array:19 [ "pii" => "X0211699502027873" "issn" => "02116995" "estado" => "S300" "fechaPublicacion" => "2002-04-01" "documento" => "article" "licencia" => "http://www.elsevier.com/open-access/userlicense/1.0/" "subdocumento" => "fla" "cita" => "Nefrologia. 2002;22 Supl 2:13" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 2437 "formatos" => array:3 [ "EPUB" => 195 "HTML" => 1935 "PDF" => 307 ] ] "itemSiguiente" => array:15 [ "pii" => "X0211699502027865" "issn" => "02116995" "estado" => "S300" "fechaPublicacion" => "2002-04-01" "documento" => "article" "licencia" => "http://www.elsevier.com/open-access/userlicense/1.0/" "subdocumento" => "fla" "cita" => "Nefrologia. 2002;22 Supl 2:14" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 2870 "formatos" => array:3 [ "EPUB" => 188 "HTML" => 2226 "PDF" => 456 ] ] "es" => array:8 [ "idiomaDefecto" => true "titulo" => "Homocisteína, hipertensión arterial y genes" "tienePdf" => "es" "tieneTextoCompleto" => "es" "paginas" => array:1 [ 0 => array:1 [ "paginaInicial" => "14" ] ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "J. C. RODRIGUEZ PÉREZ" "autores" => array:1 [ 0 => array:1 [ "nombre" => "J. C. RODRIGUEZ PÉREZ" ] ] ] ] ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/X0211699502027865?idApp=UINPBA000064" "url" => "/02116995/00000022000000S2/v0_201502091327/X0211699502027865/v0_201502091327/es/main.assets" ] "itemAnterior" => array:15 [ "pii" => "X0211699502027881" "issn" => "02116995" "estado" => "S300" "fechaPublicacion" => "2002-04-01" "documento" => "article" "licencia" => "http://www.elsevier.com/open-access/userlicense/1.0/" "subdocumento" => "fla" "cita" => "Nefrologia. 2002;22 Supl 2:12" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 1532 "formatos" => array:3 [ "EPUB" => 181 "HTML" => 1026 "PDF" => 325 ] ] "en" => array:8 [ "idiomaDefecto" => true "titulo" => "Effects of AT1 blockade on myocardial fibrosis in hypertensive heart disease. Beyond the control of blood pressure" "tienePdf" => "en" "tieneTextoCompleto" => "en" "paginas" => array:1 [ 0 => array:1 [ "paginaInicial" => "12" ] ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "J. DÍEZ" "autores" => array:1 [ 0 => array:1 [ "nombre" => "J. DÍEZ" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/X0211699502027881?idApp=UINPBA000064" "url" => "/02116995/00000022000000S2/v0_201502091327/X0211699502027881/v0_201502091327/en/main.assets" ] "en" => array:8 [ "idiomaDefecto" => true "titulo" => "Large artery damage and hypertension in end-stage renal failure (ESRD)" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:1 [ "paginaInicial" => "13" ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "G. M. LONDON" "autores" => array:1 [ 0 => array:1 [ "nombre" => "G. M. LONDON" ] ] ] ] "textoCompleto" => "NEFROLOGÍA. Vol. XXII. Suplemento 2. 2002 Large artery damage and hypertension in end-stage renal failure (ESRD) G. M. London Hospital Manhes, Fleury Mérogis. France. The ill effects of hypertension are attributed to reduction in the caliber or the number of arterioles, resulting in increased total peripheral resistance (TPR). TPR is a determinant of mean arterial pressure (MBP) considered as constant over time. This does not take into account the fact that BP is an oscillatory phenomenon with systolic and diastolic BP being the limits of these oscillations. Moreover, while MBP and diastolic BP are almost constant along the arterial tree, systolic BP is amplified from the aorta to the brachial artery whose systolic BP only indirectly reflects the pressure in the aorta and LV1. The appropriate term to define the arterial factor(s) opposing LV ejection is aortic input impedance which depends on TPR, arterial compliance, wave reflections, and inertance of blood column in the arterial tree. Arterial compliance and wave reflections are major determinants of systolic and diastolic BP, and the pressure wave amplitude, i.e. pulse pressure (PP) which is an independent cardiovascular risk factor. ALTERATIONS OF AORTIC INPUT IMPEDANCE IN ESRD AND ITS CONSEQUENCES Due to anemia or arteriovenous shunts, TPR is usually within normal values in ESRD patients. The