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Prevalence of Non–Left Anterior Descending Septal Perforator Culprit in Patients With Hypertrophic Cardiomyopathy Undergoing Alcohol Septal Ablation
Accepted Manuscript Prevalence of Non-Left Anterior Descending Septal Perforator Culprit in Patients With Hypertrophic Cardiomyopathy Undergoing Alcohol Septal Ablation Mohamad Alkhouli, MD, Waseem Sajjad, MBBS, Junsoo Lee, MD, Genaro Fernandez, MD, Bryan Waits, MD, Karl Q. Schwarz, MD, Christopher J. Cove, MD PII:
S0002-9149(16)30306-X
DOI:
10.1016/j.amjcard.2016.02.046
Reference:
AJC 21736
To appear in:
The American Journal of Cardiology
Received Date: 19 December 2015 Revised Date:
7 February 2016
Accepted Date: 16 February 2016
Please cite this article as: Alkhouli M, Sajjad W, Lee J, Fernandez G, Waits B, Schwarz KQ, Cove CJ, Prevalence of Non-Left Anterior Descending Septal Perforator Culprit in Patients With Hypertrophic Cardiomyopathy Undergoing Alcohol Septal Ablation, The American Journal of Cardiology (2016), doi: 10.1016/j.amjcard.2016.02.046. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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Prevalence of Non-Left Anterior Descending Septal Perforator Culprit in Patients With Hypertrophic Cardiomyopathy
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Undergoing Alcohol Septal Ablation
Mohamad Alkhouli MD 1, Waseem Sajjad MBBS1, Junsoo Lee MD1, Genaro Fernandez MD1,
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Bryan Waits MD1, Karl Q Schwarz MD1, Christopher J Cove MD1
University of Rochester Medical Center
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Department of Medicine
Division of Cardiovascular Disease
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Corresponding Author: Mohamad Alkhouli, MD
Division of Cardiovascular Diseases
University of Rochester, Division of Cardiovascular Disease
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Rochester, NY
601 Elmwood Avenue, Box 679C
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Rochester, NY 14642-8679 Tel: (585) 273-1147 Fax: (585) 271-7667
Email: [email protected]
Conflicts of Interest/Disclosures: None Total Word Count: 2131 3204 (including text, figure/video legends and references)
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Abstract 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
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artery/arteries (SPA) 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 between 2006-2014
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was conducted. Procedural and midterm outcomes of patients who had ASA of LAD and nonLAD culprit SPA were reported. 89 patients were included in the analysis; thirteen patients
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(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 two groups. In
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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 prior unsuccessful ASA. Systematic screening for the ideal culprit SPA with non-selective coronary injection of echo contrast should
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be utilized to avoid incomplete or failed ASA.
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Key Words: Hypertrophic obstructive cardiomyopathy; alcohol septal ablation; septal perforator artery; myocardial contrast echocardiography
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Introduction: Clinical symptoms in patients with hypertrophic obstructive cardiomyopathy are multifactorial, but are largely related to the degree of LVOT obstruction produced by: (1) severe narrowing of
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the LVOT due to asymmetric hypertrophy (2) suctioning of the anterior mitral leaflet during systole (venturi effect) manifested by systolic anterior motion of the mitral valve (SAM). The residual LVOT gradient after ASA is thought to be largely due to the difficulty in precisely
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identifying the septal perforator artery (SPA) supplying the basal septum 1,2. The introduction of myocardial contrast echocardiography (MCE) to guide ASA procedures led to the recognition
descending artery (LAD)
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that the optimal SPA for ablation is often not the first septal perforator branch of the left anterior . In approximately 15-20% 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 4. Despite the utilization of MCE, inability to identify a satisfactory culprit SPA is still reported in over 10% of ASA procedures 2. Some case reports suggested that
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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 6-8. The actual prevalence of a non-LAD culprit SPA during
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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
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obstructive 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 >18 years old who underwent elective alcohol septal ablation at our catheterization laboratory between January 2006 to October 2014. The Institutional Review Board at our institution approved the study protocol.
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At the beginning of each case, two 6 French (Fr) sheaths were inserted in the common femoral vein and the common femoral artery, respectively. Also, a 5Fr sheath was inserted in the right (or left) radial artery. A 6Fr temporary pacemaker wire (Medtronic - Minneapolis, MN) was
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inserted into the right ventricle via the femoral venous sheath. Left ventricular (LV) cavity was entered with a 5Fr multipurpose diagnostic catheter inserted via the radial artery access (Boston Scientific – Marlborough, MA). A 6Fr extra-back support Launcher guiding catheter (Medtronic
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- Minneapolis, MN) was advanced over a wire into the ascending aorta (AO) via the femoral artery access. The LV multipurpose catheter and the AO guiding catheter were connected to two
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fluid filled pressure transducers, and invasive hemodynamic assessment of the LVOT gradient was obtained at baseline resting conditions 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 –
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Marlborough, MA). Next, a small over-the-wire (OTW) Sprinter Legend balloon (typically 2.02.5x6-8mm) (Medtronic - Minneapolis, MN) was advanced to the proximal portion of this SPA.
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Injection of 0.1 ml of echo contrast (Optison – GE Healthcare) into the wired SPA through the balloon catheter along with real time 2D echocardiography was used to confirm that this SPA
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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 non-selective 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 OTW 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
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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 (0.5-1 cc over 3 minutes) until satisfactory hemodynamic
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response is observed. If there was a persistent significant resting gradient (>25 mmHg) 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,
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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 prior to discharge. Transthoracic
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echocardiography was repeated at 1 month and as needed thereafter (if symptoms recur or if the 1 month echo showed high resting LVOT gradient).
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)
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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
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into two categories: (1) Patients who underwent ASA of a SPA arising from the LAD artery (LAD culprit group). (2) Patients who underwent ASA of a SPA arising from coronary arteries
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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 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
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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 prior
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ASA compared with only 1.3% of those who underwent ASA of an LAD culprit (Figure1).
