Mid ventricular obstruction in hypertrophic obstructive cardiomyopathy. New diagnostic and therapeutic challenge.

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Abstract
Shah (1975) outlined the eventful and controversy-filled saga of hypertrophic obstructive cardiomyopathy (HOCM) (idiopathic hypertrophic subaortic stenosis, muscular subaortic stenosis, obstructive asymmetric septal hypertrophy). Concepts of the anatomical and pathophysiological mechanism(s) of left ventricular outflow obstruction present in this disease have evolved slowly over the years. Recently, echocardiographic observations have provided information regarding the possible causes of systolic outflow obstruction in hypertrophic obstructive cardiomyopathy. There is now sufficient evidence accumulated to support the concept of a spectrum of physiopathological and anatomical disorders causing left ventricular obstruction HOCM, which probably relate to the heterogeneous and disorderly hypertrophic process underlying this disease. In many cases, the abnormal systolic contraction patterns and deformed geometry of the left ventricular cavity alter the direction of papillary muscle contraction and produce hemodynamic forces which attract the anterior mitral valve leaflet against the bulging septum during systole; thus, obstruction occurs at the junction of the inflow and outflow tracts. In other instances, the hypertrophic process predominates at the mid-ventricular level, and the hypertrophic papillary muscles together with abnormal free wall trabeculations abut against the septum during systole to produce true muscular stenosis; there is a high pressure apical chamber, while both inflow and outflow tracts remain free of obstruction. The presence of atypical echocardiographic features in patients with otherwise typical HOCM may alert the clinician to the possible presence of mid-ventricular HOCM.