Left ventricular diastolic response to exercise in valvular aortic stenosis.

Exercise produces profound alterations in symptoms and hemodynamics in patients with valvular aortic stenosis (AS). Prior studies have demonstrated marked increases in late left ventricular (LV) diastolic filling pressure with exercise. Little information is available on the exercise response of indexes of early LV diastolic performance. Catheter-tip manometer recordings in 11 patients with AS and 5 age-matched controls were obtained at rest and with supine bicycle exercise at the time of cardiac catheterization. Pressure-derived indexes of LV diastolic performance, isovolumic relaxation rate, and diastolic interval data were examined. At rest, early (patients 22 +/- 6 mm Hg, controls 12 +/- 3 mm Hg; p < 0.01), minimal (patients 9 +/- 4 mm Hg, controls 4 +/- 1 mm Hg; p < 0.01), and late (patients 28 +/- 10 mm Hg, controls 13 +/- 3 mm Hg; p < 0.002) LV diastolic pressures were elevated in patients with AS. The time to onset of isovolumic relaxation (patients 422 +/- 31 ms, controls 363 +/- 40 ms; p < 0.01) and minimal LV diastolic pressure (patients 608 +/- 57 ms, controls 448 +/- 52 ms; p < 0.002) at rest were prolonged in patients with AS. With exercise, early (patients 45 +/- 14 mm Hg, controls 15 +/- 3 mm Hg; p < 0.002), minimal (patients 15 +/- 6 mm Hg, controls 2 +/- 1 mm Hg; p < 0.01), and late (patients 38 +/- 10 mm Hg, controls 18 +/- 5 mm Hg; p < 0.002) LV diastolic pressures were elevated, and the time to minimal LV diastolic pressure (patients 528 +/- 26 ms; controls 393 +/- 56 ms) and peak first derivative of LV pressure decline (-LV dP/dt) patients 395 +/- 41 ms, controls 326 +/- 59 ms) were prolonged in AS. Furthermore, patients with AS failed to comparably increase the rate of LV pressure decay and isovolumic relaxation with exercise. The LV diastolic response to exercise in patients with AS is distinguished from the control response by suboptimal and prolonged relaxation and a diminished rate of LV pressure decay. These abnormal responses in early diastolic function coupled with the known abnormal chamber distensibility in AS contribute to significant elevations in early, mid-, and late diastolic pressures with exercise.