Golden jubilee of hypertrophic cardiomyopathy: is alcohol septal ablation the gold standard?

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Abstract

In the golden jubilee year of the first recognition of hypertrophic obstructive cardiomyopathy, we are discussing the intricacies and impact of alcohol septal ablation (ASA) in the treatment of this clinical entity. Since its first revelation 14 years ago, ASA has become a well-established treatment modality for symptomatic hypertrophic obstructive cardiomyopathy patients. With better recognition of the implication of first septal branch and right dose of alcohol to be used for ablation, the incidence of complications like complete heart block are coming down along with better procedural success rates. In appropriately selected patients and in expert hands ASA has produced excellent results. Surgical myectomy, even though it has produced excellent results, is available only at a few centers and patient preference is tilted more for a less invasive procedure like ASA. This has contributed towards far more ASAs being performed worldwide than surgical myectomies. While more than 5000 ASAs have been performed in the last 14 years, the number of patients who have had myectomy remains around 3000–4000. The pendulum of gold standard may have started swinging away from surgical myectomy towards ASA.

Section snippets

The idea

The idea of septal ablation originated in the early 1980s, at the University of Lausanne in Switzerland. While studying the hemodynamics of left-sided cardiac chambers in patients with HOCM, Sigwart and the late Dr. Grbic [5] found significant reduction in left ventricular outflow tract gradient when angioplasty balloon was inflated in the first septal artery. This was further supported by the disappearance of the typical auscultatory findings, carotid pulse, and echocardiographic

Clinico-anatomical correlates

Basal interventricular septal hypertrophy and its related septal arterial branches are the core component of ASA. Recently, Angelini [8] has defined this as a new anatomic-functional entity, the first septal unit. Asymmetric septal hypertrophy (ASH) of the basal interventricular septum and systolic anterior motion (SAM) of the anterior mitral leaflet (AML) are the two most important contributors of the LVOT obstruction (LVOTO). The AML septal contact zone is the main area of interest and the

Patient selection

Appropriate selection of the patient remains vital for the success of ASA. All patients undergoing ASA should be NYHA Class III or IV despite optimal medical therapy or are intolerant to medical therapy. The LVOTO should be >30 mmHg at rest and >50 mmHg on provocation [19], [20], [21]. ASA is largely dependent on the morphology of the first septal unit. Variation in this core structure/absence of a suitable septal perforator may preclude the use of this modality in certain patient population.

The technique

Femoral access is the preferable route for ASA. A temporary transvenous pacemaker lead is placed in the apex of the right ventricle and is kept for 48 h postprocedure. The septum is avoided as the pacing site, because fluctuation in pacing threshold may occur during the procedure due to the proximity of this region to the target area for ASA. Baseline left ventriculogram is performed to assess the mitral regurgitation and the site and extent of hypertrophy. LVOTO is assessed by Doppler

Pathophysiological changes

ASA results in coagulative necrosis of both the myocardium and septal perforator arteries. Affected arteries are filled with necrotic debris and lack platelet-fibrin thrombi. In the later stages, there is a development of dense scar with adjacent area of viable myocytes [32]. Single-photon emission computed tomography imaging following ASA has shown the basal ventricular septal infarcts to be <10% of the LV myocardium. Perfusion abnormality decreases late after ASA without an increase in LVOTO

Clinical outcome of ASA

In a pooled analysis of 42 published studies between 1996 and 2005, Alam et al. [46] have analyzed the outcome of ASA in 2959 patients. After a mean follow-up of 12.7 months, there was a sustained reduction in resting and provocable LVOTO gradients from 65.3 to 15.8 mmHg and from 125.4 to 31.5 mmHg, respectively.

Basal septal diameter decreased from 20.9 to 13.9 mm. This was associated with significant improvement in symptoms and decrease in mean NYHA functional class from 2.9 to 1.2. Mean

Complications

Inhospital mortality ranges from 0% to 4%, and at experienced centers mortality is in a lower range even in high-risk patients [46], [48]. Complete heart block requiring permanent pacemaker is the most important complication associated with ASA. LAD dissection, remote infarction, ventricular fibrillation, stroke, pericardial effusion, and ventricular septal defects are relatively uncommon complications of ASA [46], [51], [52].

Surgery or ablation

Surgical myectomy essentially involves removal of a small segment of hypertrophied basal septum. Both surgical myectomy and ASA have their own advantages and disadvantages (Table 3). The real question remains as to the choice of procedure in a particular patient. There are no randomized controlled trials comparing these two strategies. The studies that have compared the two procedures are nonrandomized and retrospective in nature [62], [63], [64], [65], [66]. The patients undergoing ASA in

Alternate modalities

Recently, various alternative modalities in place of alcohol have been tried in an attempt to reduce the complication rates of ASA. Coils [69], polyvinyl alcohol particles [70], angioplasty wires [71], cyanoacrylate glue [72], gelatin particles [73], and radiofrequency ablation [74] are few such options. A 6-month follow-up of 20 patients after coil embolization of the septal artery has shown a significant reduction in LVOTO (from 80 to 35 mmHg) and a 0% incidence of complete heart block [70].

Conclusions

Half a century after the first well-documented description of HOCM and 14 years after its introduction, ASA has emerged as a safe and effective alternative in the management of symptomatic HOCM. Although the role of ASA vis-à-vis surgery is yet not clear, evaluation of long-term data may help in further defining the role of ASA in the management of HOCM. Given the rarity of the disease, diversity of the patients opting for a particular septal reduction therapy, and patients' inclination for a

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