All patients underwent a detailed hemodynamic study at the outset of the procedure to confirm the echo findings of severe resting LVOT gradient. Procedural data, in-hospital and 1-
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month outcomes as well as midterm mortality data are presented in table (2). One-month follow up was available in all but 4 patients. Mid-term follow-up (18.9±13.7 months) was available for
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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.
Thirteen patients had a culprit septal perforator that did not originate from the LAD. Of these, 6 (46%) originated from the ramus coronary artery, 5 (38%) from the posterior descending
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coronary artery (PDA) (four from right coronary artery PDA and one from a circumflex coronary artery PDA), 1 (8%) from the first diagonal branch of the LAD, and 1 (8%) from the left main
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coronary artery. Figure 2(A-C) and Video (online only) (1-5) illustrates procedural steps leading to the identification and treatment of a non-LAD culprit SPA in a patient who had a failed prior
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ASA. Figure 2 (D-F) and Video (online only) (6-7) 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 (46%) had prior 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 mmHg, 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 mmHg (Table 3). Four patients (30.8%) had successful ASA of the non-LAD septal perforator alone, and 9 patients (69.2%) had alcohol
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ablation of LAD and non-LAD septal perforators. In the majority of patients, ablation of the nonLAD septal perforators was performed after an initial LAD septal perforator ablation (Table 3). Treating non-LAD SPA was associated with longer fluoroscopy time, more contrast use,
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and higher ethanol dose with no impact on peri-procedural outcomes including the need for permanent pacemaker, unplanned ICD and length of stay. These patients also had less post-ASA resting residual gradient but similar provoked residual gradient compared with those treated with
gradient between the two groups (Table 2).
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Discussion
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LAD-SPA ablation. However, at 1 month there was no difference in symptom relief or residual
Percutaneous alcohol septal ablation was introduced in 1994 as a less invasive alternative to surgical myomectomy for symptomatic patients with obstructive HC who were deemed poor surgical candidates 9. The procedure has since undergone significant technical refinements, most important of which is the introduction of MCE for more precise localization of the target SPA
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that supplies the basal septum 3,4. The routine use of MCE significantly increased the success rate of ASA, and led to the recognition of the fact that the basal septum is often not exclusively supplied by the SPA branching off the proximal LAD 4. In some recent reports, the failure to
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identify an unusual origin of the SPA was thought to be the cause of unsuccessful ASA 2,6-8.
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Blood supply of the basal septum is complex; Autopsy and cardiac magnetic resonance
(CMR) imaging studies have shown significant variability and rich collateral blood supply of the basal septum in both normal subjected and those with obstructive HC
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. A major limitation of
ASA lays in its imprecision in identifying the optimal SPA that should be targeted with alcohol ablation. Although MCE has significantly improved our ability to identify the optimal SPA(s) prior to ASA, the procedure remains unsuccessful in reducing the LVOT gradient in a small percentage of patients. This could be related to the failure to recognize non-LAD SPA feeding
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the basal septum, rather than failure of ASA due to recruited collaterals or inadequate ethanol dose (Figure 2A-2C, Video 1-5 online only).
The prevalence, the screening techniques and the potential implications of non-LAD
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septal perforator supply of the basal septum have not been previously described. Routinely, most operators screen for the culprit SPA by selectively injecting echo contrast into the proximal LAD SPA. At our center, the screening strategy includes two additional steps: (1) If selective
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injections of the proximal LAD SPA(s) with echo-contrast did not lead to appropriate MCE staining of the basal septum on real time echo, upfront screening for atypical SPA culprit(s) was
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performed by non-selective echo-contrast injections in the left main and the right coronary arteries. (2) If selective injections of the proximal LAD SPA(s) with echo-contrast identified an appropriate SPA for septal ablation, but the LVOT gradient remained elevated (≥ 25mmHg) after successful ablation of the that branch, screening for atypical SPA culprit(s) was similarly
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performed by non-selective echo-contrast injections in the left main and the right coronary arteries. This methodology uncovered a suitable SPA for ASA in ~ 15% of patients. A significant number of these patients (46%) had undergone at least one prior unsuccessful ASA in
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the past. This suggests a possible failure to recognize the atypical or the dual septal perforator blood supply of the basal septum in these patients at the time of the initial procedure. Although
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these patients were more likely to have more than one septal branch treated and received higher doses of Ethanol than patients who had ASA of typical LAD SPA target(s), the complication rates including complete heart block, the need for a permanent pacemaker, hospital length of stay and midterm mortality were similar in the two groups.
This study has several limitations. First, the study is subject to the inherent limitations of retrospective and non-randomized studies such as selection bias and patients who were lost in follow up. Therefore, these data may not be entirely representative and generalizable for all
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patients with obstructive HC treated with ASA. Second, the study is not sufficient to detect disparities in long-term outcomes between patients undergoing alcohol ablation of LAD and nonLAD SPA. This is due to the fact that most of our patients are referred from remote
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clinics/centers, and therefore only midterm follow up is available for the majority of them. Third, blood supply of the basal septum is complex as illustrated by Singh et al 5, and this study does not include advanced imaging techniques (such as Magnetic Resonance Imaging) to precisely
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address the dual or triple supply of the basal septum by LAD and non-LAD SPA. Nevertheless, even patients who underwent alcohol ablation of non-LAD SPA alone had very small residual
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gradient after ASA.
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References: 1. Orme NM, Sorajja P, Dearani JA, Schaff HV, Gersh BJ, Ommen SR. Comparison of surgical septal myectomy to medical therapy alone in patients with hypertrophic cardiomyopathy and
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syncope. Am J Cardiol 2013;111:388-392.
2. Angelini P. The "1st septal unit" in hypertrophic obstructive cardiomyopathy: a newly
Texas Heart Institute Journal 2007;34:336-346.