aortic impedance is increased principally due to decreased arterial compliance (arterial stiffening), increased wave reflections and higher inertance 2, 3. In ESRD changes in compliance are associated with arterial remodelling, pricipally intima-media thickening and the enlargement of arterial lumen 3. The enlargement of the arteries increases the volume and mass of blood contained in the arterial tree and is responsible for increased inertance. The increased stiffness ins renal failure is due to alterations of biomaterials characterized by increased elastic modulus (Einc) 4 associated with arterial mediacalcosis, and low-grade inflammation. Besides arterial sitffness, early wave reflections represents major contribution to LV afterload and compromised coronary perfusion 1. Wave reflections are frequently increased in es- sential hypertension and almost constantly increased in ESRD 2, 3. The arterial stiffening estimated by changes in aortic pulse wave velocity is an independent predictor of survival in ESRD and general population5-6. Increased wave reflections independently from changes in arterial stiffness are also a strong predictor of survival in ESRD patients 7. Improvement of arterial compliance and decrease in the effect of wave reflections could be obtained by antihypertensive treatment as observed with the calcium-channel blocker and ACE inhibitors 8. It has been shown that improvement of aortic compliance and use of ACE inhibitors had favorable independent effect on survival in hypertensive patients with ESRD 9. REFERENCES 1. Nichols WW, O'Rourke MF: McDonald's blood flow in arteries: theoretical, experimental and clinical principles (4th edn.). Edward Arnold, London, 1998. 2. Safar ME, London GM: The arterial system in human hypertension. In: Textbook of Hypertension (ed. Swales JD). London: Blackwell Scientific. 1994. p. 85-102. 3. London GM, Guérin AP, Marchais SJ y cols.: Cardiac and arterial interactions in end-stage renal disease. Kidney Int 50: 600-8, 1996. 4. Mourad JJ, Girerd X, Boutouyrie P y cols.: Increases stiffness of radial artery wall material in end-stage renal disease. Hypertesion 30: 1425-30, 1997. 5. Blacher J, Guérin AP, Pannier B y cols.: Impact of aortic stiffness on survival in end-stage renal disease. Circulation 99: 2434-2439, 1999. 6. Laurent S, Boutouyrie P, Asmar R y cols.: Aortic sitffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension 37: 1236-41, 2001. 7. London GM, Blacher J, Pannier B y cols.: Arterial wave reflections and survival in end-stage renal failure. Hypertension 38: 434-438, 2001. 8. London GM, Pannier B, Guerin AP y cols.: Cardiac hypertrophy, aortic compliance, peripheral resistance and wave reflection in end-stage renal disease: comparative effects of ACE inhibition and calcium channel blockade. Circulation 90: 2786-96, 1994. 9. Guérin AP, Blacher J, Pannier B y cols.: Impact of aortic stiffness attenuation on survival of patients in end-stage renal failure. Circulation 103: 987-92, 2001. 13 " "pdfFichero" => "P7-E193-S140-A3681.pdf" "tienePdf" => true ] "idiomaDefecto" => "en" "url" => "/02116995/00000022000000S2/v0_201502091327/X0211699502027873/v0_201502091327/en/main.assets" "Apartado" => array:4 [ "identificador" => "35407" "tipo" => "SECCION" "es" => array:2 [ "titulo" => "Suplementos" "idiomaDefecto" => true ] "idiomaDefecto" => "es" ] "PDF" => "https://static.elsevier.es/multimedia/02116995/00000022000000S2/v0_201502091327/X0211699502027873/v0_201502091327/en/P7-E193-S140-A3681.pdf?idApp=UINPBA000064&text.app=https://revistanefrologia.com/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/X0211699502027873?idApp=UINPBA000064" ]
Información de la revista
Acceso a texto completo
Large artery damage and hypertension in end-stage renal failure (ESRD)
Visitas
5299
G. M. LONDON
Este artículo ha recibido
Información del artículo
Texto completo
