Key result
Supine bicycle exercise in patients with aortic valve stenosis yielded an attenuated stroke flow increase (229 to 256 mL/s, P<0.01) compared to controls (230 to 406 mL/s, P<0.001).
Why the study?
How do systemic arterial hemodynamics respond to exercise in patients with aortic valve stenosis compared to control subjects?
Case-Control (n=29)
How do systemic arterial hemodynamics respond to exercise in patients with aortic valve stenosis compared to control subjects?
Patients with aortic valve stenosis exhibit persistent stiffening of the arterial system during exercise, which contributes to a diminished stroke output response.
May link persistent arterial stiffening to limited exercise reserve in aortic stenosis; hypothesis-generating for combined valvular-vascular studies.
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.
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Laskey et al. (2009) conducted a case-control in Aortic Valve Stenosis (n=29). Supine bicycle exercise vs. Control subjects was evaluated on Systemic arterial hemodynamics (systemic vascular resistance, total arterial compliance, effective arterial elastance, aortic characteristic impedance). Supine bicycle exercise in patients with aortic valve stenosis yielded an attenuated stroke flow increase (229 to 256 mL/s, P<0.01) compared to controls (230 to 406 mL/s, P<0.001).
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