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

Abstract

A recent editorial by 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. At first, obstruction was attributed to a circular muscle band in the left ventricular outflow tract (Brachfeld and Gorlin, 1959;Brock, 1959;Cohen et al., 1964) but later this view was felt to be too simple, overlooking the fact that the left ventricle unlike the right does not have a true muscular outflow tract (Shah, 1975). Whether a true intraventricular pressure gradient was actually even present in hypertrophic cardiomyopathy was subsequently questioned by Criley et al. (1965). They explained recorded subaortic pressure gradients as being caused by entrapment of the catheter, based on the demonstration that high subendocardial pressures transmitted to a catheter embedded in the trabeculated left ventricular apex result in artefactual gradients (Morrow et al., 1965;Dieudonne, 1966 More recently, echocardiographic observations have provided additional information regarding the possible causes of systolic outflow obstruction in hypertrophic obstructive cardiomyopathy. The septum is disproportionately thicker than the posterior wall by a ratio of 1-3 or more (Henry et al., 1973a) and the anterior mitral leaflet moves in systole toward the septum (Shah et al., 1969). The length and degree of the systolic apposition of the mitral leaflet against the septum have correlated well with outflow gradients found at catheterisation (Henry et al., 1973b), though lack of correlation has been noted by other authors (Rossen et al., 1974). The precise mechanisms for the systolic apposition of the anterior mitral leaflet against the septum are not clearly understood, being attributed to malalignment of the anterior papillary muscle (Reis et al., 1974) or to a Venturi effect on the left ventricular outflow tract (Wigle et al., 1971) produced by the abnormal anatomy and contraction patterns. As further evidence of the role of the mitral valve, Cooley et al. (1973) showed disappearance of outflow gradients after mitral valve replacement with a 701

Midventricular obstruction—A form of hypertrophic obstructive cardiomyopathy—and systolic anterior motion of the mitral valve

“…Kuhn et al, (1 983a,b) found that SAM was present in 46% of their cases; suggestive in 23% and absent in 30%. Nor was there any SAM in the cases reported and reviewed by Falicov andResnekov (1976, 1977). Echocardiographic studies have provided some information re- Biventricular angiography in midventricular obstrucgarding the possible causes of systolic obstruction in HOCM.…”

“…Other types and mechanisms of intraventricular obstruction of the right ventricle, such as anomalous muscular bands (Forster et al, 1971;Hartmann ef al., 1964) were excluded by simultaneous biventricular angiography in the LAO position. Catheter entrapment within portions of the right and left ventricular cavities as a cause of spurious gradient was ruled out (Falicov et al, 1977).…”

Beneficial Effect of Dual-Chamber Pacing for a Left Mid-Ventricular Obstruction With Apical Aneurysm.

“…8,10 Therefore, relief of the high apical pressure may be necessary to preventing further asynergy. It has been considered that drug-refractory patients with MVO are candidates for cardiac surgery, 11,12 but recently, pacing therapy for pressure gradient reduction in patients with MVO has been reported, 6 as is the case for patients with hypertrophic LVOT obstruction. [1][2][3][4][5] Previous reports have suggested that the paradoxical motion of the interventricular septum may play a role in the relief of LVOT obstruction, [1][2][3][4][5] and another study has indicated that pacing reduces septal wall motion in patients with LVOT obstruction.…”

Midventricular Hypertrophic Obstructive Cardiomyopathy with Left Ventricular Aneurysm and Clot: The Role of Transesophageal Echocardiogram in Assessment and Management of Myomectomy

“…4 It is caused by hypertrophic septum coming in contact with a hypercontractile left ventricular free wall. 5 Long period of exposure to mid ventricular obstruction and increased left ventricular wall stress may cause apical aneurysm formation. 4 Midcavity obliteration to flow during systole might lead to compensatory apical hypertrophy, which by itself could make midventricular obstruction more severe.…”