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recognized anatomo-functional entity, identified during recent alcohol septal ablation experience.
3. Faber L, Ziemssen P, Seggewiss H. Targeting percutaneous transluminal septal ablation for
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hypertrophic obstructive cardiomyopathy by intraprocedural echocardiographic monitoring. Journal of the American Society of Echocardiography 2000;13:1074-1079. 4. Faber L, Seggewiss H, Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: results with respect to intraprocedural myocardial
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contrast echocardiography. Circulation 1998;98:2415-2421.
5. Singh M, Edwards WD, Holmes DR, Jr., Tajil AJ, Nishimura RA. Anatomy of the first septal perforating artery: a study with implications for ablation therapy for hypertrophic
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cardiomyopathy. Mayo Clinic Proceedings 2001;76:799-802. 6. Noble S, Frangos C, L'Allier P L. Alcohol septal ablation for obstructive hypertrophic
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cardiomyopathy: the perfect septal branch may originate from an atypical location. The Canadian Journal of Cardiology 2012;28:245 e241-243. 7. Doran GC, Burns CM, Murdoch DJ, Incani A, Walters DL. A repeat alcohol septal ablation procedure for hypertrophic obstructive cardiomyopathy where the first septal branch arose from the intermediate (ramus) artery. Heart, lung & circulation 2013;22:1026-1029.
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8. Toutouzas K, Karanasos A, Anastasakis A, Vavuranakis M, Seggewiss H, Stefanadis C, Rigopoulos A. Optimal branch selection in alcohol septal ablation. International Journal of Cardiology 2011;147:143-144.
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9. Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet 1995;346:211-214.
10. Valeti US, Nishimura RA, Holmes DR, Araoz PA, Glockner JF, Breen JF, Ommen SR,
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Gersh BJ, Tajik AJ, Rihal CS, Schaff HV, Maron BJ. Comparison of surgical septal myectomy and alcohol septal ablation with cardiac magnetic resonance imaging in patients with
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hypertrophic obstructive cardiomyopathy. J AmColl Cardiol 2007;49:350-357.
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Figure and Video Legends: Figure (1): The Incidence of Failed Prior Alcohol Septal Ablation Procedures Among Patients with LAD and Non-LAD Septal Perforator Culprit. LAD, left anterior descending.
Non-LAD Culprit Septal Perforator Artery.
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Figure (2): Still Images of Cine Angiography in two Patients who Underwent ASA of a
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Patient 1 (A-C): had initial ASA of an LAD culprit, and a repeat ASA of a non-LAD culprit
A- Left coronary angiography showing an LAD septal treated at the time of the first ASA
echocardiography (Video2).
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procedure (S1). This branch was thought to partially supply the basal septum on contrast
B- Right coronary angiography showing an RCA septal treated at the time of the repeat procedure (PDA-S). This branch was confirmed to supply the basal septum on contrast
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echocardiography (Video4).
C- Staining of the basal septum after ASA of the RCA septal perforator (arrow). Patient 2 (E-G): had one ASA of a non-LAD culprit
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D- Left coronary angiography showing that the septal perforator originating from the LAD
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(S1,S2) did not seem to supply the basal septum (suboptimal culprits) E- Right coronary angiography showing a potentially optimal RCA septal culprit. This branch was found to be the main vessel supplying the basal septum on myocardial contrast echocardiography (Video6).
F- Staining of the basal septum after ASA of the RCA septal perforator (arrow)
Video (1-5): Procedural cine angiograms and myocardial echo contrast images in a patient who
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underwent two alcohol septal ablation procedures (1st of an LAD septal perforator and 2nd of a non-LAD septal perforator). Video 1: Cine runs of the left coronary artery angiography. The first run illustrates the absence
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of a proximal SPA suitable for septal ablation; the second run shows balloon occlusion of the main body of the first LAD septal perforator; the third run shows balloon occlusion of the upper branch of the LAD septal perforator; the fourth run shows staining of myocardium in the
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territory of the treated LAD septal perforator.
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Video 2: Myocardial contrast echocardiography at the time of the first ASA procedure. The first run illustrates that selective injection of echo contrast in the first LAD septal perforator leads to suboptimal opacification of basal septum (distal basal septum and proximal mid septum). The second run illustrates that selective injection of echo contrast in the upper branch of the first LAD septal perforator leads to better but no ideal opacification of the basal septum.
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Video 3: 3-month post 1st ASA follow-up transthoracic echocardiogram. This video illustrates that the septal area treated with the first septal ablation (LAD septal perforator) resulted in
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reduction of the septal myocardium distal to the basal septum. It also showed a persistent SAM and flow acceleration in the LVOT.
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Video 4: Myocardial contrast echocardiography at the time of the second procedure (6 months later). The video illustrates that selective injection of echo contrast in the distal PDA septal perforator artery (PDA S3) resulted in no opacification of the septum (first run), while selective injection of echo contrast in a more proximal PDA septal perforator artery (PDA S2) resulted in opacification of the basal septum (second run) making this septal an ideal target for ASA.
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Video 5: Cine runs of the right coronary artery angiography at the time of the second procedure. The angiogram shows abundance of septal perforators originating from the PDA. The proximal PDA septal perforator artery that was confirmed to be the prominent vessel supplying the basal
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septum by myocardial contrast echocardiography (video 4), was treated with ASA. The final cine run shows staining at the basal septum at the conclusion of the procedure.
Video (6-7): Procedural cine angiograms and myocardial echo contrast images in a patient who
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underwent an initial alcohol septal ablation of a non-LAD septal perforator culprit.
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Video 6: Screening contrast echocardiography at the beginning of the procedure. Non-selective injection of echo contrast in the left main coronary artery resulted in no opacification of the basal septum (first run). Non-selective injection of echo contrast in the right coronary artery resulted in opacification of the basal septum (second run) suggesting that the ideal septal perforator artery for ASA originates from the right coronary artery.
