The Mechanism of the Intraventricular Pressure Gradient in Idiopathic Hypertrophic Subaortic Stenosis

Abstract

The evidence favoring the existence of obstruction, clinical observations, such as the presence of a systolic murmur in patients without demonstrable mitral regurgitation, and the relief of angina and syncope by operations designed to relieve outflow tract obstruction should be mentioned. In addition, the marked reduction or elimination of the pressure gradient by these operations further supports the concept that obstruction plays a significant role in this disease. According to conventional hemo-dynamic usage, pressure differences should not be termed "pressure gradients;" the term "intraventricular pressure differences" perhaps better describes their nature, and this terminology also might be preferable in referring to elevated pressures measured in empty portions of the ventricular cavity in patients with IHSS. It can be stated with assurance that obstruction to outflow, of greater or lesser severity, does exist in patients with IHSS in whom an elevated systolic pressure is present to nonobliterated portions of the left ventricular cavity. Following the onset of left ventricular contraction, isometric pressure development and early ventricular ejection appear to proceed at a more rapid rate than in the normal subject, and approximately 30% of the forward stroke volume is ejected while there is no significant pressure gradient. This phase of systole is responsible for the sharp upstroke of the arterial pressure pulse. Subsequently, the hypertrophied in-terventricular septum approaches the anterior surface of the closed mitral valve, and the intraventricular pressure at all points in the cavity below this site begins to exceed that in the outflow tract. The pressure gradient from the body of the ventricle to the outflow tract then increases progressively as further narrowing of this region occurs, and orthograde flow consequently diminishes, the remaining 70% of the stroke volume being ejected during this phase. Finally, hi late systole, obstruction in the outflow tract becomes essentially complete, and elevated pressure persists in both obliterated and in nonobliterated portions of the ventricle, at a time when forward flow cannot be detected. In addition to obstruction to left ventricular emptying, the reduced compliance of the thickened ventricular wall in IHSS also interferes with left ventricular filling and accordingly, ventricular end-diastolic volume may be reduced despite an elevated left ventricular diastolic pressure. The relative importance of such impedance to left ventricular filling during diastole, and the obstruction to outflow during systole, undoubtedly varies among individual patients.