Hypertrophic Cardiomyopathy: Surgical Perspectives

Abstract

Hypertrophic cardiomyopathy is a unique myocardial disorder that can present in all ages from neonate to adults and has strong genetic basis. Several key features characterize hypertrophic cardiomyopathy. These include: the presence of left ventricular hypertrophy that can not be explained by another etiology, and left ventricular outflow tract obstruction secondary to systolic anterior motion of the anterior mitral valve leaflet with varying degrees of mitral valve regurgitation. Surgical septal myectomy continues to be the standard line of treatment when medical therapy fails or become intolerable. We summarize in the current chapter the technical tips and pitfall of septal myectomy, its alternatives/adjuncts and its outcomes.

1. Introduction: history

Brock and Teare in 1958 reported the first pathological case that drew the attention to HCM, while the first surgical procedure to address HCM was credited to Cleland and colleagues in the same year [1]. The “Morrow” operation was the main surgical procedure for years since it was initially reported by Morrow and Brockenbrough in 1960 [2].

Mitral valve replacement has been historically considered a way of eliminating the LVOTO by eliminating SAM, however with appropriate and complete septal myectomy, this is rarely considered an option in the current era except in the presence of unrepairable concomitant mitral valve disease.

Surgical septal myectomy; however, has evolved over the years from the traditional “Morrow” operation to the current “extended left ventricular septal myectomy” to ensure complete elimination of recurrence or residual LVOTO as will be discussed in the current chapter.

2. Background

Hypertrophic cardiomyopathy (HCM) is a unique myocardial disorder that is characterized by the presence of dynamic left ventricular outflow tract (LVOT) obstruction (LVOTO) and systolic anterior motion (SAM) of the anterior mitral valve leaflet with resultant various degrees of mitral regurgitation. HCM was previously known as idiopathic hypertrophic subaortic stenosis (IHSS) or asymmetric septal hypertrophy which is due to the presence of left ventricular hypertrophy that can not be explained by other pathology. Another key feature in this unique disease.

HCM has been one of the main causes of sudden death in young adults and athletes. Patients may present with a variety of clinical pictures that range from completely asymptomatic to exertional fatigue, chest pain, and/or shortness of breath.

The first line treatment in HCM continued to be medical therapy especially in those symptomatic with LVOTO [3]. Septal reduction therapy should be considered for those who failed or became intolerant to medical therapy [4].

3. Morphological variants of hypertrophic cardiomyopathy

HCM is characterized by varying degree of septal hypertrophy and this led to the emergence of several morphological variants of HCM. These variants include basal septal hypertrophy, apical, midventricular or combination of any [5]. A key feature in the basal variant is the presence of SAM of the anterior mitral valve leaflet, while a key feature in the apical variant is the presence of small left ventricular cavity and absence of SAM.

Recognition of these variants is critical especially when considering patients for septal reduction therapy to ensure delivering the right modality and decrease the chance of persistence or recurrence of the LVOT obstruction.

4. Current indications for septal myectomy

Surgical septal myectomy should be considered for those symptomatic patients who failed medical treatment or for those who are intolerant to medical therapy. Morphological variants may play a role in proceeding with surgery as well. Variants like apical and midventricular level of obstruction are difficult to manage medically and do not respond to Alcohol septal ablation.

5. Surgical approaches for septal myectomy

Understanding the different morphological variants of HCM is critical in selecting the right surgical approach for the patient. This ensures elimination of the LVOT obstruction and minimizes if not prevents any residual/recurrent significant gradient/obstruction.

The procedure is done through a standard median sternotomy with central aortic and single venous (right atrial) cannulation. Although septal myectomy has been reported via a minimally invasive approaches such as endoscopic [6] and robotic [7], we do believe median sternotomy should be considered the gold standard for these cases as it provides adequate exposure to the heart and mediastinal structures and facilitates performing all maneuvers that are needed to facilitate exposure to the interventricular septum and performance of an adequate septal myectomy.

Prior to venous cannulation, we measure the gradient across the LVOT directly by placing a needle in the distal ascending aorta and another one in the left ventricular cavity (via the right ventricle free wall) simultaneously (Figure 1A and B). This measures the resting LVOT gradient (Figure 2) and then provocative maneuvers are performed. These maneuvers are important to evaluate the LVOT gradient as it occurs with exercise. A variant of HCM is known as “Latent obstruction” will be discussed later but patients with this variant do not have any significant gradient at rest but they do with exercise. These provocative maneuvers can be either an induction of a premature ventricular contraction (Brockenbrough-Braunwald-Morrow) (Figure 3) or administration of isoproterenol.

