C. Movsowitz et al., LEFT-VENTRICULAR DIASTOLIC RESPONSE TO EXERCISE IN VALVULAR AORTIC-STENOSIS, The American journal of cardiology, 77(4), 1996, pp. 275-280
Exercise produces profound alterations in symptoms and hemodynamics in
patients with valvular aortic stenosis (AS). Prior studies have demon
strated marked increases in late left ventricular (LV) diastolic filli
ng pressure with exercise. Little information is available on the exer
cise response of indexes of early LV diastolic performance. Catheter-t
ip manometer recordings in 11 patients with AS and 5 age-matched contr
ols 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 w
ere 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 wit
h AS. The time to onset of isovolumic relaxation (patients 422 +/- 31
ms, controls 363 +/- 40 ms; p <0.01) arid minimal LV diastolic pressur
e (patients 608 +/- 57 ms, controls 448 +/- 52 ms; p <0.002) at rest w
ere 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 (patient
s 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 re
laxation with exercise. The LV diastolic response to exercise in patie
nts with AS is distinguished from the control response by suboptimal a
nd prolonged relaxation and a diminished rate of LV pressure decay. Th
ese abnormal responses in early diastolic function coupled with the kn
own abnormal chamber distensibility in AS contribute to significant el
evations in early, mid-, and late diastolic pressures with exercise.