Retrospective analysis was performed of consecutive HOCM patients who underwent ASA at a single tertiary center. The indications for ASA in these patients were dyspnea NYHA class III or IV, CCS class II or III angina or exertional syncope in association with significant dynamic LVOT obstruction (defined as >50 mmHg at rest and/or >70 mmHg with provocation). Patients with previous permanent pacemaker or implantable cardio-defibrillator were excluded from this analysis.

The procedure was performed as described previously by Fiarresga et al.10 1.7–3 cm3 of 98% dehydrated ethanol was used for ASA. All patients were admitted to the cardiac intensive care unit (ICU) with a temporary pacemaker device placed during the procedure as a precaution for the development of a high-grade atrioventricular (AV) block, usually during 24–48 hours. A risk score for AV block was used to predict pacemaker dependency and select the patients for prolonged monitoring and/or PPM implantation, as described by Faber et al.11 All patients without previous PPM had continuous telemetry monitoring and daily 12-lead electrocardiogram until discharge. The risk score was applied at 24 h after ASA in all patients who did not develop persistent complete AV block. This score stratifies patients into three categories of pacemaker dependency risk (low, intermediate, and high risks). Patients with a low-risk score at 24 h after ASA were transferred to a cardiology ward under continuous telemetry monitoring; intermediate risk patients underwent prolonged monitoring in the ICU for up to 4–5 days plus corticoid therapy (prednisolone 1 mg/kg/day for four days) to assess the reversibility of AV conduction disturbances. In high-risk patients, the PPM indication was established on the second day after ASA. All the patients underwent a transthoracic echocardiogram before discharge and were followed up periodically. Patients who received a PPM had device analysis at one month after implantation and then annually thereafter.

The included patients were divided in two groups: PPM placement after ASA and those who do not undergo the procedure) and were followed for a minimum period of three years. The baseline characteristics, procedure data and outcomes were noted and compared. The long-term pacing rates in the PPM group and the PPM implantation rate in the no-PPM group during follow-up were also evaluated. The primary endpoint was composite all-cause mortality and all-cause hospitalization, and the secondary endpoint was composite all-cause mortality and hospitalization due to a cardiac cause.

Continuous variables are presented as mean value and standard deviation and categorical variables in absolute and relative values. The comparative analysis was performed using the Student's T test and chi-square test for the categorical variables. The results were presented as odds ratio (OR), 95% confidence interval (CI) and p-value and endpoints were also displayed in Kaplan-Meier curves. Statistical analysis was performed using SPSS version 25.0.

Between 2009 and 2020, 109 consecutive patients underwent ASA. 97 patients were included in this analysis (68% female, mean age 65.2 years old). 16 patients (16.5%) required PPM implantation for CHB. In these patients, no vascular access, pacemaker pocket or pulmonary parenchyma complications were noted. The baseline characteristics of comorbidities, symptoms, echocardiographic and electrocardiographic findings (Table 1) were identical in the two groups. There were statistically significant differences in the mean age (70.6 years old in the PPM group vs. 64.1 years old in the non-PPM group) and in the beta-blocker therapy rates prior to the intervention (56% in the PPM group vs. 84%). Procedure-related data showed higher creatine kinase (CK) peaks in the PPM group (1692 U/L vs. 1243 U/L, p=0.05), with no significant differences in the alcohol dose (2.1 ml in both groups, p=0.33).

In all patients, implantation of a device during hospitalization after ASA was due to AV conduction disturbances. However, in three out of 16 patients (19%) a defibrillation lead was placed in the right ventricle (RV) to perform anti-tachycardia therapies as primary prevention. 13 patients (81%) implanted a dual chamber pacemaker. In the remaining three, a single lead was placed due to permanent atrial fibrillation. Regarding the site of RV pacing, the lead was placed in an apical position in 11 patients (69%) and septal in five patients (31%). The mean programmed base rates was 55±7 bpm. Minimal pacing algorithms were used in all patients with a dual chamber pacemaker to reduce RV pacing in patients with intermittent AV conduction disturbances and enable longer intrinsic AV delay in patients with first degree AV block.

In the PPM group, the median (inter-quartile range) pacing rates (Table 2) at one month, one year and two years were 89.0 (59.0), 40.0 (90.2) and 48.5 (83.0), respectively. Two patients (12.5%) had 1–5% pacing and none had pacing <1% at two years.

In the group without PPM, five patients (6.2%) required PPM implantation at a later date, during the follow-up (six months, one year, one year, two years and three years after ASA), all of them for AV conduction disturbances. No other patients received an ICD during the follow-up period under analysis.

In the 16 patients who implanted PPM after ASA during hospitalization, no vascular, pocket-related or pulmonary complications were recorded. During the three-year follow-up, there were no recorded pocket-related, device or lead complications.

In this analysis, no in-hospital deaths occurred during hospitalization for the procedure. There were no statistically significant differences in the two groups regarding one year mortality or re-hospitalization (Table 3). There was no difference in the primary endpoint of composite all-cause mortality and all-cause hospitalization (Figure 1) between the two groups, showing, however, a trend toward a lower event rate in the PM group (p=0.09). This difference appears to be attributable to a lower rate of all-cause re-hospitalization (19% vs. 43%, p=0.07). There was no difference in the secondary endpoint of composite all-cause mortality and hospitalization due to a cardiac cause (Figure 2) between the two groups (p=0.22).

Figure 1.

Kaplan-Meier curves of event-free time for the primary endpoint of all-cause mortality and all-cause hospitalization.

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Figure 2.

Kaplan-Meier curves of event-free time of the primary endpoint all-cause mortality and cardiac cause hospitalization.

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This study has some limitations such as the reduced sample size and a reduced event rate in the follow-up period, mainly regarding mortality, which does not allow a proper characterization of this component endpoint. Also, the follow-up period used does not encompass potential hospitalizations and complications in the PPM group associated with replacement of the device's generator.