Methods

The study protocol was approved by the Institutional Ethics Committee of Fuwai Hospital. All patients gave informed consent before enrollment in the study. We studied 38 patients with obstructive HC who underwent ASA procedures from August 2005 to December 2012. Indications for ASA included severe, drug-refractory, New York Heart Association functional class III or IV heart failure with an LVOT gradient >50 mm Hg at rest or >100 mm Hg during provocation. No patients had previous surgical myectomy, aortic valvular disease, intrinsic mitral disease, or general contraindications to CMR.

The ASA procedure was performed using a method previously described, under continuous electrocardiographic and blood pressure monitoring. In brief, through a 6Fr or 7Fr left coronary guiding catheter, an oversized over-the-wire angioplasty balloon (diameter 1.5 to 2.5 mm) was placed in the proximal part of the septal perforator artery. After the balloon was inflated (pressure 6 bar), the supply area of the closed septal branch was determined by injection of angiographic contrast together with simultaneous transthoracic echocardiographic registration. After delineation of the size of targeted myocardium, 1 to 3 ml of ethanol was slowly injected. A successful procedure was defined by a reduction in the LVOT pressure gradient of >50% of the baseline value.

CMR imaging studies were performed with a 1.5-T speed clinical scanner. All images were acquired with an electrocardiographically gated breath-hold technique. First, steady-state free precession cine images were acquired in 3 long-axis 4-chamber, 3-chamber, and 2-chamber long- and short-axis views with the following protocol: repetition time 2.7 ms, echo time 1.2 ms, flip angle 70°, temporal resolution 40 ms, field of view 360 × 315 mm ² , matrix size 192 × 162; slice thickness 6 mm, and slice gap 2 mm. Finally, late gadolinium enhancement images were acquired 10 minutes after the intravenous administration of 0.2 mmol/kg gadodiamide hydrate using a segmented phase-sensitive inversion-recovery spoiled gradient-echo sequence.

All CMR image analysis was performed by experienced radiologic technicians using dedicated software (Medis Medical Imaging Systems, Leiden, the Netherlands). Epicardial and endocardial borders of the LV and RV myocardium before and after ASA were manually traced during the whole cardiac phase on each cine short-axis image to obtain LV and RV end-diastolic and end-systolic volumes, ejection fractions, and myocardial mass ( Figure 1 ). Myocardial mass was calculated by multiplying the volume of the myocardium calculated at end-diastole by the specific gravity of the myocardium (1.05 g/ml). The end-diastolic volume index, end-systolic volume index, and mass index were indexed to body surface area. Infarct size after ASA was evaluated by manual tracing of the hyperenhanced area, which was defined as the area within the septal myocardium with pixel signal intensity >4 SDs of remote, nonenhanced myocardium. Central dark zones within the area of hyperenhancement were included. Interventricular septum was defined as the myocardium between the anterior and posterior junctions of the right ventricle to the left ventricle. Remote LV mass was measured as LV mass minus interventricular septal mass. Mitral regurgitation severity was measured by color Doppler and grading by vena contracta width and proximal isovelocity surface area according as follows: 1+ = mild, 2+ = moderate, 3+ = moderate to severe, and 4+ = severe.

Short-axis slice through the ventricles shows epicardial and endocardial border segmentation of the right and left ventricles before ASA (A) and after ASA (B) .

Data are expressed as mean ± SD for normally distributed continuous variables and as medians and interquartile ranges for non–normally distributed continuous variables. Differences between means were measured by paired Student’s t tests. Wilcoxon-Mann-Whitney U tests were used to examine differences in medians. Noncontinuous data were compared by chi-square or Fisher’s exact tests as appropriate. The relations between the changes of parameters were assessed using linear regression analysis. Statistical significance was defined as p <0.05. Statistical analysis was conducted using SPSS version 18.0 for Windows (SPSS, Inc., Chicago, Illinois).

Results

The study cohort had a mean age of 48 ± 9 years, and 28 of the 38 patients (74%) were men. Thirteen patients (34%) had angina pectoris, 8 (21%) had syncope, 29 (76%) had New York Heart Association functional class III or IV symptoms, and 8 (21%) had family histories of HC or sudden cardiac death ( Table 1 ). The median follow-up time was 16 months (range 9 to 39).

ASA resulted in significant reductions of LVOT gradient at rest in all patients. The mean LVOT gradient decreased from 89 ± 22 to 34 ± 23 mm Hg (p <0.001) after the procedure and further decreased from 34 ± 23 to 24 ± 12 mm Hg (p <0.001) during the 16-month follow-up period ( Figure 2 ). The favorable LVOT gradient reduction was associated with significant improvement of functional status: 35 patients (92%) had improved New York Heart Association functional class at follow-up ( Figure 3 ). The median New York Heart Association functional class improved from 3 (1 to 4) to 1 (1 to 3) (p <0.001) at follow-up. Furthermore, mitral regurgitation severity reduced significantly in 33 patients (87%) ( Figure 3 ). The median mitral regurgitation severity grade decreased from 2+ (0 to 4) at baseline to 1+ (0 to 2) at follow-up (p <0.001).

ASA results in a significant reduction of LVOT gradient before ASA, after the procedure, and at 16-month (interquartile range 9 to 39) follow-up.

Changes of New York Heart Association functional class (A) and mitral regurgitation severity (B) at baseline and 16-month (interquartile range 9 to 39) follow-up.

At 16-month follow-up, a clearly demarcated area of hyperenhancement was seen in the basal part of the interventricular wall in all patients. The mean myocardial infarct size was 13 ± 5 g and involved 19% of the septal mass at 16 months after ASA. A larger infarct size was associated with a larger decrease of septal mass (r = −0.467, p = 0.003) as well as LVOT gradient reduction (r = −0.632, p <0.001) at follow-up. Septal thickness reduced from 20 ± 1 mm at baseline to 15 ± 1 mm (−5 mm, p <0.001) at follow-up. LV end-diastolic dimension increased from 46 ± 3 to 48 ± 3 mm (p <0.001) at follow-up. LV mass, septal mass, and LV remote mass all decreased significantly (−13%, −12%, and −14%, respectively (p <0.001 for all)) at follow-up. Furthermore, LV end-diastolic volume and LV end-diastolic volume index increased significantly (p <0.001 for both) at follow-up. There was no significant difference (p = 0.324) in the LV ejection fraction between baseline and follow-up ( Table 2 ).

RV mass and RV mass index decreased significantly (−7 g and −2 g/m ² , p <0.001 for both). In contrast, RV end-diastolic volume and RV end-diastolic volume index increased significantly (by 13 ml and 7 ml/m ² , respectively, p <0.001 for both). The RV ejection fraction increased significantly from 40 ± 3% to 46 ± 3% (p <0.001) during follow-up ( Table 3 ).

Table 3

Changes in right ventricular structure and function after alcohol septal ablation

	Baseline (n = 38 )	Follow-up (n = 38 )	p-Value
Right ventricular mass (g)	54 ± 7	47 ± 6	<0.001
Right ventricular mass index (g/m 2 )	29 ± 4	27 ± 4	<0.001
Right ventricular end-diastolic volume (ml)	111 ± 22	124 ± 24	<0.001
Right ventricular end-diastolic volume index (ml/m 2 )	60 ± 10	67 ± 11	<0.001
Right ventricular stroke volume (ml)	44 ± 11	57 ±12	<0.001
Right ventricular stroke volume index (ml/m 2 )	24 ± 5	31 ± 6	<0.001
Right ventricular ejection fraction (%)	40 ± 3	46 ± 3	<0.001

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