Effects of afterload reduction on vena contracta width in mitral regurgitation

Ali M. Kizilbash, Duwayne L. Willett, M. Elizabeth Brickner, Sheila K. Heinle, Paul A. Grayburn

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)427-431
Number of pages5
JournalJournal of the American College of Cardiology
Volume32
Issue number2
DOIs
StatePublished - Aug 1998

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Mitral Valve Insufficiency
Nitroprusside
Blood Pressure
Rheumatic Heart Disease
Mitral Valve Prolapse
Dilated Cardiomyopathy
Endocarditis
Vasodilation
Ischemia
Color

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Effects of afterload reduction on vena contracta width in mitral regurgitation. / Kizilbash, Ali M.; Willett, Duwayne L.; Brickner, M. Elizabeth; Heinle, Sheila K.; Grayburn, Paul A.

In: Journal of the American College of Cardiology, Vol. 32, No. 2, 08.1998, p. 427-431.

Research output: Contribution to journalArticle

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abstract = "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.",
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T1 - Effects of afterload reduction on vena contracta width in mitral regurgitation

AU - Kizilbash, Ali M.

AU - Willett, Duwayne L.

AU - Brickner, M. Elizabeth

AU - Heinle, Sheila K.

AU - Grayburn, Paul A.

PY - 1998/8

Y1 - 1998/8

N2 - 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.

AB - 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.

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