Figure 1.

Intraoperative photos showing the technique of direct pressure measurement of the left ventricular outflow tract gradient prior to initiation of cardiopulmonary bypass. In (A), a needle is placed in the distal ascending aorta, and in (B) the second needle is placed into the left ventricular cavity indirectly via the free wall of the right ventricle (RV) and the interventricular septum. PA: Pulmonary artery; RV: Right ventricle.

Figure 2.

Intraoperative pressure tracing showing the resting left ventricular outflow tract gradient by direct needle pressures. The left ventricular pressure is in white, while the aortic pressure is in light blue colors. LVOT: Left ventricular outflow tract.

Figure 3.

Intraoperative pressure tracing from the same patient showing positive Brockenbrough-Braunwald-Morrow maneuver by induction of premature ventricular contraction. The left ventricular pressure (white color) increased, while the aortic pressure (light blue) decreased, resulting in significant left ventricular outflow tract gradient.

This will be repeated after coming off cardiopulmonary bypass to document elimination of any significant gradient across the LVOT. Based on the variant of septal hypertrophy and the level of obstruction, the technique of myectomy may differ or be a combination of the following:

5.1 Trans-aortic myectomy

This is the most common approach and is used for the most common variant which is basal or subaortic obstruction. The technical details have been described before [8]. Once the heart is arrested with antegrade cardioplegia, a hockey-stick aortotomy is performed down to the base of the non-coronary sinus of Valsalva. The aortotomy in these cases has to be a bit lower than standard aortotomy for aortic valve replacement to provide adequate exposure to the LVOT.

Stay sutures are then applied and the LVOT is assessed. This is a 360-degree visual assessment of the LVOT and the mitral apparatus prior to performing any resection (Figure 4). The result of this assessment determines the degree of septal bulge, how far down in the left ventricular cavity the resection has to extend, the abnormalities that may coexist in the mitral subvalvular apparatus such as anomalous chordae (Figure 5) and/or papillary muscles. These all can lead to persistent or recurrent LVOT gradient. A variety of instruments – seen in Figure 6- are needed to perform the myectomy.

Figure 4.

The anatomic landmarks of the left ventricular outflow tract after performing the aortotomy and prior to the myectomy. The area of the interventricular septum (IVS) is visualized, as well as the membranous septum (*) where resection should be avoided. The mitral valve (MV) is visualized deep in the left ventricle. RCA: Right coronary artery ostium; RCC: Right coronary cusp; LCA: Left coronary artery ostium; LCC: Left coronary cusp; NCC: Non-coronary cusp; MV: Mitral valve; IVS: Interventricular septum.

Figure 5.

An intraoperative view through the aortotomy showing an anomalous mitral valve chord in the left ventricular outflow tract. These chordae can result in persistent or recurrence of gradient after an initial myectomy as it limits the mobility of the anterior mitral valve leaflet and can result in persistence of systolic anterior motion (SAM).

Figure 6.

The variety of surgical instruments that are useful during the myectomy procedure. Different types of surgical blades, aortic cusp retractors, pituitary Rongeurs to help with removal of the muscle pieces.

The resection then starts below the nadir of the right coronary cusp (Figure 7) and extends in an anti-clockwise direction towards the commissure between the left and non-coronary cusps. Scissors are then used to complete the resection. This is the initial resection which serves to widen the subaortic area and facilitates further access to the left ventricular cavity. Further resection has to be performed along the interventricular septum and towards the left ventricular apex to ensure complete elimination of any residual gradient. Some maneuvers can help with exposing that part of the septum such as placing a sponge stick on the free wall of the right ventricle that helps bringing the interventricular septum in view (Figure 8). The area of resection is further widened as we go deeper into the ventricular cavity which what makes this “extended” in comparison to the initial “Morrow” operation.

Figure 7.

The resection starts below the nadir of the right coronary cusp (RCC) and goes into anti-clockwise direction towards the anterior mitral valve leaflet and chordal structures (*). RCC: Right coronary cusp; LCC: Left coronary cusp; NCC: Non-coronary cusp.

Figure 8.

One of the helpful maneuvers to facilitate exposure of the lower part of the interventricular septum is using a sponge stick (*) to depress the free wall of the right ventricular and rotate the septum, thus bringing it in view to the surgeon.

