to our protocol, frequently due to significant overshadowing of the myocardial contrast depot or inability to identify the extent of the ablation lesion in a stop-frame image at follow-up. Patients were examined in a supine position during percutaneous septal ablation and a left lateral position at follow-up, so that the apical four-chamber views selected for analysis were not exactly comparable. These points raise general concern about the practical applicability of quantitative analysis of intraprocedural contrast echocardiography. However, it has to be taken into consideration that due to growing practical experience with echo-guided percutaneous septal ablation and a critical selection process of patients eligible for intervention, optimal clinical and hemodynamic results could in fact be achieved just by qualitative judgement of the intraprocedural echo in 33 of the 34 patients examined in this study. Therefore, the lack of patients in our study population treated unsuccessfully might render it impossible to identify quantitative echocardiographic cut-off values entailing a poor result. Finally, morphologic changes of the left ventricular outflow tract geometry following percutaneous septal ablation involve a complex three-dimensional remodeling process, whose time course and extent cannot be characterized adequately by quantitative measurements in a single imaging plane. Theoretically, the predictive accuracy of quantitative echocardiographic measurements may be increased by combining information from multiple echocardiographic windows, or with a three-dimensional approach. However, quantitative measurements in multiple echocardiographic windows are cumbersome to obtain and interpret in clinical routine and suffer from the practical limitations mentioned above.
In summary, in our single-center experience with a limited patient population, additional quantitative echocardiographic examination of intraprocedural contrast echocardiography failed to offer an incremental benefit over mere qualitative assessment.
|
Notes |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionNotesReferences |
|---|
Presented at EUROECHO 7, 3–6 December 2003, Barcelona, Spain. |
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionNotesReferences |
|---|
- Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet (1995) 346:211–214.[CrossRef][Web of Science][Medline]
- Seggewiss H. Current status of alcohol septal ablation for patients with hypertrophic cardiomyopathy. Curr Cardiol Rep (2001) 3:160–166.[Medline]
- Seggewiss H., Faber L., Gleichmann U. Percutaneous transluminal septal ablation in hypertrophic obstructive cardiomyopathy. Thorac Cardiovasc Surg (1999) 47:94–100.[Web of Science][Medline]
- Gietzen F.H., Leuner C.J., Raute-Kreinsen U., et al. Acute and long-term results after transcoronary ablation of septal hypertrophy (TASH). Catheter interventional treatment for hypertrophic obstructive cardiomyopathy. Eur Heart J (1999) 20:1342–1354.
[Abstract/Free Full Text] - Faber L., Seggewiss H., Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy. Results with respect to intraprocedural myocardial contrast echocardiography. Circulation (1998) 98:2415–2421.
[Abstract/Free Full Text] - Faber L., Seggewiss H., Ziemssen P., Gleichmann U. Intraprocedural myocardial contrast echocardiography as a routine procedure in percutaneous transluminal septal myocardial ablation: detection of threatening myocardial necrosis distant from the septal target area. Catheter Cardiovasc Interv (1999) 47:462–466.[CrossRef][Web of Science][Medline]
- Faber L., Ziemssen P., Seggewiss H. Targeting percutaneous transluminal septal ablation for hypertrophic obstructive cardiomyopathy by intraprocedural echocardiographic monitoring. J Am Soc Echocardiogr (2000) 13:1074–1079.[CrossRef][Web of Science][Medline]
- Knight C.J., Kurbaan A.S., Seggewiss H., et al. Non-surgical septal reduction for hypertrophic obstructive cardiomyopathy: outcome in the first series of patients. Circulation (1997) 95:2075–2081.
[Abstract/Free Full Text] - Kuhn H., Gietzen F., Leuner C., Gerenkamp T. Induction of subaortic septal ischemia to reduce obstruction in hypertrophic obstructive cardiomyopathy. Eur Heart J (1997) 18:846–851.
[Abstract/Free Full Text]
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||