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Video 7: Cine runs of the left and the right coronary artery angiography. The angiograms show a lack of an appropriate septal perforator originating from the proximal LAD, but identify an
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appropriate septal perforator originating from the RCA PDA. The PDA septal perforator artery was confirmed to be the culprit septal supplying the basal septum by myocardial contrast
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echocardiography (video6), and was therefore treated with ASA. The final cine run shows staining at the basal septum at the conclusion of the procedure.
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Table (1): Key Baseline Characteristics of Patients Who Underwent Alcohol Septal Ablation of a
Septal Perforator Arteries
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Typical (Left Anterior Descending) and Atypical (Non- Left Anterior Descending)
LAD Septal (N=76)
Non-LAD Septal (N=13)
P value
Age (mean±SD) Women Hypertension Atrial Fibrillation Prior Stroke Diabetes Mellitus Coronary Artery Disease Prior Septal Ablation Family History of HC Family History of Sudden Cardiac Death NYHA Class III/IV Syncope Implantable Cardioverter Defibrillator Prior Pacemaker Left Bundle Branch Block Left Ventricular Ejection Fraction Maximum Wall Thickness (mm) Echo Resting Gradient (mmHg) Echo Provoked Gradient (mmHg)
64±13 51 (67%) 60 (79%) 14 (18%) 2 (2.6%) 9 (12%) 20 (26%) 1 (1.3%) 4 (5%) 9 (12%) 66 (88%) 12 (16%) 5 (7%) 6 (8%) 13 (18%) 69.3±8.1 19.5±4.7 70.1±49 106.2±51
58±11.5 6 (46%) 9 (72%) 3 (23%) 1 (8%) 1 (8%) 3 (25%) 6 (46%) 2 (15%) 4 (31%) 13 (100%) 1 (8%) 3 (23%) 1 (8%) 2 (15%) 74±4.9 19.6±3.8 90.9±55 170.3±64
0.1 0.21 0.48 0.71 0.38 1 1 <0.001 0.21 0.09 0.35 0.68 0.09 1 1 0.046 0.94 0.17 <0.001
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Variable
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LAD, left anterior descending; SD, standard deviation; n, number; HC, hypertrophic cardiomyopathy; NYHA, New York heart association. Variables are expressed in (mean±SD) or number (%).
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Table (2): Procedural and Long-Term Outcomes of Patients Who Underwent Alcohol Septal Ablation
Septal Perforator Arteries
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of a Typical (Left Anterior Descending) and Atypical (Non- Left Anterior Descending)
LAD Septal (N=76)
Non-LAD Septal (N=13)
P value
Cath Resting Gradient (mean±SD) Cath Provoked Gradient Left Ventricular End Diastolic Pressure Number of Septal Perforator Treated Septal Perforator Size Ethanol Volume (ml) Post Ablation Resting Gradient Post Ablation Provoked Gradient Fluoroscopy Time Contrast Volume (cc) Creatine Kinase (unit/liter)* Creatine Kinase Isoenzyme MB** Temporary Pacemaker Needed Permanent Pacemaker Implantation Cardioverter Defibrillator Implantation Coronary Artery Dissection Length of Stay In-Hospital Death Echo Resting Gradient at 1 month Echo Provoked Gradient at 1 month NYHA Class at 1 month Death During Maximum Follow up
81.3±37 156.5±50 19.6±7.9 1.2±0.4 2.3±0.4 2.6±1 7.7±4.8 38.3±37.6 20.1±14.7 143±86 1072±612 126±70 26 (34%) 12 (16%) 2 (2.7%) 0 (0%) 2.7±1.7 0 (0%) 18±12.5 29.2±24.5 1.2±0.5 2 (2.6%)
85.4±35 154.3±37 21.1±5.8 2.1±0.9 2.0±0.1 3.9±1.1 4.7±4.0 37.7±29.3 29.1±12.6 196±97 863±361 99±37 4 (31%) 1 (8%) 0 (0%) 1 (8%) 2±0 0 (0%) 21±18 26.4±22.5 1.3±0.5 0 (0%)
0.1 0.88 0.51 <0.001 0.009 <0.001 0.036 0.95 0.04 0.047 0.23 0.18 1 0.68 1 0.15 0.14 1 0.45 0.7 0.5 1
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Variable
LAD, left anterior descending; SD, standard deviation; n, number; NYHA, New York heart association;. Variables are expressed in (mean±SD) or number (%). * Normal range for Creatine Kinase is 46-171 units/liter. ** Normal range for Creatine Kinase Isoenzyme MB is 0-10.4 ng/mL.
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Table (3): Procedural Details of Patients who Underwent Alcohol Septal Ablation of
2 2 3 3 1 2 1 3 3 2 3 1 1
LAD, Ramus LAD, Left Main LAD, Ramus LAD, Ramus Right LAD, Right Ramus LAD, Right LAD, LPDA LAD, Right LAD, Ramus Diagonal Ramus
Ramus Left Main LAD LAD Right Right Ramus LAD LAD LAD LAD Diagonal Ramus
r-LVOT gradient at beginning of the procedure*
r-LVOT gradient at end of the procedure*
NA NA NA NA NA NA NA 7 24 8 14 8 44
187 110 78 160 45 30 62 170 55 150 45 52 73
12 8 0 0 5 0 5 8 5 10 0 0 5
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N N N N N N N Y Y Y Y Y Y
Time since prior ASA
NA NA NA NA NA NA NA 8 5 45 5 5 8
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1 2 3 4 5 6 7 8 9 10 11 12 13
r-LVOT # of Coronary origin 1st gradient at Septal of Treated Septal end of Treated* Septals* Treated* prior ASA
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Subject
Prior LAD Septal ASA
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Non-Left Anterior Descending Septal Perforator Arteries
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LAD, left anterior descending; ASA, alcohol septal ablation; r-LVOT, resting left ventricular outflow gradient; LPDA, left posterior descending artery; NA, non-applicable * data at the time of second procedure if the patient had a prior ASA. Gradient is expressed in mmHg.
