Contribution of volume overload and angiotensin II to the increased pulse wave velocity of hemodialysis patients

Aortic compliance is decreased in patients with end-stage renal disease. This malfunction contributes to high aortic systolic pressures and thus to the development of left ventricular hypertrophy. It was hypothesized that besides structural vascular changes, functional changes as a result of hypervo...

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Veröffentlicht in:Journal of the American Society of Nephrology 2002, Vol.13 (1), p.177-183
Hauptverfasser: TYCHO VUURMANS, J. L, BOER, Walther H, BOS, Willem-Jan W, BLANKESTIJN, Peter J, KOOMANS, Hein A
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container_issue 1
container_start_page 177
container_title Journal of the American Society of Nephrology
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creator TYCHO VUURMANS, J. L
BOER, Walther H
BOS, Willem-Jan W
BLANKESTIJN, Peter J
KOOMANS, Hein A
description Aortic compliance is decreased in patients with end-stage renal disease. This malfunction contributes to high aortic systolic pressures and thus to the development of left ventricular hypertrophy. It was hypothesized that besides structural vascular changes, functional changes as a result of hypervolemia and increased vasoconstrictor activity, in particular angiotensin II, play a role in decreasing aortic compliance. Nineteen hemodialysis patients were studied before and 24 h after they had been dialyzed to dry weight. Applanation tonometry of peripheral arteries was used to estimate aortic pulse wave velocity (PWV), known to depend on aortic compliance, and aortic systolic pressure augmentation (augmentation index [Aix]). Predialysis aortic PWV was increased in the dialysis patients compared with matched healthy subjects (9.9 +/- 3.1 versus 7.5 +/- 1.1 m/s; P < 0.05). The AIx was also increased (35 +/- 6 versus 25 +/- 10; P < 0.05). Volume reduction with dialysis had no significant effect on PWV (9.3 +/- 1.5 m/s), but the AIx decreased (28 +/- 7; P < 0.05). A subset of 10 patients were restudied after 1 wk of angiotensin-converting enzyme inhibition (ACEi) with enalapril 5 mg once daily. ACEi decreased both predialysis as postdialysis BP but had no effect on pulse pressure and heart rate, which remained elevated compared with healthy subjects. ACEi also decreased predialysis aortic PWV, from 11.0 +/- 3.5 to 9.1 +/- 2.1 m/s (P < 0.05) but had no significant effect on AIx. During treatment with ACEi, the same volume reduction with dialysis decreased aortic PWV further to 8.0 +/- 1.4 m/s (P < 0.05), a figure not different from PWV in healthy subjects. AIx decreased to an even slightly subnormal value (12 +/- 23; P < 0.05). It was concluded that volume overload and angiotensin II both contribute to elevated PWV and AIx in dialysis patients. Volume reduction and ACEi both improve the aortic PWV and AIx. Combined volume reduction and ACEi has an enhanced effect that, in the present patients, was so large that PWV and AIx were no longer elevated. Monitoring and correcting of arterial pressure waves is feasible and may be an important tool in the treatment of patients with end-stage renal disease.
