Systemic arterial response to exercise in patients with aortic valve stenosis.

BACKGROUND Systemic arterial hemodynamics play an important role in the assessment of the severity and hemodynamic consequences of aortic valve stenosis (AVS). METHODS AND RESULTS Systemic vascular resistance, total arterial compliance, effective arterial elastance, and aortic characteristic impedance were derived from high-fidelity catheter recordings of ascending aortic pressure and blood flow velocity at rest and with supine bicycle exercise in 18 patients with AVS and 11 control subjects. Mean aortic pressure was similar between groups. At rest, systemic vascular resistance (AVS patients, 1426+/-318 dynes . s . cm(-5); control subjects, 107+/-228 dynes . s . cm(-5); P<0.01), arterial elastance (AVS patients, 1.38+/-0.36 mm Hg/mL; control subject, 0.99+/-0.15 mm Hg/mL; P<0.002), and aortic characteristic impedance (AVS patients, 107+/-23 dynes . s . cm(-5); control subjects, 76+/-30 dynes . s . cm(-5); P<0.01) were increased, whereas total arterial compliance was lower (AVS patients, 0.737+/-0.19x10(-3) cm(5)/dyne; control subjects, 1.155+/-0.27x10(-3) cm(5)/dyne; P<0.001) in AVS. With exercise, total arterial compliance increased in control subjects (rest, 1.155+/-0.27x10(-3) cm(5)/dyne; exercise, 1.421+/-0.49x10(-3) cm(5)/dyne; P<0.05) but did not change in AVS patients (rest, 0.737+/-0.19x10(-3) cm(5)/dyne; exercise, 0.769+/-0.21x10(-3) cm(5)/dyne; P=0.2). Arterial elastance increased on exercise in AVS patients (rest, 1.38+/-0.36 mm Hg/mL; exercise, 1.57+/-0.44; P<0.01). Aortic characteristic impedance remained elevated on exercise (AVS patients, 122+/-30 dynes . s . cm(-5); control subjects, 80+/-43 dynes . s . cm(-5); P=0.01). Stroke flow increased significantly in both AVS patients (rest, 229+/-69 mL/s; exercise, 256+/-78 mL/s; P<0.01) and control subjects (rest, 230+/-37 mL/s; exercise, 406+/-69 mL/s; P<0.001), although the increment was much attenuated in AVS. On multiple regression, the increase in stroke flow was related to the decrease in systemic vascular resistance (P=0.03), increase in total arterial compliance (P=0.03), and decrease in arterial elastance (P=0.02). CONCLUSIONS These results indicate a pressure-independent increase in the steady and pulsatile components of the arterial load in patients with AVS under resting conditions. Persistent "stiffening" of the arterial system is an important contributor to the diminished stroke output response to exercise in AVS.