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S0002-9149(16)30306-X
DOI:
10.1016/j.amjcard.2016.02.046
Reference:
AJC 21736
To appear in:
The American Journal of Cardiology
Received Date: 19 December 2015 Revised Date:
7 February 2016
Accepted Date: 16 February 2016
Please cite this article as: Alkhouli M, Sajjad W, Lee J, Fernandez G, Waits B, Schwarz KQ, Cove CJ, Prevalence of Non-Left Anterior Descending Septal Perforator Culprit in Patients With Hypertrophic Cardiomyopathy Undergoing Alcohol Septal Ablation, The American Journal of Cardiology (2016), doi: 10.1016/j.amjcard.2016.02.046. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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Prevalence of Non-Left Anterior Descending Septal Perforator Culprit in Patients With Hypertrophic Cardiomyopathy
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Undergoing Alcohol Septal Ablation
Mohamad Alkhouli MD 1, Waseem Sajjad MBBS1, Junsoo Lee MD1, Genaro Fernandez MD1,
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Bryan Waits MD1, Karl Q Schwarz MD1, Christopher J Cove MD1
University of Rochester Medical Center
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Department of Medicine
Division of Cardiovascular Disease
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Corresponding Author: Mohamad Alkhouli, MD
Division of Cardiovascular Diseases
University of Rochester, Division of Cardiovascular Disease
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Rochester, NY
601 Elmwood Avenue, Box 679C
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Rochester, NY 14642-8679 Tel: (585) 273-1147 Fax: (585) 271-7667
Email: [email protected]
Conflicts of Interest/Disclosures: None Total Word Count: 2131 3204 (including text, figure/video legends and references)
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Abstract 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
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artery/arteries (SPA) 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 between 2006-2014
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was conducted. Procedural and midterm outcomes of patients who had ASA of LAD and nonLAD culprit SPA were reported. 89 patients were included in the analysis; thirteen patients
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(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 two groups. In
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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 prior unsuccessful ASA. Systematic screening for the ideal culprit SPA with non-selective coronary injection of echo contrast should
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be utilized to avoid incomplete or failed ASA.
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Key Words: Hypertrophic obstructive cardiomyopathy; alcohol septal ablation; septal perforator artery; myocardial contrast echocardiography
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Introduction: Clinical symptoms in patients with hypertrophic obstructive cardiomyopathy are multifactorial, but are largely related to the degree of LVOT obstruction produced by: (1) severe narrowing of
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the LVOT due to asymmetric hypertrophy (2) suctioning of the anterior mitral leaflet during systole (venturi effect) manifested by systolic anterior motion of the mitral valve (SAM). The residual LVOT gradient after ASA is thought to be largely due to the difficulty in precisely
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identifying the septal perforator artery (SPA) supplying the basal septum 1,2. The introduction of myocardial contrast echocardiography (MCE) to guide ASA procedures led to the recognition
descending artery (LAD)
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that the optimal SPA for ablation is often not the first septal perforator branch of the left anterior . In approximately 15-20% 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 4. Despite the utilization of MCE, inability to identify a satisfactory culprit SPA is still reported in over 10% of ASA procedures 2. Some case reports suggested that
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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 6-8. The actual prevalence of a non-LAD culprit SPA during
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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
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obstructive 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 >18 years old who underwent elective alcohol septal ablation at our catheterization laboratory between January 2006 to October 2014. The Institutional Review Board at our institution approved the study protocol.
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At the beginning of each case, two 6 French (Fr) sheaths were inserted in the common femoral vein and the common femoral artery, respectively. Also, a 5Fr sheath was inserted in the right (or left) radial artery. A 6Fr temporary pacemaker wire (Medtronic - Minneapolis, MN) was
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inserted into the right ventricle via the femoral venous sheath. Left ventricular (LV) cavity was entered with a 5Fr multipurpose diagnostic catheter inserted via the radial artery access (Boston Scientific – Marlborough, MA). A 6Fr extra-back support Launcher guiding catheter (Medtronic
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- Minneapolis, MN) was advanced over a wire into the ascending aorta (AO) via the femoral artery access. The LV multipurpose catheter and the AO guiding catheter were connected to two
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fluid filled pressure transducers, and invasive hemodynamic assessment of the LVOT gradient was obtained at baseline resting conditions 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 –
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Marlborough, MA). Next, a small over-the-wire (OTW) Sprinter Legend balloon (typically 2.02.5x6-8mm) (Medtronic - Minneapolis, MN) was advanced to the proximal portion of this SPA.
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Injection of 0.1 ml of echo contrast (Optison – GE Healthcare) into the wired SPA through the balloon catheter along with real time 2D echocardiography was used to confirm that this SPA
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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 non-selective 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 OTW 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
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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 (0.5-1 cc over 3 minutes) until satisfactory hemodynamic
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response is observed. If there was a persistent significant resting gradient (>25 mmHg) 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,
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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 prior to discharge. Transthoracic
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echocardiography was repeated at 1 month and as needed thereafter (if symptoms recur or if the 1 month echo showed high resting LVOT gradient).
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)
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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
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into two categories: (1) Patients who underwent ASA of a SPA arising from the LAD artery (LAD culprit group). (2) Patients who underwent ASA of a SPA arising from coronary arteries
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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 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
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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 prior
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ASA compared with only 1.3% of those who underwent ASA of an LAD culprit (Figure1).
All patients underwent a detailed hemodynamic study at the outset of the procedure to confirm the echo findings of severe resting LVOT gradient. Procedural data, in-hospital and 1-
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month outcomes as well as midterm mortality data are presented in table (2). One-month follow up was available in all but 4 patients. Mid-term follow-up (18.9±13.7 months) was available for
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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.