NEFROLOGÍA. Vol. XXII. Suplemento 2. 2002 Large artery damage and hypertension in end-stage renal failure (ESRD) G. M. London Hospital Manhes, Fleury Mérogis. France. The ill effects of hypertension are attributed to reduction in the caliber or the number of arterioles, resulting in increased total peripheral resistance (TPR). TPR is a determinant of mean arterial pressure (MBP) considered as constant over time. This does not take into account the fact that BP is an oscillatory phenomenon with systolic and diastolic BP being the limits of these oscillations. Moreover, while MBP and diastolic BP are almost constant along the arterial tree, systolic BP is amplified from the aorta to the brachial artery whose systolic BP only indirectly reflects the pressure in the aorta and LV1. The appropriate term to define the arterial factor(s) opposing LV ejection is aortic input impedance which depends on TPR, arterial compliance, wave reflections, and inertance of blood column in the arterial tree. Arterial compliance and wave reflections are major determinants of systolic and diastolic BP, and the pressure wave amplitude, i.e. pulse pressure (PP) which is an independent cardiovascular risk factor. ALTERATIONS OF AORTIC INPUT IMPEDANCE IN ESRD AND ITS CONSEQUENCES Due to anemia or arteriovenous shunts, TPR is usually within normal values in ESRD patients. The aortic impedance is increased principally due to decreased arterial compliance (arterial stiffening), increased wave reflections and higher inertance 2, 3. In ESRD changes in compliance are associated with arterial remodelling, pricipally intima-media thickening and the enlargement of arterial lumen 3. The enlargement of the arteries increases the volume and mass of blood contained in the arterial tree and is responsible for increased inertance. The increased stiffness ins renal failure is due to alterations of biomaterials characterized by increased elastic modulus (Einc) 4 associated with arterial mediacalcosis, and low-grade inflammation. Besides arterial sitffness, early wave reflections represents major contribution to LV afterload and compromised coronary perfusion 1. Wave reflections are frequently increased in es- sential hypertension and almost constantly increased in ESRD 2, 3. The arterial stiffening estimated by changes in aortic pulse wave velocity is an independent predictor of survival in ESRD and general population5-6. Increased wave reflections independently from changes in arterial stiffness are also a strong predictor of survival in ESRD patients 7. Improvement of arterial compliance and decrease in the effect of wave reflections could be obtained by antihypertensive treatment as observed with the calcium-channel blocker and ACE inhibitors 8. It has been shown that improvement of aortic compliance and use of ACE inhibitors had favorable independent effect on survival in hypertensive patients with ESRD 9. REFERENCES 1. Nichols WW, O'Rourke MF: McDonald's blood flow in arteries: theoretical, experimental and clinical principles (4th edn.). Edward Arnold, London, 1998. 2. Safar ME, London GM: The arterial system in human hypertension. In: Textbook of Hypertension (ed. Swales JD). London: Blackwell Scientific. 1994. p. 85-102. 3. London GM, Guérin AP, Marchais SJ y cols.: Cardiac and arterial interactions in end-stage renal disease. Kidney Int 50: 600-8, 1996. 4. Mourad JJ, Girerd X, Boutouyrie P y cols.: Increases stiffness of radial artery wall material in end-stage renal disease. Hypertesion 30: 1425-30, 1997. 5. Blacher J, Guérin AP, Pannier B y cols.: Impact of aortic stiffness on survival in end-stage renal disease. Circulation 99: 2434-2439, 1999. 6. Laurent S, Boutouyrie P, Asmar R y cols.: Aortic sitffness is an independent predictor of all-cause and cardiovascular mortality in hypertensive patients. Hypertension 37: 1236-41, 2001. 7. London GM, Blacher J, Pannier B y cols.: Arterial wave reflections and survival in end-stage renal failure. Hypertension 38: 434-438, 2001. 8. London GM, Pannier B, Guerin AP y cols.: Cardiac hypertrophy, aortic compliance, peripheral resistance and wave reflection in end-stage renal disease: comparative effects of ACE inhibition and calcium channel blockade. Circulation 90: 2786-96, 1994. 9. Guérin AP, Blacher J, Pannier B y cols.: Impact of aortic stiffness attenuation on survival of patients in end-stage renal failure. Circulation 103: 987-92, 2001. 13