A proper septal myectomy is a 3-dimensional operation in regards to the extent of resection [9], and all other potential causes of recurrent/residual LVOT obstruction have to be addressed such as resection of anomalous papillary muscles and/or chordae (Figure 9). The aortotomy is then closed in two-layers and the heart is de-aired and the aortic cross clamp is removed.

Figure 9.

The completed myectomy specimen with two anomalous chordae. Notice the contact lesion (white scar) on the resected specimen. This occurs as a result of the anterior mitral vale leaflet hitting the septum during systole (systolic anterior motion).

5.2 Trans-apical myectomy

Trans-apical approach can be done for one of three main indications: (1) midventricular variant, where the transaortic approach may not be adequate, (2) apical variant, and (3) in those patients who do not have adequate left ventricular cavity and non-obstructive variant of HCM where left ventricular enlargement can be performed to improve their left ventricular end-diastolic volume.

We have described the technique previously [10], but briefly, after the cardioplegic arrest, the left ventricular apex is delivered into the field and the left anterior descending (LAD) coronary artery is identified. An apical incision is done 1 cm to the left and parallel of the LAD (Figure 10). In the apical variant, the left ventricular apex is quite obliterated with muscles and it is critical to stay on the interventricular septum side (Figure 11) to avoid risk of injury of the mitral valve papillary muscles which are usually apical displaced and hypertrophied in these cases (Figure 12). Once the left ventricular cavity is entered, further resection is performed and the cavity is further widened. The apex is then closed in two layers and suture line is supported with Teflon felt.

Figure 10.

An apical incision is made in the left ventricular apex which facilitates myectomy in patients with midventricular and apical hypertrophic cardiomyopathy.

Figure 11.

A view through the opened left ventricular apex showing the resected muscle specimen-in progress- and the interventricular septum (IVS). It is important for the surgeon to stay on the IVS side during resection till he/she able to visualize the papillary muscles of the mitral valve to avoid inadvertent injury to the mitral subvalvular structures. IVS: Interventricular septum.

Figure 12.

After the resection, the left ventricular cavity now is widened and the mitral valve subvalvular structures can be easily visualized.

5.3 Trans-mitral myectomy

This is a left atrial approach to the interventricular septum through the mitral valve. It has been used by some authors as an alternative to the transaortic approach but it requires detachment of the anterior leaflet of the mitral valve followed most likely by patch augmentation after completing the resection [11]. One has to be familiar with this approach as the anatomy of the interventricular septum differs through this approach compared to the trans-aortic exposure.

We believe this may be more of value in children and those with small aortic root where the trans-aortic approach may not be adequate. Another potential advantage is that it helps addressing the mitral valve pathology and performing the myectomy through one incision.

6. Adjuncts to septal myectomy

6.1 Abnormalities of the mitral subvalvular apparatus

6.1.1 Papillary muscle abnormalities

Detection of papillary muscle abnormalities on preoperative echocardiogram can be challenging, therefore, it is important for the surgeon to evaluate the mitral subvalvular apparatus as part of the overall thorough evaluation of the LVOT. Anomalous papillary muscle can be a cause of persistent/recurrent gradient after an initial-what it seems like- a complete myectomy [12].

It is critical to differentiate these anomalous muscles from the true papillary muscles of the mitral valve. A key difference is the insertion of the anomalous papillary muscle into the body of the leaflet, rather than the free edge and therefore, it can be excised safely.

6.1.2 Anomalous chordae

These anomalous chordae are attached to the body of the anterior mitral valve leaflets and not to the free edge which helps differentiating these chordae from primary chordal structures of the mitral valve. These can limit the mobility of the anterior mitral leaflet and result in SAM as well.

Some anomalous chordae can cause adherence of the papillary muscles to the septum and cutting this helps mobilizing these papillary muscles and minimize the gradient and the chance of SAM after septal myectomy. In general, there should be no chordal attachment between the mitral valve apparatus and the interventricular septum.

6.2 Management of concomitant atrial fibrillation

Due to the elevated left ventricular end-diastolic pressure and subsequently left atrial pressure secondary to the significant LVOTO, it is not uncommon for patients with HCM to present with atrial fibrillation (AFib). Losing the atrial kick in those with HCM and diastolic dysfunction results in significant drop in their cardiac output and symptoms, therefore, it is important to maintain normal sinus rhythm in these patients [13].

