Muscular subaortic stenosis: The interrelation of wall tension, outflow tract “distending pressure” and orifice radius

Abstract

Various pharmacologic agents were administered in 10 cases of muscular subaortic stenosis at the time of left heart catheterization in an attempt to determine the various factors affecting the severity of the outflow tract obstruction. Amyl nitrite-induced vasodilatation increased the degree of stenosis in 5 cases, whereas systemic vasoconstriction induced by angiotensin II, norepinephrine and methoxamine significantly decreased the degree of stenosis. These agents were believed to have affected the degree of stenosis principally by virtue of the changes they caused in the systolic “distending pressure” in the left ventricular outflow tract. This pressure, being equal to the aortic systolic pressure, would be decreased by vasodilatation, and increased by vasoconstriction. A decrease in the systolic “distending pressure” in the outflow tract would allow closer apposition of the walls of this tract in systole and result in increased severity of the muscular stenosis. A vasoconstriction-induced increase in this pressure would tend to distend the walls of the outflow tract in systole and decrease the severity of the muscular stenosis. By altering aortic diastolic pressure and, hence, the time of onset of ventricular ejection, these effects of vasodilatation and vasoconstriction on the degree of stenosis would be accentuated. By interrelating the outflow tract “distending pressure” (P) with the linear tension (T) initially developed by the deep constrictor muscles and the over-all ventricular volume (V), variations in severity of muscular subaortic stenosis were explicable. Any influence acting to increase T or decrease P or V would increase the severity of the stenosis (decrease orifice size); any influence acting to decrease T or increase P or V would decrease the severity of the stenosis (increase orifice size). By considering the orifice size of the left ventricular outflow tract in muscular subaortic stenosis to be governed in the above manner, the effect of arterial vasodilatation and vasoconstriction as well as the effect of acetylstrophanthidin, isoproterenol and most other reported influences on the degree of muscular subaortic stenosis could be explained.