Guidelines for HOCM Treatment: A Moving Target?

Ulrich Sigwart


Eur Heart J. 2019;40(21):1688-1689. 

Hypertrophic obstructive cardiomyopathy (HOCM) is a two-component disease: there is the anatomical part (hypertrophy) and the dynamic component (obstruction); the latter phenomenon appears only during systole. Possible treatment addresses these components individually either by focusing on the dynamic part through the reduction of contractility or by focusing on the anatomical component through surgical resection.

Both treatment modalities were introduced more than half a century ago in the UK: the pharmacological reduction of overall myocardial contractility through beta-blockers by Sir James Black[1] and/or calcium channel blockers such as verapamil, and the surgical removal of excessive obstruction (Figure 1) by Cleland upon the suggestion of Lord Brock.[2] An alternative to surgery was launched a quarter of a century later when a small amount of a toxic substance, i.e. 96% alcohol, was locally injected via catheters with the intention to address both problems in patients in whom the pharmacological reduction of contractility did not suffice.[3] The procedure is nowadays known as alcohol septal ablation (ASA). In contrast to the surgical removal of the excessive tissue which obstructs the ejection of blood from the left ventricular outflow tract to the aorta during systole, ASA locally reduces septal myocardial contraction immediately as well as volume during the healing process (Figure 2A and B). The procedure is crucially dependent on the individual blood supply and the speed of administration and volume of the injected toxin.

Figure 1.

Surgical resection of obstructing septal myocardium within the left ventricular outflow tract.

Figure 2.

(A) and (B) Creation of a localized myocardial infarction after septal alcohol injection immediately (left) and following shrinkage some 8 weeks later.

The first patients treated in June 1994 suffered from severe, highly symptomatic myocardial hypertrophy with impressive outflow tract gradients resistant to drug treatment and right ventricular pacing. They refused surgical myectomy, which made them acceptable for this type of 'experimental' therapy. Guidelines created by the American Heart Association and by the European Society of Cardiology regarding the indication for alcohol ablation or surgical myectomy appeared much later.[4,5] They specified that the thickness of the interventricular septum should measure at least 16 mm—evaluated by echocardiography—mainly in order to avoid the occurrence of septal defects. As the majority of HOCM patients present with this type of septal hypertrophy, most clinicians followed the recommendations proposed by the guidelines.

The retrospective analysis of 1505 consecutive ASA procedures from high-volume European centres published in this issue of the European Heart Journal addresses this particular topic.[6] The authors used propensity scoring to match 172 pairs (344 patients) divided into echocardiographically measured interventricular septal thickness of >16 mm or up to 16 mm. The mean follow-up was 5.4 ± 4.3 years.

Interestingly, no septal defects occurred in either group, and there were no early (up to 30 days) deaths in the thinner septum patients. The need for pacemaker implantation, however, was slightly higher in patients with a lower septal thickness (13% vs. 8%). During long-term follow-up, more patients died with septal thickness >16 mm (3.2 deaths per 100 patient-years) as compared with 1.8 for the thinner septum group; details of the cause of death, however, are not reported in this paper. Repeat interventions were carried out more frequently in patients with a greater degree of hypertrophy.

The overall amount of alcohol injected was slightly higher in patients with a thicker septum, which indicates the desire to adjust the volume of toxic substance to the volume of the observed target. The authors do not give an explanation regarding a common strategy addressing recommended volume, possibly in relation to septal thickness, nor do they indicate the speed of injection. This may turn out to be a confounding factor.

This analysis, despite a few shortcomings, calls for a timely adaptation of the existing guidelines. It took more than a decade and a half to produce the first published recommendations for the treatment of HOCM. It is now urgent to implement facts that have appeared over the last quarter of a century on the application of an alternative to surgical myectomy in HOCM. It may also be useful to implement some practical tips such as ways to identify the target vessel, the amount of alcohol injected, and the speed of injection in order to standardize the procedure. Regarding the indication for invasive therapy, i.e. ASA vs. surgical myectomy, the revised guidelines ought to avoid obsolete recommendations regarding age limits of either treatment option or septal thickness.

It is unfortunate that the heated debate about the best treatment for symptomatic HOCM continues among surgeons and cardiologists. After 25 years of experience with a less invasive interventional approach, it appears that the time has come to perform a randomized international trial comparing ASA with surgical myectomy within a few highly experienced high-volume centres.