Thirteen patients had a culprit septal perforator that did not originate from the LAD. Of these, 6 (46%) originated from the ramus coronary artery, 5 (38%) from the posterior descending
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coronary artery (PDA) (four from right coronary artery PDA and one from a circumflex coronary artery PDA), 1 (8%) from the first diagonal branch of the LAD, and 1 (8%) from the left main
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coronary artery. Figure 2(A-C) and Video (online only) (1-5) illustrates procedural steps leading to the identification and treatment of a non-LAD culprit SPA in a patient who had a failed prior
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ASA. Figure 2 (D-F) and Video (online only) (6-7) 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 (46%) had prior 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 mmHg, 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 mmHg (Table 3). Four patients (30.8%) had successful ASA of the non-LAD septal perforator alone, and 9 patients (69.2%) had alcohol
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ablation of LAD and non-LAD septal perforators. In the majority of patients, ablation of the nonLAD septal perforators was performed after an initial LAD septal perforator ablation (Table 3). Treating non-LAD SPA was associated with longer fluoroscopy time, more contrast use,
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and higher ethanol dose with no impact on peri-procedural outcomes including the need for permanent pacemaker, unplanned ICD and length of stay. These patients also had less post-ASA resting residual gradient but similar provoked residual gradient compared with those treated with
gradient between the two groups (Table 2).
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Discussion
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LAD-SPA ablation. However, at 1 month there was no difference in symptom relief or residual
Percutaneous alcohol septal ablation was introduced in 1994 as a less invasive alternative to surgical myomectomy for symptomatic patients with obstructive HC who were deemed poor surgical candidates 9. The procedure has since undergone significant technical refinements, most important of which is the introduction of MCE for more precise localization of the target SPA
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that supplies the basal septum 3,4. The routine use of MCE significantly increased the success rate of ASA, and led to the recognition of the fact that the basal septum is often not exclusively supplied by the SPA branching off the proximal LAD 4. In some recent reports, the failure to
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identify an unusual origin of the SPA was thought to be the cause of unsuccessful ASA 2,6-8.
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Blood supply of the basal septum is complex; Autopsy and cardiac magnetic resonance
(CMR) imaging studies have shown significant variability and rich collateral blood supply of the basal septum in both normal subjected and those with obstructive HC
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. A major limitation of
ASA lays in its imprecision in identifying the optimal SPA that should be targeted with alcohol ablation. Although MCE has significantly improved our ability to identify the optimal SPA(s) prior to ASA, the procedure remains unsuccessful in reducing the LVOT gradient in a small percentage of patients. This could be related to the failure to recognize non-LAD SPA feeding
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the basal septum, rather than failure of ASA due to recruited collaterals or inadequate ethanol dose (Figure 2A-2C, Video 1-5 online only).
The prevalence, the screening techniques and the potential implications of non-LAD
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septal perforator supply of the basal septum have not been previously described. Routinely, most operators screen for the culprit SPA by selectively injecting echo contrast into the proximal LAD SPA. At our center, the screening strategy includes two additional steps: (1) If selective
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injections of the proximal LAD SPA(s) with echo-contrast did not lead to appropriate MCE staining of the basal septum on real time echo, upfront screening for atypical SPA culprit(s) was
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performed by non-selective echo-contrast injections in the left main and the right coronary arteries. (2) If selective injections of the proximal LAD SPA(s) with echo-contrast identified an appropriate SPA for septal ablation, but the LVOT gradient remained elevated (≥ 25mmHg) after successful ablation of the that branch, screening for atypical SPA culprit(s) was similarly
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performed by non-selective echo-contrast injections in the left main and the right coronary arteries. This methodology uncovered a suitable SPA for ASA in ~ 15% of patients. A significant number of these patients (46%) had undergone at least one prior unsuccessful ASA in
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the past. This suggests a possible failure to recognize the atypical or the dual septal perforator blood supply of the basal septum in these patients at the time of the initial procedure. Although
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these patients were more likely to have more than one septal branch treated and received higher doses of Ethanol than patients who had ASA of typical LAD SPA target(s), the complication rates including complete heart block, the need for a permanent pacemaker, hospital length of stay and midterm mortality were similar in the two groups.
This study has several limitations. First, the study is subject to the inherent limitations of retrospective and non-randomized studies such as selection bias and patients who were lost in follow up. Therefore, these data may not be entirely representative and generalizable for all
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patients with obstructive HC treated with ASA. Second, the study is not sufficient to detect disparities in long-term outcomes between patients undergoing alcohol ablation of LAD and nonLAD SPA. This is due to the fact that most of our patients are referred from remote
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clinics/centers, and therefore only midterm follow up is available for the majority of them. Third, blood supply of the basal septum is complex as illustrated by Singh et al 5, and this study does not include advanced imaging techniques (such as Magnetic Resonance Imaging) to precisely
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address the dual or triple supply of the basal septum by LAD and non-LAD SPA. Nevertheless, even patients who underwent alcohol ablation of non-LAD SPA alone had very small residual
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gradient after ASA.
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References: 1. Orme NM, Sorajja P, Dearani JA, Schaff HV, Gersh BJ, Ommen SR. Comparison of surgical septal myectomy to medical therapy alone in patients with hypertrophic cardiomyopathy and
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syncope. Am J Cardiol 2013;111:388-392.
2. Angelini P. The "1st septal unit" in hypertrophic obstructive cardiomyopathy: a newly
Texas Heart Institute Journal 2007;34:336-346.
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recognized anatomo-functional entity, identified during recent alcohol septal ablation experience.
3. Faber L, Ziemssen P, Seggewiss H. Targeting percutaneous transluminal septal ablation for
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hypertrophic obstructive cardiomyopathy by intraprocedural echocardiographic monitoring. Journal of the American Society of Echocardiography 2000;13:1074-1079. 4. Faber L, Seggewiss H, Gleichmann U. Percutaneous transluminal septal myocardial ablation in hypertrophic obstructive cardiomyopathy: results with respect to intraprocedural myocardial
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contrast echocardiography. Circulation 1998;98:2415-2421.