Our strategy is to offer biatrial Cox-maze IV procedure using a combination of radiofrequency and cryoablation for those with chronic persistent AFib, while in those with paroxysmal AFib, bilateral pulmonary vein isolation is sufficient. Routine excision or exclusion of the left atrial appendage is part of either procedures.

6.3 Mitral valve surgery

Historically, mitral valve replacement was one of the proposed solutions to LVOTO in patients with HCM, however this is not currently the case. With adequate extended left ventricular septal myectomy, all SAM is eliminated and the mitral regurgitation-even if severe- is significantly improved if not completely eliminated.

Our approach is to perform mitral valve surgery in the settings of septal myectomy only in the presence of intrinsic mitral valve pathology and mitral regurgitation that is not the result of SAM and the dynamic nature of the LVOTO in HCM. Repair is preferred over replacement in all cases due to the long-term survival benefit of mitral repair that is documented across multiple studies in the literature. Mitral valve repair techniques may also need to be modified in these cases to avoid recreating SAM after the repair such as if a ring to be used, a one size larger may be preferred.

In some cases, when there is a question about the need for mitral valve repair or if the mechanism of regurgitation is unclear, we will perform a complete myectomy, and then come off cardiopulmonary bypass and re-evaluate the mitral valve and make the decision if interventions on the mitral valve is necessary at this stage.

If mitral valve replacement is necessary, then it is important to choose a mechanical or a low profile bioprosthesis that does not project into the LVOT and results in LVOT gradient.

6.4 Myocardial bridging

Myocardial bridging (MB) is a challenging problem in the presence of HCM. It can cause significant symptoms (chest pain) after an initial septal myectomy and at the same time not all patients with MB requires unroofing of their MB. A challenging task is to identify those who will benefit from concomitant unroofing of MB and septal myectomy. Currently no guidelines or recommendations regarding the optimal management of these patients.

Wang and colleagues reported their midterm results of different treatment methods for MB in patients with HCM after their septal myectomy [14]. A total of 823 patients were included, where the authors identified 31 events with mortality in 24 patients and nonfatal myocardial infarction (MI) in 7. The three-year cumulative event-free survival of all cause-death was 100% for both those who underwent coronary artery bypass grafting, and unroofing, however, the 3-year cumulative event-free survival of non-fatal MI and the combined endpoints were significantly lower in the un-treated group. The authors concluded that surgical treatment of MB at the time of septal myectomy is beneficial.

We do perform coronary angiography in the majority of these patients especially when the presentation is of a chest pain. If a MB is identified, a hemodynamic evaluation of the bridge is performed to determine its significance and help making the decision for concomitant unroofing.

We have described the technique previously [15] and we prefer performing the unroofing procedure on the arrested heart to avoid inadvertent injury of the coronary artery. A combination of sharp and electrocautery dissection is used to unroof the entire bridged segment (Figure 13). It is critical to remember that the bridged segment of the coronary artery is always fragile and the unroofing process has to be done with extreme caution.

Figure 13.

Intraoperative photo of a patient with hypertrophic cardiomyopathy who underwent repeat operation with unroofing of a long segment of the left anterior descending coronary artery due to missed diagnosis of myocardial bridge after his initial septal myectomy. LAD: Left anterior descending coronary artery.

6.5 Left ventricular apical aneurysm

These are outpouchings that appear at the left ventricular apex and can occur in those with HCM. The aneurysms are usually thin-walled and either dyskinetic or akinetic on echocardiographic images. It has been reported to occur in 15–30% of patients with the apical and midventricular variants of HCM [16], however detection of these aneurysms is not always straightforward. In the study by Yang and colleagues, the authors analyzed 1332 patients with apical HCM with cardiac magnetic resonance imaging (cMRI), and 31 patients had an apical aneurysm (2.3%). The rate of missed diagnosis of apical aneurysms by echocardiogram was 64.5% [17].

Several adverse events have been reported with apical aneurysms such as ventricular arrhythmias, heart failure and up to sudden cardiac death. These apical aneurysms are not amenable to medical treatment and in many cases, surgical resection is recommended at the time of septal myectomy [18]. In those with midventricular obstruction, access to the left ventricular cavity can be facilitated through the aneurysm with less risk of injury to the mitral valve apparatus. Small aneurysms can be plicated, while larger ones should be resected.

