Treatment of Symptomatic Left Ventricular Outflow Tract Obstruction

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Summary

Treatment of Symptomatic Left Ventricular Outflow Tract Obstruction

Currently, there is no evidence that asymptomatic patients with LVOTO benefit from treatment to reduce the severity of obstruction; treatment is reserved for patients with LVOTO and drug-refractory symptoms.^43,44 A contemporary treatment algorithm for symptomatic patients with LVOTO is summarised in Figure 3. The first-line treatment for symptoms associated with LVOTO is correction of exacerbating factors (e.g. vasodilating antihypertensives, anaemia) followed by pharmacological therapy with β-blockers, verapamil and disopyramide, which modulate the dynamic physiology of obstruction through their negative inotropic and chronotropic effects.^43–46 In patients with drug-refractory symptoms or unacceptable side effects, invasive treatments should be considered by a multidisciplinary team following a comprehensive evaluation of the mechanism of obstruction:

• Surgical myectomy involves excision of the hypertrophied septum at the point of mitral contact through an aortotomy under cardiopulmonary bypass.⁴⁷ Surgical myectomy is a technically demanding operation, but with improved peri-operative care and surgical techniques the current peri-operative mortality is low in high volume centres. In addition to the general complications of open heart surgery, specific peri-operative complications of myectomy include ventricular septal defects, aortic regurgitation and complete heart block requiring pacemaker implantation.^48,49
• Mitral valve repair/replacement may be required as an adjunct to myectomy.^50–52 Mitral valve replacement in isolation also abolishes SAM and LVOTO, but is considered only when there are other indications for valve replacement such as intrinsic mitral valve disease.^53,54
• Alcohol septal ablation aims to reproduce the effects of myectomy via a minimally invasive percutaneous approach.^55,56 Ethanol is injected via the septal perforator branches of the left anterior descending artery to the hypertrophied septum to induce a myocardial infarction and necrosis. Scar formation causes remodelling of the LVOT with relief of obstruction. ASA is discussed in more detail below.
• Atrioventricular (AV) sequential pacing from the right ventricular apex using dual-chamber pacemakers with short AV delay reduces LVOTO by causing septal dysynchrony and modifying preload.⁵⁷ Placebo-controlled trials showed an improvement in symptoms but with a less consistent reduction in LVOTO.^58–62

ASA is currently the most frequently used invasive therapy, and while it is efficacious, relatively safe and minimally invasive, outcomes from randomised trials comparing different invasive techniques are not yet available. Several experienced opinions still regard surgical treatment as the ‘gold standard’.^43,44 Currently, patients must be counselled that choices between ASA, surgery and pacing are made on the basis of considerations other than proven differences in outcome.

In general, ASA may be unsuitable in the presence of co-existing mid-cavity obstruction and/or intrinsic mitral valve disease; in such cases a surgical approach should be considered. Septal reduction either by ASA or myectomy when the septal wall thickness is <15 mm at the site of mitral contact is also challenging, and alternatives such as mitral valve repair/replacement or AV sequential pacing should be considered. AV sequential pacing can also be useful in selected patients where aggressive pharmacological treatment with a β-blocker, verapamil and disopyramide is contemplated, and in patients too frail to tolerate more invasive treatment. In others, pacing may be considered as an initial therapeutic trial before progression to more invasive treatment. This may include individuals with conventional indicators for device therapy (including pacing and defibrillator treatment) and patients at high risk of developing heart block following invasive treatment. Patient preference is also a key factor in decision-making.