5. Singh M, Edwards WD, Holmes DR, Jr., Tajil AJ, Nishimura RA. Anatomy of the first septal perforating artery: a study with implications for ablation therapy for hypertrophic
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cardiomyopathy. Mayo Clinic Proceedings 2001;76:799-802. 6. Noble S, Frangos C, L'Allier P L. Alcohol septal ablation for obstructive hypertrophic
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cardiomyopathy: the perfect septal branch may originate from an atypical location. The Canadian Journal of Cardiology 2012;28:245 e241-243. 7. Doran GC, Burns CM, Murdoch DJ, Incani A, Walters DL. A repeat alcohol septal ablation procedure for hypertrophic obstructive cardiomyopathy where the first septal branch arose from the intermediate (ramus) artery. Heart, lung & circulation 2013;22:1026-1029.
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8. Toutouzas K, Karanasos A, Anastasakis A, Vavuranakis M, Seggewiss H, Stefanadis C, Rigopoulos A. Optimal branch selection in alcohol septal ablation. International Journal of Cardiology 2011;147:143-144.
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9. Sigwart U. Non-surgical myocardial reduction for hypertrophic obstructive cardiomyopathy. Lancet 1995;346:211-214.
10. Valeti US, Nishimura RA, Holmes DR, Araoz PA, Glockner JF, Breen JF, Ommen SR,
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Gersh BJ, Tajik AJ, Rihal CS, Schaff HV, Maron BJ. Comparison of surgical septal myectomy and alcohol septal ablation with cardiac magnetic resonance imaging in patients with
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hypertrophic obstructive cardiomyopathy. J AmColl Cardiol 2007;49:350-357.
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Figure and Video Legends: Figure (1): The Incidence of Failed Prior Alcohol Septal Ablation Procedures Among Patients with LAD and Non-LAD Septal Perforator Culprit. LAD, left anterior descending.
Non-LAD Culprit Septal Perforator Artery.
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Figure (2): Still Images of Cine Angiography in two Patients who Underwent ASA of a
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Patient 1 (A-C): had initial ASA of an LAD culprit, and a repeat ASA of a non-LAD culprit
A- Left coronary angiography showing an LAD septal treated at the time of the first ASA
echocardiography (Video2).
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procedure (S1). This branch was thought to partially supply the basal septum on contrast
B- Right coronary angiography showing an RCA septal treated at the time of the repeat procedure (PDA-S). This branch was confirmed to supply the basal septum on contrast
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echocardiography (Video4).
C- Staining of the basal septum after ASA of the RCA septal perforator (arrow). Patient 2 (E-G): had one ASA of a non-LAD culprit
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D- Left coronary angiography showing that the septal perforator originating from the LAD
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(S1,S2) did not seem to supply the basal septum (suboptimal culprits) E- Right coronary angiography showing a potentially optimal RCA septal culprit. This branch was found to be the main vessel supplying the basal septum on myocardial contrast echocardiography (Video6).
F- Staining of the basal septum after ASA of the RCA septal perforator (arrow)
Video (1-5): Procedural cine angiograms and myocardial echo contrast images in a patient who
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underwent two alcohol septal ablation procedures (1st of an LAD septal perforator and 2nd of a non-LAD septal perforator). Video 1: Cine runs of the left coronary artery angiography. The first run illustrates the absence
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of a proximal SPA suitable for septal ablation; the second run shows balloon occlusion of the main body of the first LAD septal perforator; the third run shows balloon occlusion of the upper branch of the LAD septal perforator; the fourth run shows staining of myocardium in the
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territory of the treated LAD septal perforator.
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Video 2: Myocardial contrast echocardiography at the time of the first ASA procedure. The first run illustrates that selective injection of echo contrast in the first LAD septal perforator leads to suboptimal opacification of basal septum (distal basal septum and proximal mid septum). The second run illustrates that selective injection of echo contrast in the upper branch of the first LAD septal perforator leads to better but no ideal opacification of the basal septum.
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Video 3: 3-month post 1st ASA follow-up transthoracic echocardiogram. This video illustrates that the septal area treated with the first septal ablation (LAD septal perforator) resulted in
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reduction of the septal myocardium distal to the basal septum. It also showed a persistent SAM and flow acceleration in the LVOT.
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Video 4: Myocardial contrast echocardiography at the time of the second procedure (6 months later). The video illustrates that selective injection of echo contrast in the distal PDA septal perforator artery (PDA S3) resulted in no opacification of the septum (first run), while selective injection of echo contrast in a more proximal PDA septal perforator artery (PDA S2) resulted in opacification of the basal septum (second run) making this septal an ideal target for ASA.
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Video 5: Cine runs of the right coronary artery angiography at the time of the second procedure. The angiogram shows abundance of septal perforators originating from the PDA. The proximal PDA septal perforator artery that was confirmed to be the prominent vessel supplying the basal
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septum by myocardial contrast echocardiography (video 4), was treated with ASA. The final cine run shows staining at the basal septum at the conclusion of the procedure.
Video (6-7): Procedural cine angiograms and myocardial echo contrast images in a patient who
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underwent an initial alcohol septal ablation of a non-LAD septal perforator culprit.
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Video 6: Screening contrast echocardiography at the beginning of the procedure. Non-selective injection of echo contrast in the left main coronary artery resulted in no opacification of the basal septum (first run). Non-selective injection of echo contrast in the right coronary artery resulted in opacification of the basal septum (second run) suggesting that the ideal septal perforator artery for ASA originates from the right coronary artery.