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L ; BOER, Walther H ; BOS, Willem-Jan W ; BLANKESTIJN, Peter J ; KOOMANS, Hein A</creator><creatorcontrib>TYCHO VUURMANS, J. L ; BOER, Walther H ; BOS, Willem-Jan W ; BLANKESTIJN, Peter J ; KOOMANS, Hein A</creatorcontrib><description><![CDATA[Aortic compliance is decreased in patients with end-stage renal disease. This malfunction contributes to high aortic systolic pressures and thus to the development of left ventricular hypertrophy. It was hypothesized that besides structural vascular changes, functional changes as a result of hypervolemia and increased vasoconstrictor activity, in particular angiotensin II, play a role in decreasing aortic compliance. Nineteen hemodialysis patients were studied before and 24 h after they had been dialyzed to dry weight. Applanation tonometry of peripheral arteries was used to estimate aortic pulse wave velocity (PWV), known to depend on aortic compliance, and aortic systolic pressure augmentation (augmentation index [Aix]). Predialysis aortic PWV was increased in the dialysis patients compared with matched healthy subjects (9.9 +/- 3.1 versus 7.5 +/- 1.1 m/s; P < 0.05). The AIx was also increased (35 +/- 6 versus 25 +/- 10; P < 0.05). Volume reduction with dialysis had no significant effect on PWV (9.3 +/- 1.5 m/s), but the AIx decreased (28 +/- 7; P < 0.05). A subset of 10 patients were restudied after 1 wk of angiotensin-converting enzyme inhibition (ACEi) with enalapril 5 mg once daily. ACEi decreased both predialysis as postdialysis BP but had no effect on pulse pressure and heart rate, which remained elevated compared with healthy subjects. ACEi also decreased predialysis aortic PWV, from 11.0 +/- 3.5 to 9.1 +/- 2.1 m/s (P < 0.05) but had no significant effect on AIx. During treatment with ACEi, the same volume reduction with dialysis decreased aortic PWV further to 8.0 +/- 1.4 m/s (P < 0.05), a figure not different from PWV in healthy subjects. AIx decreased to an even slightly subnormal value (12 +/- 23; P < 0.05). It was concluded that volume overload and angiotensin II both contribute to elevated PWV and AIx in dialysis patients. Volume reduction and ACEi both improve the aortic PWV and AIx. Combined volume reduction and ACEi has an enhanced effect that, in the present patients, was so large that PWV and AIx were no longer elevated. Monitoring and correcting of arterial pressure waves is feasible and may be an important tool in the treatment of patients with end-stage renal disease.]]></description><identifier>ISSN: 1046-6673</identifier><identifier>EISSN: 1533-3450</identifier><identifier>DOI: 10.1681/asn.v131177</identifier><identifier>PMID: 11752035</identifier><identifier>CODEN: JASNEU</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams &amp; Wilkins</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. 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Applanation tonometry of peripheral arteries was used to estimate aortic pulse wave velocity (PWV), known to depend on aortic compliance, and aortic systolic pressure augmentation (augmentation index [Aix]). Predialysis aortic PWV was increased in the dialysis patients compared with matched healthy subjects (9.9 +/- 3.1 versus 7.5 +/- 1.1 m/s; P < 0.05). The AIx was also increased (35 +/- 6 versus 25 +/- 10; P < 0.05). Volume reduction with dialysis had no significant effect on PWV (9.3 +/- 1.5 m/s), but the AIx decreased (28 +/- 7; P < 0.05). A subset of 10 patients were restudied after 1 wk of angiotensin-converting enzyme inhibition (ACEi) with enalapril 5 mg once daily. ACEi decreased both predialysis as postdialysis BP but had no effect on pulse pressure and heart rate, which remained elevated compared with healthy subjects. ACEi also decreased predialysis aortic PWV, from 11.0 +/- 3.5 to 9.1 +/- 2.1 m/s (P < 0.05) but had no significant effect on AIx. During treatment with ACEi, the same volume reduction with dialysis decreased aortic PWV further to 8.0 +/- 1.4 m/s (P < 0.05), a figure not different from PWV in healthy subjects. AIx decreased to an even slightly subnormal value (12 +/- 23; P < 0.05). It was concluded that volume overload and angiotensin II both contribute to elevated PWV and AIx in dialysis patients. Volume reduction and ACEi both improve the aortic PWV and AIx. Combined volume reduction and ACEi has an enhanced effect that, in the present patients, was so large that PWV and AIx were no longer elevated. Monitoring and correcting of arterial pressure waves is feasible and may be an important tool in the treatment of patients with end-stage renal disease.]]