Doppler evidence that true left ventricular-to-aortic pressure gradients exist in hypertrophic cardiomyopathy

Abstract

The etiology of systolic left ventricular-to-aortic pressure gradients in hypertrophic cardiomyopathy is still controversial. While cavity obliteration has been proposed by some investigators as the cause for recording of a high left ventricular systolic pressure, the concept of left ventricular outflow tract obstruction has received more experimental support. To investigate further whether left ventricular pressure truly exceeds aortic pressure and implies obstruction, we studied, with imaging and Doppler echocardiographic techniques, five patients with asymmetric septal hypertrophy and systolic anterior movement of the mitral valve occasionally causing it to abut upon the septum. All had outflow tract pressure gradients (peak 85 ± 10 mm Hg) and trace to mild mitral regurgitation. Continuous wave Doppler study recorded peak flow velocities in the outflow tract (4.6 ± 0.3 m/sec), and mitral regurgitant (mean 6.6 ± 0.3 m/sec) jets. Aortic systolic and diastolic blood pressures were measured by cuff sphygmomanometry, and simultaneous carotid pulse tracings were recorded. The magnitude of systolic aortic pressure was determined at the time of peak velocity in the mitral regurgitant jet. Since the poak systolic pressure gradient across the mitral valve (left ventricular minus left atrial pressure) should equal 4 times the square of the peak velocity (V) in the mitral regurgitant jet, peak left ventricular systolic pressure should equal 4 × V 2 plus the height of left atrial pressure at the time of peak mitral regurgitant velocity. In each case, calculations were made assuming an upper normal left atrial pressure of 10 mm Hg. If actual obstruction were present, that estimate of peak systolic left ventricular pressure should equal the sum of the aortic systolic pressure and the outflow tract pressure gradient, both measured at the time of peak mitral flow velocity. By paired t tests, estimated values for left ventricular systolic pressures by both techniques were equivalent (both 187 ± 18 mm Hg). During the recording of a left ventricular-to-aortic gradient, the basal ventricular cavity was not obliterated on two-dimensional imaging, and ventricular shortening continued. Ventricular systolic dimension at the time of peak mitral regurgitant and outflow tract velocities (2.9 ± 0.4 cm) was greater in each patient than minimal systolic dimension (2.3 ± 0.4 cm, p = 0.01). The combination of marked elevation of the systolic pressure gradient across the mitral valve, relative to simultaneous aortic systolic pressure, and continued ventricular shortening indicates that true outflow obstruction can elevate left ventricular systolic pressure in hypertrophic cardiomyopathy.