Identifying the coronary branch that supplies the basal septum is the cornerstone for successful alcohol septal ablation (ASA). The basal septum is often supplied by septal perforator artery/arteries (SPA/SPAs) not originating from the left anterior descending (LAD) coronary artery. We aim to investigate the prevalence and significance of non-LAD septal “culprit” in patients undergoing ASA. A retrospective review of patients who underwent ASA from 2006 to 2014 was conducted. Procedural and midterm outcomes of patients who had ASA of LAD and non-LAD culprit SPA were reported. A total 89 patients were included in the analysis; 13 patients (15%) had ASA of non-LAD SPA. These patients were more likely to have a history of failed ASA, more than one SPA treated, more ethanol dose injected, longer procedures, and higher contrast use compared with those who had ASA of LAD-SPA. In-hospital outcomes, residual gradient, symptom improvement, and midterm mortality were similar in the 2 groups. In conclusion, in a cohort of patients undergoing ASA, 15% had ablation of SPA culprit that did not originate from the LAD. Half of these patients had previous unsuccessful ASA. Systematic screening for the ideal culprit SPA with nonselective coronary injection of echo contrast should be used to avoid incomplete or failed ASA.
Clinical symptoms in patients with hypertrophic obstructive cardiomyopathy are multifactorial but are largely related to the degree of left ventricular outflow tract (LVOT) obstruction produced by: (1) severe narrowing of the LVOT because of asymmetric hypertrophy and (2) suctioning of the anterior mitral leaflet during systole (Venturi effect) manifested by systolic anterior motion of the mitral valve. The residual LVOT gradient after alcohol septal ablation (ASA) is believed to be largely due to the difficulty in precisely identifying the septal perforator artery (SPA) supplying the basal septum. The introduction of myocardial contrast echocardiography (MCE) to guide ASA procedures led to the recognition that the optimal SPA for ablation is often not the first septal perforator branch of the left anterior descending artery (LAD). In approximately 15% to 20% of cases, the use of MCE results in changing the target SPA to a more proximal or a more distal branch than what appears to be the culprit SPA on angiography. Despite the utilization of MCE, inability to identify a satisfactory culprit SPA is still reported in more than 10% of ASA procedures. Some case reports suggested that the ideal SPA for ASA could arise from an atypical location such as the ramus coronary artery or the first diagonal branch of the LAD. The actual prevalence of a non-LAD culprit SPA during ASA and their significance are unknown. We sought to investigate the prevalence and the potential implications of non-LAD SPA culprit in a large series of symptomatic patients with obstructive hypertrophic cardiomyopathy (HC) undergoing ASA at a tertiary reference center.
Methods
A retrospective chart review study design was used. The study population consisted of 92 consecutive patients aged >18 years who underwent elective ASA at our catheterization laboratory from January 2006 to October 2014. The institutional review board at our institution approved the study protocol.
At the beginning of each case, 2 6 French (Fr) sheaths were inserted in the common femoral vein and the common femoral artery, respectively. In addition, a 5Fr sheath was inserted in the right (or left) radial artery. A 6Fr temporary pacemaker wire (Medtronic, Minneapolis, Minnesota) was inserted into the right ventricle through the femoral venous sheath. Left ventricular (LV) cavity was entered with a 5Fr multipurpose diagnostic catheter inserted through the radial artery access (Boston Scientific, Marlborough, Massachusetts). A 6Fr extra-back support Launcher guiding catheter (Medtronic) was advanced over a wire into the ascending aorta through the femoral artery access. The LV multipurpose catheter and the ascending aorta guiding catheter were connected to 2 fluid filled pressure transducers, and invasive hemodynamic assessment of the LVOT gradient was obtained at baseline conditions at rest and after inducing premature ventricular contractions. The left main coronary artery was then engaged with the guiding catheter, and coronary angiography was performed. If the angiogram suggested an appropriate LAD proximal SPA for ASA, the SPA was wired with a 300 cm 0.014″ Choice Floppy wire (Boston Scientific). Next, a small over-the-wire Sprinter Legend balloon (typically 2.0 to 2.5 × 6 to 8 mm; Medtronic) was advanced to the proximal portion of this SPA. Injection of 0.1 ml of echo contrast (Optison; GE Healthcare, Princeton, NJ) into the wired SPA through the balloon catheter along with real-time 2-dimensional echocardiography was used to