></description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Angiotensin II - physiology</subject><subject>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</subject><subject>Aorta - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Brachial Artery - physiopathology</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>Enalapril - therapeutic use</subject><subject>Female</subject><subject>Humans</subject><subject>Hyperemia - physiopathology</subject><subject>Intensive care medicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pulse</subject><subject>Reference Values</subject><subject>Renal Dialysis</subject><issn>1046-6673</issn><issn>1533-3450</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0DtrwzAQB3BRWpo07dS9aOlUnEqW5McYQh-B0A59rOZsnxoVRzKW7JJvX4cEMhx3w4_j7k_ILWdznmT8EbydD1xwnqZnZMqVEJGQip2PM5NJlCSpmJAr738Z4ypO00syGa2KmVBT0i6dDZ0p-2CcpU7TwTX9FqkbsGsc1BTsvn6MC2i9sXS1osHRsEFqbNUheKxp2zce6R8MSAdsXGXCbr9qg1tXG2h23njaQjBog78mFxpGfnPsM_L1_PS5fI3W7y-r5WIdVZJnIUpFXFZlLmSZlDxlYrwcVA4ac455kiVaKZ3lMlOghZJMjv8DaF4iCCwVSDEjD4e9Vee871AXbWe20O0Kzop9bsXi4634PuQ26ruDbvtyi_XJHoMawf0RgK-g0R3YyviTE5KxWDLxD2RNd44</recordid><startdate>2002</startdate><enddate>2002</enddate><creator>TYCHO VUURMANS, J. 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Cell therapy and gene therapy</topic><topic>Angiotensin II - physiology</topic><topic>Angiotensin-Converting Enzyme Inhibitors - therapeutic use</topic><topic>Aorta - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Brachial Artery - physiopathology</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>Enalapril - therapeutic use</topic><topic>Female</topic><topic>Humans</topic><topic>Hyperemia - physiopathology</topic><topic>Intensive care medicine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pulse</topic><topic>Reference Values</topic><topic>Renal Dialysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>TYCHO VUURMANS, J. 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It was hypothesized that besides structural vascular changes, functional changes as a result of hypervolemia and increased vasoconstrictor activity, in particular angiotensin II, play a role in decreasing aortic compliance. Nineteen hemodialysis patients were studied before and 24 h after they had been dialyzed to dry weight. Applanation tonometry of peripheral arteries was used to estimate aortic pulse wave velocity (PWV), known to depend on aortic compliance, and aortic systolic pressure augmentation (augmentation index [Aix]). Predialysis aortic PWV was increased in the dialysis patients compared with matched healthy subjects (9.9 +/- 3.1 versus 7.5 +/- 1.1 m/s; P < 0.05). The AIx was also increased (35 +/- 6 versus 25 +/- 10; P < 0.05). Volume reduction with dialysis had no significant effect on PWV (9.3 +/- 1.5 m/s), but the AIx decreased (28 +/- 7; P < 0.05). A subset of 10 patients were restudied after 1 wk of angiotensin-converting enzyme inhibition (ACEi) with enalapril 5 mg once daily. ACEi decreased both predialysis as postdialysis BP but had no effect on pulse pressure and heart rate, which remained elevated compared with healthy subjects. ACEi also decreased predialysis aortic PWV, from 11.0 +/- 3.5 to 9.1 +/- 2.1 m/s (P < 0.05) but had no significant effect on AIx. During treatment with ACEi, the same volume reduction with dialysis decreased aortic PWV further to 8.0 +/- 1.4 m/s (P < 0.05), a figure not different from PWV in healthy subjects. AIx decreased to an even slightly subnormal value (12 +/- 23; P < 0.05). It was concluded that volume overload and angiotensin II both contribute to elevated PWV and AIx in dialysis patients. Volume reduction and ACEi both improve the aortic PWV and AIx. Combined volume reduction and ACEi has an enhanced effect that, in the present patients, was so large that PWV and AIx were no longer elevated. Monitoring and correcting of arterial pressure waves is feasible and may be an important tool in the treatment of patients with end-stage renal disease.]]></abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams &amp; Wilkins</pub><pmid>11752035</pmid><doi>10.1681/asn.v131177</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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subjects Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Angiotensin II - physiology
Angiotensin-Converting Enzyme Inhibitors - therapeutic use
Aorta - physiopathology
Biological and medical sciences
Blood Pressure - drug effects
Brachial Artery - physiopathology
Emergency and intensive care: renal failure. Dialysis management
Enalapril - therapeutic use
Female
Humans
Hyperemia - physiopathology
Intensive care medicine
Male
Medical sciences
Middle Aged
Pulse
Reference Values
Renal Dialysis
title Contribution of volume overload and angiotensin II to the increased pulse wave velocity of hemodialysis patients
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