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Video 7: Cine runs of the left and the right coronary artery angiography. The angiograms show a lack of an appropriate septal perforator originating from the proximal LAD, but identify an
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appropriate septal perforator originating from the RCA PDA. The PDA septal perforator artery was confirmed to be the culprit septal supplying the basal septum by myocardial contrast
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echocardiography (video6), and was therefore treated with ASA. The final cine run shows staining at the basal septum at the conclusion of the procedure.
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Table (1): Key Baseline Characteristics of Patients Who Underwent Alcohol Septal Ablation of a
Septal Perforator Arteries
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Typical (Left Anterior Descending) and Atypical (Non- Left Anterior Descending)
LAD Septal (N=76)
Non-LAD Septal (N=13)
P value
Age (mean±SD) Women Hypertension Atrial Fibrillation Prior Stroke Diabetes Mellitus Coronary Artery Disease Prior Septal Ablation Family History of HC Family History of Sudden Cardiac Death NYHA Class III/IV Syncope Implantable Cardioverter Defibrillator Prior Pacemaker Left Bundle Branch Block Left Ventricular Ejection Fraction Maximum Wall Thickness (mm) Echo Resting Gradient (mmHg) Echo Provoked Gradient (mmHg)
64±13 51 (67%) 60 (79%) 14 (18%) 2 (2.6%) 9 (12%) 20 (26%) 1 (1.3%) 4 (5%) 9 (12%) 66 (88%) 12 (16%) 5 (7%) 6 (8%) 13 (18%) 69.3±8.1 19.5±4.7 70.1±49 106.2±51
58±11.5 6 (46%) 9 (72%) 3 (23%) 1 (8%) 1 (8%) 3 (25%) 6 (46%) 2 (15%) 4 (31%) 13 (100%) 1 (8%) 3 (23%) 1 (8%) 2 (15%) 74±4.9 19.6±3.8 90.9±55 170.3±64
0.1 0.21 0.48 0.71 0.38 1 1 <0.001 0.21 0.09 0.35 0.68 0.09 1 1 0.046 0.94 0.17 <0.001
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Variable
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LAD, left anterior descending; SD, standard deviation; n, number; HC, hypertrophic cardiomyopathy; NYHA, New York heart association. Variables are expressed in (mean±SD) or number (%).
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Table (2): Procedural and Long-Term Outcomes of Patients Who Underwent Alcohol Septal Ablation
Septal Perforator Arteries
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of a Typical (Left Anterior Descending) and Atypical (Non- Left Anterior Descending)
LAD Septal (N=76)
Non-LAD Septal (N=13)
P value
Cath Resting Gradient (mean±SD) Cath Provoked Gradient Left Ventricular End Diastolic Pressure Number of Septal Perforator Treated Septal Perforator Size Ethanol Volume (ml) Post Ablation Resting Gradient Post Ablation Provoked Gradient Fluoroscopy Time Contrast Volume (cc) Creatine Kinase (unit/liter)* Creatine Kinase Isoenzyme MB** Temporary Pacemaker Needed Permanent Pacemaker Implantation Cardioverter Defibrillator Implantation Coronary Artery Dissection Length of Stay In-Hospital Death Echo Resting Gradient at 1 month Echo Provoked Gradient at 1 month NYHA Class at 1 month Death During Maximum Follow up
81.3±37 156.5±50 19.6±7.9 1.2±0.4 2.3±0.4 2.6±1 7.7±4.8 38.3±37.6 20.1±14.7 143±86 1072±612 126±70 26 (34%) 12 (16%) 2 (2.7%) 0 (0%) 2.7±1.7 0 (0%) 18±12.5 29.2±24.5 1.2±0.5 2 (2.6%)
85.4±35 154.3±37 21.1±5.8 2.1±0.9 2.0±0.1 3.9±1.1 4.7±4.0 37.7±29.3 29.1±12.6 196±97 863±361 99±37 4 (31%) 1 (8%) 0 (0%) 1 (8%) 2±0 0 (0%) 21±18 26.4±22.5 1.3±0.5 0 (0%)
0.1 0.88 0.51 <0.001 0.009 <0.001 0.036 0.95 0.04 0.047 0.23 0.18 1 0.68 1 0.15 0.14 1 0.45 0.7 0.5 1
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Variable
LAD, left anterior descending; SD, standard deviation; n, number; NYHA, New York heart association;. Variables are expressed in (mean±SD) or number (%). * Normal range for Creatine Kinase is 46-171 units/liter. ** Normal range for Creatine Kinase Isoenzyme MB is 0-10.4 ng/mL.
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Table (3): Procedural Details of Patients who Underwent Alcohol Septal Ablation of
2 2 3 3 1 2 1 3 3 2 3 1 1
LAD, Ramus LAD, Left Main LAD, Ramus LAD, Ramus Right LAD, Right Ramus LAD, Right LAD, LPDA LAD, Right LAD, Ramus Diagonal Ramus
Ramus Left Main LAD LAD Right Right Ramus LAD LAD LAD LAD Diagonal Ramus
r-LVOT gradient at beginning of the procedure*
r-LVOT gradient at end of the procedure*
NA NA NA NA NA NA NA 7 24 8 14 8 44
187 110 78 160 45 30 62 170 55 150 45 52 73
12 8 0 0 5 0 5 8 5 10 0 0 5
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N N N N N N N Y Y Y Y Y Y
Time since prior ASA
NA NA NA NA NA NA NA 8 5 45 5 5 8
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1 2 3 4 5 6 7 8 9 10 11 12 13
r-LVOT # of Coronary origin 1st gradient at Septal of Treated Septal end of Treated* Septals* Treated* prior ASA
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Subject
Prior LAD Septal ASA
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Non-Left Anterior Descending Septal Perforator Arteries
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LAD, left anterior descending; ASA, alcohol septal ablation; r-LVOT, resting left ventricular outflow gradient; LPDA, left posterior descending artery; NA, non-applicable * data at the time of second procedure if the patient had a prior ASA. Gradient is expressed in mmHg.
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