Methods

Patients with HC who underwent ASA at the hospital of the University of Alabama at Birmingham from September 2003 to April 2008 were included in the study. ASA is performed at our institution for patients with HC and severe symptoms that are unresponsive to maximally tolerated medical therapy and a left ventricular outflow gradient ≥30 mm Hg at rest or ≥50 mm Hg with provocation.

MPI was performed at a median of 2 days after ASA (interquartile range 1 to 2) using gated single-photon emission computed tomography 60 minutes after intravenous injection of technetium-99m sestamibi 20 to 40 mCi at rest. Images were acquired with a dual-head detector (Phillips, Miltipas, California) with and without attenuation correction using emission line source. Images were obtained in 32 projections (30 seconds/projection) using 180° anterior elliptical arc with 20% energy window centered on 140 keV. The RR cycle was divided into 8 to 16 frames and gating was done with a ±50% window. Rotating images were reviewed for motion and reconstructed with filtered backprojection using Butterworth filter and realigned to the long axis of the heart. The present results are without attenuation correction. Images were interpreted quantitatively using an automated operator-independent method based on polar maps and a customized database of patients with HC as previously described. It is important to note that using proprietary software will lead to errors because this population is known to have asymmetric septal hypertrophy. Images were interpreted blindly without knowledge of serum markers and vice versa.

ASA was performed as previously described. Briefly, a Sprinter 1.5- to 3.0- × 6-mm balloon (Medtronic, Minneapolis, Minnesota) was inflated in the septal artery and a small amount of absolute alcohol was injected with the balloon in the inflated position to prevent leakage into the main artery. The balloon was deflated 5 minutes after infusion of alcohol. All procedures were guided by contrast echocardiography.

Serum levels of creatine kinase (CK), CK-MB, cardiac troponin I, and brain natriuretic peptide were routinely checked before ASA and then at 6, 12, 18, 24, 30, 36, and 42 hours afterward. All serum markers were analyzed in the local institutional laboratory.

All patients gave informed consent for their procedure after understanding the available alternatives. This study was a retrospective review of their medical records and the laboratory and imaging results. Chart review was approved by the local institution review board.

All statistical analyses are carried out using SPSS 11.5 for Windows (SPSS, Inc., Chicago, Illinois). Continuous variables are presented as mean ± SD and discrete variables as frequencies and percentages. Chi-square test was used for categorical variables when appropriate. Linear regression analysis was used to determine the relation between serial markers and defect size as determined by MPI. Serial changes in serum markers were analyzed using analysis of variance for repeated measures. All tests were 2-tailed, and a p value ≤0.05 was considered statistically significant.

Results

During the specified period 66 patients with HC underwent ASA at our institution. MPI studies were available for assessment of infarct size in 54 patients (82%). Serum markers were available for all patients at some of the specified time points. Baseline characteristics of patients are listed in Table 1 and medications at the time of their ASA are listed in Table 2 . These characteristics were similar between the 2 populations.

The ASA procedure was technically successful in all patients. The amount of absolute alcohol injected per patient was 2.21 ± 1.15 ml and the mean diameter of the balloons inflated in the coronary arteries was 2.17 ± 0.33 mm (range 1.3 to 3.0). On average, patients stayed in the hospital 4.3 ± 2.6 days (range 2 to 14).

All 3 serum markers of myocardial necrosis (CK, CK-MB, and troponin I) showed a pattern of increase after alcohol infusion to peak levels at 12 hours and then a trend down toward baseline (p <0.0001; Figure 1 , Table 3 ). Brain natriuretic peptide was increased at baseline but did not show any appreciable change after ASA (p = 1.0). Alcohol infusion produced, in general, small infarcts at the base of the left ventricular septum. The infarct size was quantified as described in the Methods section ( Table 4 ).

Change of serum markers after MI. Concentrations of CK (A) , CK-MB (B) , troponin I (C) , and brain naturetic peptide (BNP) (D) are shown at different time points after infusion of alcohol in a septal coronary artery of patients with HC. Time points are listed as median and interquartile range with the 95th percentile confidence interval. The number of patients with available data at each time point is listed below the graph. A clear peak at 12 hours is seen for CK, CK-MB, and troponin I, after which the concentrations trend back toward baseline. There is no clear change in BNP after MI when followed serially for 42 hours. It is noted that BNP is significantly increased at baseline in these symptomatic patients with HC.

Serum markers of myocardial necrosis after ASA showed significant correlations with the size of the infarct as assessed by MPI ( Figure 2 ); the highest correlation was with CK at 12 hours, which was even better than the total amount released as measured by the area under the curve for each patient. Brain natriuretic peptide at baseline was only weakly correlated with infarct size ( Table 5 ). Multivariate models using linear regression were then constructed for the prediction of the size of the infarct as assessed by MPI using the 3 serum markers (CK, CK-MB, and troponin I) measured at 12 hours, at peak level for each patient, or as the total amount released. In each instance the model showed statistical significance in the prediction of the infarct size, with the highest contribution coming from CK. At 12 hours, CK was the only variable that showed statistical significance in the multivariate model with a slope of 0.729 ( Table 6 ).

Correlation between serum markers and infarct mass measured with MPI. There is a linear correlation between CK (A) and troponin I (B) measured at 12 hours after inducing MI by the infusion of alcohol in a septal coronary artery of patients with HC. The correlation coefficient (r) is shown at the top of the graph with the corresponding p value. The regression line (straight line) is bounded by the 95th percentile confidence interval.

Table 5

Factors correlated with size of infarct as assessed by myocardial perfusion imaging

	r	p Value
Creatine kinase
At 12 hours	0.609	<0.0001
Peak	0.581	<0.0001
Cumulative ⁎	0.544	<0.0001
Creatine kinase-MB
At 12 hours	0.446	0.002
Peak	0.454	0.001
Cumulative ⁎	0.408	0.003
Troponin I
At 12 hours	0.480	0.002
Peak	0.445	0.001
Cumulative ⁎	0.477	0.001
Brain natruretic peptide at baseline	0.130	0.007

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