6.6 Internal cardioverter defibrillator (ICD) placement

Those with risk factors of sudden cardiac death and history of sustained ventricular tachycardia/fibrillation benefit from placement of internal cardioverter defibrillator (ICD) [19].

Several strategies and techniques have been proposed for placement of ICD such as endovenous, subcutaneous [20] and epicardial (Figure 14A and B). If the patient did not have ICD prior to surgery, and meets the criteria, our practice is to place the ICD prior to hospital discharge after septal myectomy. In children, the preference has been to perform concomitant myectomy with epicardial ICD placement through the sternotomy incision.

Figure 14.

In children who needed an internal cardioverter defibrillator placement, the procedure is usually done after completion of the myectomy where an epicardial system is placed and the defibrillator coil (visualized in figure A) is secured to the pericardium below the phrenic nerve, while the sensing epicardial leads are secured to the epicardial surface of the right ventricle (seen in figure B) and the device is placed in the epigastric area behind the rectus abdominis muscle.

7. Alterantive surgical options to septal myectomy

7.1 Mobilization of the right and left fibrous trigones

Yacoub et al. has pioneered this technique as an alternative to septal myectomy in those with obstructive type of HCM [21]. It is based on the role of the right and left fibrous trigones in the functional anatomy of the LVOT. The authors proposed that LVOTO is secondary to connection of the both the right and left fibrous trigones by a complete fibromuscular ring which is needed to be excised and both trigones be mobilized to ensure complete relief of the LVOT gradient.

After resection of a fibromuscular wedge of tissue from the interventricular septum, the left fibrous trigone is mobilized be extending the incision laterally to open the hinge mechanism between the septum and the subaortic curtain. Mobilization of the right fibrous trigone is done by excision of a wedge of abnormal tissue in the angle between the membranous septum and the subaortic curtain.

7.2 Modified Konno procedure

While extended left ventricular septal myectomy is considered the gold standard surgery for HCM with obstruction, the procedure is quite challenging in young children and in those with right ventricular outflow tract (RVOT) obstruction.

Modified Konno emerged as an alternative and another tool in the box for some of these cases. The procedure is performed after cardioplegic arrest by making a transverse incision in the (RVOT) and through the aortotomy, a right-angled instrument is passed and used to perforate the interventricular septum. This provides the upper limit for the septal incision. The conal septum is then incised towards the apex and away from the conduction tissue. Myectomy is performed on both sides of the septum, followed by patch closure of the created ventricular septal defect.

The long-term results of modified Konno have been reported in 79 patients with 38% of them below the age of five years, and 25% had Noonan syndromes with RVOTO present in 28% of them. Survival without death or transplantation was 82% at 20 years [22].

8. Latent obstruction

A subgroup of HCM patients have symptoms despite what appears to be a low LVOT gradient at rest and it is important to differentiate between diastolic dysfunction and labile LVOT gradient as an etiology for their symptoms. It is critical in evaluating these patients, to perform provocative maneuvers such as exercise, amyl nitrite, and/or Valsalva maneuver. If provocative maneuvers revealed significant LVOT gradient, the patient should be offered septal myectomy as symptoms in these patients are related to a latent form of obstruction rather than to diastolic dysfunction.

A report of 249 patients with latent obstruction (gradient <30 mmHg at rest) was compared to those who had severe LVOT gradient at rest and both underwent septal myectomy. Early mortality was 1% with comparable long-term survival to that of an age-matched population [23].

9. Recurrent left ventricular outflow tract obstruction after septal myectomy

With complete and proper septal myectomy (Figure 15), recurrence is quite low, especially in adults. As discussed previously, anatomic causes of recurrence such as mitral subvalvular abnormalities (anomalous papillary muscles, and anomalous chordae) should be ruled out during the initial myectomy to avoid reoperation or persistence/recurrence of symptoms.

Figure 15.

Intraoperative tracing after a complete myectomy showing no resting gradient between the left ventricle and the aorta with negative Brockenbrough-Braunwald-maneuver.

Other possible etiology includes unidentified midventricular obstruction which is being unmasked by the initial subaortic resection. Muscle growth is rare to occur in adults and is most likely to occur in those with congenital subaortic stenosis.

The following mechanisms were identified in more than 50 patients with redo myectomy: limited initial myectomy, midventricular obstruction, and anomalous papillary muscles [24]. The repeat septal myectomy remains safe and feasible and should be the main treatment for those with recurrent/persistent LVOT gradient after initial limited resection.

