Surgical Versus Alcohol Septal Ablation for Hypertrophic Obstructive Cardiomyopathy

Since the original description of hypertrophic cardiomyopathy by Donald Teare1 and Lord Brock2 nearly 50 years ago, management of this condition has attracted the attention of surgeons,3–5 clinical and intervention cardiologists,6–10 epidemiologists,11 and, more recently, molecular biologists. To date, the emphasis has been directed toward symptomatic patients or those who are at high risk of dying or developing severe symptoms. The association between left ventricular outflow tract obstruction and poor outcome was recognized since the initial description of the condition, which resulted in Lord Brock attempting to surgically dilate the left ventricular outflow tract (LVOT). More recently it was shown that the LVOT obstruction is an independent predictor of progression to severe symptoms of heart failure and death,7 and this has stimulated additional intensive studies to define the exact pathophysiology of the obstruction. Although the main cause of the obstruction is the abnormal bulge of the interventricular septum into the outflow tract, the mitral valve plays an important role in producing the obstruction with echocardiographic demonstration of systolic anterior motion (SAM) of the mitral valve, SAM being an essential feature12,13 of diagnosing obstruction. The cause of SAM is multifactorial and is thought to be produced by the Venturi effect, which is produced by acceleration of blood secondary to the septal bulge and upward displacement of the line of coaptation of the posterior to the anterior leaflet of the mitral valve, ending in a more mobile distal part of the anterior leaflet. Other factors include anterior displacement of the anterior papillary muscle14 and fusion of the papillary muscle to the lateral left ventricular wall as well as other structural abnormalities. The close interaction between the mitral valve and LVOT stems from the fact that the 2 structures share the same orifice in the …