Tools and Techniques: Alcohol septal ablation for hypertrophic obstructive cardiomyopathy

. It is associated with an increased risk of arrhythmic sudden cardiac death and heart failure either from diastolic (or in later stages systolic) dysfunction or left ventricular outflow tract obstruction with or without mitral regurgitation 2 . At rest, a left ventricular outflow tract obstruction is seen in 25% of patients (hypertrophic obstructive cardiomyopathy, HOCM) 3 . Importantly, this is a dynamic phenomenon. A significant pressure gradient is seen in the majority of HCM patients with exercise or provocative manoeuvres 4 . It is the consequence of severe basal interventricular septal hypertrophy causing (via its interaction with the mitral valve) a left ventricular outflow tract gradient very similar to the gradient seen in patients with aortic valve stenosis. Though bulging of the hypertrophic asymmetric interventricular septal muscle itself with a reduction in the outflow tract diameter and area may contribute to the creation of the gradient, the most important mechanism is systolic anterior motion (SAM) of the anterior mitral valve leaflet into the outflow tract 5-10 caused by a Venturi effect due to high flow velocities as well as by displacement of the mitral valve apparatus toward the outflow tract 11 . In addition, in some cases, the abundant and elongated mitral support structures facilitate systolic anterior mitral leaflet motion 12 . Furthermore, SAM changes the geometry of the mitral valve during systole allowing mitral regurgitation 13-15 . Both outflow tract gradients and mitral regurgitation can cause an important increase in diastolic left ventricular and atrial pressure, causing shortness of breath and eventually heart failure and reduction in myocardial perfusion pressure at the level of the subendocardium due to an increase in left ventricular wall stress causing angina pectoris. In cases of severe outflow gradients, syncope, frequently with exertion, may occur. The outflow tract obstruction is dynamic. Any manoeuvres or interventions that cause a reduction in left ventricular cavity size such as shortening the diastolic filling time (tachycardia), Valsalva manoeuvre, standing from a sitting position, the administration of preload reducing agents such as nitrates or inotropic agents or exercise will reduce the left ventricular cavity size, thereby increasing the outflow tract gradient and exacerbating symptoms. Likewise, any interventions that increase the cavity size such as increasing the diastolic filling time, squatting, increasing preload or administration of negative inotropic agents may diminish symptoms. This has been the basis for the recommended avoidance of preload reducing agents and for the administration of agents that have negative chronotropic and inotropic properties such as beta-blockers, calcium channel blockers and disopyramide. Though disopyramide may decrease the outflow tract gradient at rest 16 , beta-blockers diminish the gradient only with exertion 17