Catheter Treatment for Hypertrophic Obstructive Cardiomyopathy

ypertrophic cardiomyopathy is a relatively recent con- cept. It occurs not infrequently; 1 in 500 individuals within the general population is a carrier of the disease.1 The main genes responsible for hypertrophic cardiomyopathy have been characterized and can be determined with relative ease.2 Some patients develop subaortic obstruction. The original term, idiopathic hypertrophic subaortic stenosis, dates to 1964;3 since then, it has become obvious that the obstructive component has its own prognostic meaning. The obstruction occurs in 25% of all humans with hypertrophic cardiomyopathy,4 and the entity is now called hypertrophic obstructive cardiomyopathy. Article p 131 Surgery for elimination of the obstructive element via resection of the subaortic septal bulge (myectomy) has been, since its introduction by Cleland at the Brompton in London exactly half a century ago, the only rational option for patients with clinically relevant left ventricular outflow tract obstruction that is refractory to optimal medical therapy. At experienced centers, the operation can be performed with low mortality and excellent clinical improvement.5 The concept of using transluminal techniques to reduce septal hypertrophy in patients with hypertrophic obstructive cardiomyopathy was not based on the hope of achieving better results than with surgery, but primarily to reduce morbidity. In the early 1980s, while performing coronary angiography on patients with hypertrophic obstructive car- diomyopathy, I noticed that in some patients, the first septal perforator branches appeared to irrigate primarily the area of the septal bulge responsible for outflow tract obstruction. During systole, these branches seemed to be compressed by the surrounding hyperabundant myocardium. Interfering with the proper irrigation of this territory became only logical with the advent of intracoronary manipulations, and the temporary gradient reduction observed when a regular