Marked respiratory variations in left ventricular outflow were noted in 8 of 9 patients with hypertrophie obstructive cardiomyopathy. Maximal systolic gradients were noted at the end of expiration, the smallest gradients at the end of inspiration. The reductions in left ventricular systolic pressures were accompanied by a rise in arterial systolic pressures and vice versa. These effects were not abolished by beta-adrenergic blockage and were exaggerated after “vensection.”

The Valsalva maneuver resulted in increased obstruction during the period of peak strain, and after release the obstruction was diminished during the overshoot period. These responses persisted after beta-adrenergic blockade.

The probable underlying mechanisms of varying obstruction observed with respiration and with the Valsalva maneuver are related to changes in volume of the left ventricle. The left ventricular outflow obstruction in hypertrophie obstructive cardiomyopathy is increased by a diminished ventricular volume, and relieved by an increased ventricular volume.