confirm that this SPA supplied the basal septum at the septal–mitral contact. Selective echo-contrast injections were repeated in the proximal LAD septal perforators if the first SPA was not deemed an appropriate target for ASA. If no suitable SPA was identified, systematic screening for non-LAD culprit SPA was performed by nonselective injection of 0.1 ml of echo contrast into the left main and the right coronary arteries. If the screening suggests an atypical location of the target SPA, the branch was wired with the same 0.014″ wire, and an over-the-wire balloon was advanced into this potential target. A selective injection of 0.1 ml of echo contrast was then used to confirm that this branch supply the basal septum. Once the target SPA is identified, further confirmation was performed by injecting iodine intravenous contrast into the culprit septal perforator to demonstrate staining in the basal septum on fluoroscopy. The target SPA was then treated with repeated injections of 95% ethanol (0.5 to 1 cc over 3 minutes) until satisfactory hemodynamic response is observed. If there was a persistent significant gradient at rest (>25 mm Hg) at the end of the treatment, other septal perforators were evaluated for dual supply of the basal septum and were treated if appropriate. If there was transient or complete heart block during the procedure, the pacemaker lead was secured in place. Patients were observed in the hospital for 48 hours and received a repeat echocardiogram and a 48-hour Holter monitor before discharge. Transthoracic echocardiography was repeated at 1 month and as needed thereafter (if symptoms recur or if the 1 month echo showed high LVOT gradient at rest).
Electronic medical records and ASA reports were reviewed to obtain baseline characteristics, hemodynamic data, procedural data, and short-midterm outcomes. SPSS version 20 (IBM, Armonk, New York) and Excel 2010 (Microsoft Corporation, Redmond, Washington) were used for all statistical analyses. Data are expressed as mean ± SD for continuous variables and as percentages for discrete variables. Patients who underwent ASA procedures were divided into 2 categories: (1) patients who underwent ASA of an SPA arising from the LAD artery (LAD culprit group) and (2) patients who underwent ASA of an SPA arising from coronary arteries other than the LAD (non-LAD culprit group). Continuous variables were compared with the use of the paired Student t test. Categorical variables were compared with the use of the chi-square test. All calculated p values were 2-sided, and the differences were considered to be statistically significant when their p values were <0.05.
Results
During the study period, 92 patients underwent ASA at our institution. Three patients were excluded for missing key data, and 89 patients were included in the analysis. The culprit septal perforator for ASA arose from the LAD in 76 patients (85.3%) and from other coronary arteries in 13 patients (14.7%). The baseline characteristics for these patients are listed in Table 1 . Notably, among patients who underwent ASA of a non-LAD culprit SPA, 46% had previous ASA compared with only 1.3% of those who underwent ASA of an LAD culprit ( Figure 1 ).
| Variable | LAD Septal (N=76) | Non-LAD Septal (N=13) | P value |
|---|---|---|---|
| Age (mean±SD) | 64±13 | 58±11.5 | 0.1 |
| Women | 51 (67%) | 6 (46%) | 0.21 |
| Hypertension | 60 (79%) | 9 (72%) | 0.48 |
| Atrial Fibrillation | 14 (18%) | 3 (23%) | 0.71 |
| Prior Stroke | 2 (2.6%) | 1 (8%) | 0.38 |
| Diabetes Mellitus | 9 (12%) | 1 (8%) | 1 |
| Coronary Artery Disease | 20 (26%) | 3 (25%) | 1 |
| Prior Septal Ablation | 1 (1.3%) | 6 (46%) | <0.001 |
| Family History of HC | 4 (5%) | 2 (15%) | 0.21 |
| Family History of Sudden Cardiac Death | 9 (12%) | 4 (31%) | 0.09 |
| NYHA Class III/IV | 66 (88%) | 13 (100%) | 0.35 |
| Syncope | 12 (16%) | 1 (8%) | 0.68 |
| Implantable Cardioverter Defibrillator | 5 (7%) | 3 (23%) | 0.09 |
| Prior Pacemaker | 6 (8%) | 1 (8%) | 1 |
| Left Bundle Branch Block | 13 (18%) | 2 (15%) | 1 |
| Left Ventricular Ejection Fraction | 69.3±8.1 | 74±4.9 | 0.046 |
| Maximum Wall Thickness (mm) | 19.5±4.7 | 19.6±3.8 | 0.94 |
| Echo Resting Gradient (mmHg) | 70.1±49 | 90.9±55 | 0.17 |
| Echo Provoked Gradient (mmHg) | 106.2±51 | 170.3±64 | <0.001 |
All patients underwent a detailed hemodynamic study at the outset of the procedure to confirm the echo findings of severe LVOT gradient at rest. Procedural data, in-hospital, and 1-month outcomes as well as midterm mortality data are presented in Table 2 . One-month follow-up was available in all but 4 patients. Midterm follow-up (18.9 ± 13.7 months) was available for 80% of patients. There was no significant difference between the groups in terms of in-hospital outcomes, gradient and symptoms improvement at 1 month, or mortality during follow-up.
