European Heart Journal Advance Access published online on May 22, 2008
European Heart Journal, doi:10.1093/eurheartj/ehn209
Systemic pressure does not directly affect pressure gradient and valve area estimates in aortic stenosis in vitro
1 Department of Cardiology, Medical University of Vienna, Vienna General Hospital, Vienna, Austria
2 Department of Bioengineering, Medical University of Vienna, Vienna General Hospital, Vienna, Austria
3 Department of Medical Statistics, Medical University of Vienna, Vienna General Hospital, Vienna, Austria
Received 25 January 2008; revised 22 April 2008; accepted 24 April 2008.
* Corresponding author: Adult Congenital and Valvular Heart Disease Center, University Hospital Münster, Albert-Schweitzer-Str. 33, D-48149 Münster, Germany. Tel: +49 251 46110, Fax: +49 251 46109, Email: julia.mascherbauer{at}ukmuenster.de
Aims: Hypertension is a frequent finding in patients with aortic stenosis (AS). However, controversial data about the influence of systemic blood pressure on the quantification of AS have been published.
Methods and results: Various models of AS (plates and biological valves) were studied in an in vitro circuit. Valve areas were calculated with the Doppler continuity equation and the Gorlin formula. Systolic systemic pressures were increased from 80 to 200 mmHg while flow rates were maintained constant. In addition, a computational fluid dynamics (CFD) model was constructed to test the effect of systemic pressures on pressure gradient and valve area estimates.
When systemic pressure was raised, pressure gradients as well as valve areas did not change (mean difference 3.4 ± 1.8 mmHg, range 0.4–6.8 mmHg; mean difference 0.01 ± 0.03 cm2, range –0.02 to 0.05 cm2). By multivariable analysis, neither valve area nor pressure gradient were independently affected by systemic pressure. In addition, CFD analysis revealed no effect of systemic pressure on pressure gradient and valve area.
Conclusion: Our results suggest that blood pressure itself does not directly affect pressure gradients and valve area estimates in AS. Thus, when observed in vivo, these changes are most likely due to afterload-related variations of ejection fraction and, therefore, flow rate.
Key Words: Aortic stenosis • Haemodynamics • Hypertension
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