10. Septal myectomy after alcohol septal ablation

Alcohol septal ablation (ASA) has been considered as an alternative to septal myectomy in suitable patients. It relies on septal artery ablation with subsequent reduction in the basal septal thickness. We do believe it is an alternative for high risk patients and those who deemed not suitable for standard surgical septal myectomy.

However, it is important to be aware that patients who require septal myectomy after ASA are at high risk for needing a permanent pacemaker and have lower survival compared with those who receive primary surgical septal myectomy [25]. ASA results in right bundle branch block and standard myectomy will result in left bundle branch block (Figure 16), thus increasing the chance for needing permanent pacing after surgery.

Figure 16.

It is not uncommon after septal myectomy to have a left bundle branch block as visualized on this patient postoperative electrocardiogram.

There are also some anatomic substrates that will not be suitable for ASA such as the midventricular and apical variants so as those with significant basal septal thickness (3 cm or more) where surgical septal myectomy would be considered the first line septal reduction modality.

11. Right ventricular myectomy

A subgroup of patients with HCM, particularly in association with genetic syndromes such as Noonan’s, can present with biventricular outflow tract obstruction. This is important to recognize during their evaluation and especially if they are being offered surgical myectomy on the left side.

Septal myectomy on the right side is a bit different from the left side. Shaving on the right side of the interventricular septum has to be done with caution to avoid injury to conduction tissue and/or the tricuspid valve apparatus which is different from the left side where there is no septal attachment to the mitral valve. This is usually done through an infundibular incision, followed by patch augmentation of the RVOT (Figure 17) [26].

Figure 17.

Right ventricular septal myectomy is done through an incision in the right ventricular outflow tract (RVOT) followed by patch augmentation after completion of the myectomy. RVOT: Right ventricular outflow tract.

12. Outcomes

12.1 Surgical outcomes in adults

In a report form Mayo Clinic, the risk of hospital death after isolated septal myectomy for obstructive HCM is less than 1%. Reported complications after septal myectomy such as need for permanent pacemaker secondary to complete heart block, and iatrogenic ventricular septal defect occur in about 2% of patients and are considered uncommon. Approximately 90% of patients reported significant improvement in their symptoms after extended left ventricular septal myectomy. Late survival after myectomy has been also reported to be equivalent to an age-matched population and the risk of ICD discharges decreased significantly with elimination of the LVOT obstruction [27].

The transapical approach has been reported in 113 patients with apical HCM. Early mortality was 4% and at late follow-up, 76% of these patients reported improvement in their symptoms. Three patients (3%) underwent heart transplantation due to recurrent heart failure. Survival of this group was superior in comparison to those waiting for heart transplantation [28].

12.2 Surgical outcomes in children

Children with HCM can present in a similar fashion to adults, with a wide variety of presentations. These symptoms are mostly related to a combination of diastolic dysfunction and significant mitral regurgitation. Sudden death as an initial presentation is more common in children compared to adults [29].

The operation is technically more challenging in children compared to adults due to the obvious anatomic barriers secondary to the small aortic annulus and LVOT. A report from Mayo Clinic included 127 patients who underwent septal myectomy with age ranging from 2 months to 21 years old. There was no early mortality, and the most common concomitant procedures were resection of accessory papillary muscles, mitral valve repair, and closure of an atrial level shunt. Complications included two patients with iatrogenic injury to the mitral valve and seven with aortic valve injury and all were repaired. One iatrogenic ventricular septal defect occurred. There were four late death but the remaining patients reported improvement of their symptoms with 96% being in NYHA class I or II. Repeat septal myectomy was needed in six patients [30].

12.3 Septal myectomy versus alcohol septal ablation

ASA as mentioned previously has emerged as an alternative to surgical septal myectomy. It can decrease the gradient in the LVOT and improve symptoms, however several studies confirmed the better long-term symptom relief by surgical septal myectomy.

The success rate for septal myectomy is higher and the complication rate is lower when it is performed with experienced hands. In a report of 138 patients who underwent ASA, mortality and morbidity were higher than that of age- and gender-matched population who underwent septal myectomy [31]. Survival with septal myectomy is also better in those 65 years of age or younger, in addition to the immediate relief of LVOT gradient and symptoms that is provided by proper septal myectomy.

As mentioned earlier patient selection is a key for either procedure and important to be aware with the risks inherent in those who will undergo septal myectomy after ASA prior to committing them to ASA.