OBJECTIVES: We used color Doppler flow mapping to determine whether vena contracta width (VCW) is a load-independent measure of the severity of mitral regurgitation. BACKGROUND: VCW has been proposed to be a relatively load-independent measure of mitral regurgitation severity in flow models using a fixed orifice. However, in patients with mitral regurgitation, VCW may not be load independent because of a dynamic regurgitant orifice. METHODS: VCW, effective regurgitant orifice area and regurgitant volume were measured by quantitative Doppler mapping in 31 patients with chronic mitral regurgitation at baseline and during nitroprusside infusion. Patients with rheumatic heart disease, annular calcification or endocarditis were considered to have a fixed regurgitant orifice, whereas patients with mitral valve prolapse, dilated cardiomyopathy or ischemia were considered to have a dynamic regurgitant orifice. RESULTS: Systolic blood pressure (148 +/- 27 to 115 +/- 25 mm Hg) and end-systolic wall stress (121 +/- 50 to 89 +/- 36) decreased with nitroprusside (p < 0.05). Although nitroprusside did not significantly change mean values for VCW (0.5 +/- 0.2 to 0.5 +/- 0.2 cm), regurgitant volume (69 +/- 47 to 69 +/- 56 ml) or effective regurgitant orifice area (0.5 +/- 0.4 to 0.5 +/- 0.6 cm2), individual patients exhibited marked directional variability. Specifically, VCW decreased in 16 patients (improved mitral regurgitation), remained unchanged in 7 patients and increased in 8 patients (worsened mitral regurgitation) with nitroprusside. Also, the VCW response to nitroprusside was concordant with changes in effective regurgitant orifice area and regurgitant volume, and was not different between dynamic and fixed orifice groups. CONCLUSIONS: Contrary to the results from in vitro studies, VCW is not load independent in patients with mitral regurgitation caused by dynamic changes in the regurgitant orifice. The origin of mitral regurgitation does not predict accurately whether the regurgitant orifice is fixed or dynamic. Finally, short-term vasodilation with nitroprusside may significantly worsen the severity of mitral regurgitation in some patients.
OBJECTIVES: We used color Doppler flow mapping to determine whether vena contracta width (VCW) is a load-independent measure of the severity of mitral regurgitation. BACKGROUND: VCW has been proposed to be a relatively load-independent measure of mitral regurgitation severity in flow models using a fixed orifice. However, in patients with mitral regurgitation, VCW may not be load independent because of a dynamic regurgitant orifice. METHODS: VCW, effective regurgitant orifice area and regurgitant volume were measured by quantitative Doppler mapping in 31 patients with chronic mitral regurgitation at baseline and during nitroprusside infusion. Patients with rheumatic heart disease, annular calcification or endocarditis were considered to have a fixed regurgitant orifice, whereas patients with mitral valve prolapse, dilated cardiomyopathy or ischemia were considered to have a dynamic regurgitant orifice. RESULTS: Systolic blood pressure (148 +/- 27 to 115 +/- 25 mm Hg) and end-systolic wall stress (121 +/- 50 to 89 +/- 36) decreased with nitroprusside (p < 0.05). Although nitroprusside did not significantly change mean values for VCW (0.5 +/- 0.2 to 0.5 +/- 0.2 cm), regurgitant volume (69 +/- 47 to 69 +/- 56 ml) or effective regurgitant orifice area (0.5 +/- 0.4 to 0.5 +/- 0.6 cm2), individual patients exhibited marked directional variability. Specifically, VCW decreased in 16 patients (improved mitral regurgitation), remained unchanged in 7 patients and increased in 8 patients (worsened mitral regurgitation) with nitroprusside. Also, the VCW response to nitroprusside was concordant with changes in effective regurgitant orifice area and regurgitant volume, and was not different between dynamic and fixed orifice groups. CONCLUSIONS: Contrary to the results from in vitro studies, VCW is not load independent in patients with mitral regurgitation caused by dynamic changes in the regurgitant orifice. The origin of mitral regurgitation does not predict accurately whether the regurgitant orifice is fixed or dynamic. Finally, short-term vasodilation with nitroprusside may significantly worsen the severity of mitral regurgitation in some patients.
Authors: Robert A Levine; Albert A Hagége; Daniel P Judge; Muralidhar Padala; Jacob P Dal-Bianco; Elena Aikawa; Jonathan Beaudoin; Joyce Bischoff; Nabila Bouatia-Naji; Patrick Bruneval; Jonathan T Butcher; Alain Carpentier; Miguel Chaput; Adrian H Chester; Catherine Clusel; Francesca N Delling; Harry C Dietz; Christian Dina; Ronen Durst; Leticia Fernandez-Friera; Mark D Handschumacher; Morten O Jensen; Xavier P Jeunemaitre; Hervé Le Marec; Thierry Le Tourneau; Roger R Markwald; Jean Mérot; Emmanuel Messas; David P Milan; Tui Neri; Russell A Norris; David Peal; Maelle Perrocheau; Vincent Probst; Michael Pucéat; Nadia Rosenthal; Jorge Solis; Jean-Jacques Schott; Ehud Schwammenthal; Susan A Slaugenhaupt; Jae-Kwan Song; Magdi H Yacoub Journal: Nat Rev Cardiol Date: 2015-10-20 Impact factor: 32.419
Authors: Paul A Grayburn; Lilin She; Brad J Roberts; Krzysztof S Golba; Krzysztof Mokrzycki; Jaroslaw Drozdz; Alexander Cherniavsky; Roman Przybylski; Krzysztof Wrobel; Federico M Asch; Thomas A Holly; Haissam Haddad; Michael Yii; Gerald Maurer; Irving Kron; Hartzell Schaff; Eric J Velazquez; Jae K Oh Journal: Am J Cardiol Date: 2015-06-25 Impact factor: 2.778
Authors: Catherine Szymanski; Robert A Levine; Christophe Tribouilloy; Hui Zheng; Mark D Handschumacher; Ahmed Tawakol; Judy Hung Journal: Am J Cardiol Date: 2011-09-21 Impact factor: 2.778