| Variable | LAD Septal (N=76) | Non-LAD Septal (N=13) | P value |
|---|---|---|---|
| Cath Resting Gradient (mean±SD) | 81.3±37 | 85.4±35 | 0.1 |
| Cath Provoked Gradient | 156.5±50 | 154.3±37 | 0.88 |
| Left Ventricular End Diastolic Pressure | 19.6±7.9 | 21.1±5.8 | 0.51 |
| Number of Septal Perforator Treated | 1.2±0.4 | 2.1±0.9 | <0.001 |
| Septal Perforator Size | 2.3±0.4 | 2.0±0.1 | 0.009 |
| Ethanol Volume (ml) | 2.6±1 | 3.9±1.1 | <0.001 |
| Post Ablation Resting Gradient | 7.7±4.8 | 4.7±4.0 | 0.036 |
| Post Ablation Provoked Gradient | 38.3±37.6 | 37.7±29.3 | 0.95 |
| Fluoroscopy Time | 20.1±14.7 | 29.1±12.6 | 0.04 |
| Contrast Volume (cc) | 143±86 | 196±97 | 0.047 |
| Creatine Kinase (unit/liter) ∗ | 1072±612 | 863±361 | 0.23 |
| Creatine Kinase Isoenzyme MB † | 126±70 | 99±37 | 0.18 |
| Temporary Pacemaker Needed | 26 (34%) | 4 (31%) | 1 |
| Permanent Pacemaker Implantation | 12 (16%) | 1 (8%) | 0.68 |
| Cardioverter Defibrillator Implantation | 2 (2.7%) | 0 (0%) | 1 |
| Coronary Artery Dissection | 0 (0%) | 1 (8%) | 0.15 |
| Length of Stay | 2.7±1.7 | 2±0 | 0.14 |
| In-Hospital Death | 0 (0%) | 0 (0%) | 1 |
| Echo Resting Gradient at 1 month | 18±12.5 | 21±18 | 0.45 |
| Echo Provoked Gradient at 1 month | 29.2±24.5 | 26.4±22.5 | 0.7 |
| NYHA Class at 1 month | 1.2±0.5 | 1.3±0.5 | 0.5 |
| Death During Maximum Follow up | 2 (2.6%) | 0 (0%) | 1 |
∗ Normal range for creatine kinase is 46 to 171 units/L.
† Normal range for creatine kinase isoenzyme MB is 0 to 10.4 ng/ml.
Thirteen patients had a culprit septal perforator that did not originate from the LAD. Of these, 6 patients (46%) originated from the ramus coronary artery, 5 patients (38%) from the posterior descending coronary artery (PDA; 4 from right coronary artery PDA and one from a circumflex coronary artery PDA), 1 patient (8%) from the first diagonal branch of the LAD, and 1 patient (8%) from the left main coronary artery. Figure 2 and Supplementary Videos 1 to 5 illustrates procedural steps leading to the identification and treatment of a non-LAD culprit SPA in a patient who had a failed previous ASA. Figure 2 and Supplementary Videos 6 to 7 illustrated the treatment of non-LAD culprit SPA for a patient presenting for ASA for the first time. Among patients treated with ASA of a non-LAD culprit septal perforator, 6 patients (46%) had previous ASA of an LAD septal perforator. In these 6 patients; the number of LAD septal perforators treated at the first procedure was 1.8 ± 0.4, the residual LVOT gradient at the end of the first procedure was 16.3 ± 15.2 mm Hg, the time between the first and the second ablation procedure was 17.5 ± 14.5 months, and the LVOT gradient at the time of the second ablation procedure was 85.5 ± 59.5 mm Hg ( Table 3 ). Four patients (30.8%) had successful ASA of the non-LAD septal perforator alone, and 9 patients (69.2%) had alcohol ablation of LAD and non-LAD septal perforators. In most patients, ablation of the non-LAD septal perforators was performed after an initial LAD septal perforator ablation ( Table 3 ).
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