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European Heart Journal 2004 25(9):787-793; doi:10.1016/j.ehj.2004.02.011
Copyright © 2004 by the European Society of Cardiology.
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Preclinical research

Value and limitations of aortic valve resistance with particular consideration of low flow–low gradient aortic stenosis: an in vitro study

Julia Mascherbauera,d, Heinrich Schimab, Raphael Rosenheka,d, Martin Czernyc, Gerald Maurera,d and Helmut Baumgartnera,d,*

a Department of Cardiology, Vienna General Hospital, University of Vienna, Währinger Gürtel 18-20, A-1090 Vienna, Austria
b Department of Bioengineering, Vienna General Hospital, University of Vienna, Vienna, Austria
c Department of Cardiothoracic Surgery, Vienna General Hospital, University of Vienna, Vienna, Austria
d Ludwig Bolzmann Institutes of Cardiovascular and Cardiosurgical Research, Vienna, Austria

Received October 26, 2003; revised January 14, 2004; accepted February 13, 2004 * Corresponding author. Tel.: +43-1-40-400-4614; fax: +43-1-408-11-48
E-mail address: helmut.baumgartner{at}univie.ac.at

Abstract

Background The calculation of valve resistance rather than aortic valve area (AVA) has been proposed for the assessment of aortic stenosis (AS), based on the claim that it is less flow-dependent. Even more importantly, valve resistance has been reported to distinguish between truly severe and "pseudosevere" AS in patients with low cardiac output. However, the diagnostic value of valve resistance remains controversial.

Methods and results Models of stenotic aortic valves (plates and nozzles) and biological stenotic valves were studied in a pulsatile in vitro circuit using Doppler ultrasound and direct pressure and flow measurements. Anatomic AVAs ranged from 0.5 to 1.25 cm2; cardiac output varied from 1.8 to 9.0 l/min. Effective AVA was calculated with the continuity equation. The orifices of the biological valves were recorded with a video camera for planimetry. In low flow–low gradient AS, truly severe stenosis was defined by an AVA remaining 0.85 cm2 after flow normalisation, whereas AVA increased beyond 0.85 cm2 in pseudosevere AS.

In rigid stenoses, valve resistance increased significantly with flow, while in bioprostheses this flow dependence was partially masked by an actual increase of the anatomic orifice area. In low flow–low gradient AS, valve resistance was significantly smaller in pseudosevere AS compared to truly severe AS (129±28 vs. 176±33 dynescm–5; ) at a similar baseline effective AVA. After the exclusion of datasets with mean gradients 15 and 35 mmHg, the difference in valve resistance between truly severe and pseudosevere AS was no longer significant (162±26 vs. 141±22 dynescm–5; ). Nevertheless, valve resistance 120 dynescm–5 was found only in pseudosevere stenoses while valve resistance 180 dynescm–5 marked truly severe stenosis.

Conclusions Valve resistance is flow-dependent and not superior to calculated AVA for the assessment of AS. In low flow–low gradient AS, valve resistance 120 dynescm–5 identifies pseudosevere AS, whereas valve resistance 180 dynescm–5 implies truly severe AS. However, values between 120 and 180 dynescm–5 are nondiagnostic, requiring repeated AVA calculations after flow normalisation.

Key Words: Valve resistance • Aortic stenosis • Haemodynamics


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