Cardiovascular Risk in Hypertension - Can We Ask for More?
Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has res...
Ausführliche Beschreibung
Autor*in: |
Volpe, Massimo [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2008 |
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Anmerkung: |
© Adis Data Information BV 2008 |
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Übergeordnetes Werk: |
Enthalten in: High blood pressure & cardiovascular prevention - [S.l.] : Springer International, 2003, 15(2008), 4 vom: Okt., Seite 255-268 |
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Übergeordnetes Werk: |
volume:15 ; year:2008 ; number:4 ; month:10 ; pages:255-268 |
Links: |
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DOI / URN: |
10.2165/0151642-200815040-00005 |
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Katalog-ID: |
SPR036366129 |
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520 | |a Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has resulted in a better control of CV disease. The renin-angiotensin system (RAS) is involved in many pathophysiological processes underlying the development of major CV and renal diseases and, thus, it represents an ‘ideal’ target for the pharmacological treatment of these clinical conditions. Recently, in addition to the traditional therapeutic approaches, mostly based on the use of ACE inhibitors and/or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), the scientific and medical community have focused on a new therapeutic possibility to interfere with RAS activity. Indeed, the first compound of the new drug class of direct renin inhibitors, aliskiren, has been made available for clinical use. The therapeutic properties of aliskiren are of particular interest, since it interferes with the enzymatic activities of renin, the key rate-limiting step of the RAS cascade. This unique mechanism of action, e.g. occupation of the renin active site, provides an ‘upstream’ modulation in the RAS enzymatic-proteic cascade. This results in an inhibition of the biological properties of renin to promote the cleavage of the angiotensin I peptide from the angiotensinogen substrate. Clinical studies have demonstrated that the use of aliskiren provides antihypertensive efficacy comparable with, or even superior to, that observed with other classes of antihypertensive drugs. Also, the addition of aliskiren to different antihypertensive strategies results in a further significant increase in blood pressure (BP) reduction than those achieved with monotherapy based on diuretics, calcium-channel antagonists, ACE inhibitors and ARBs. The overall safety and tolerability of aliskiren are comparable with other classes of antihypertensive drugs and almost overlap with placebo. Recent evidence also demonstrates that aliskiren is effective in promoting the regression of organ damage (e.g. microalbuminuria and left ventricular hypertrophy), beyond its BP-lowering properties and in addition to standard therapies, including ARBs. An ambitious programme of clinical development of this modern antihypertensive drug will investigate whether aliskiren may further limit the incidence of major CV and renal events in hypertensive patients with co-morbidities, treated with the available therapeutic strategies, including ACE inhibitors and ARBs. | ||
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10.2165/0151642-200815040-00005 doi (DE-627)SPR036366129 (SPR)0151642-200815040-00005-e DE-627 ger DE-627 rakwb eng Volpe, Massimo verfasserin aut Cardiovascular Risk in Hypertension - Can We Ask for More? 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Adis Data Information BV 2008 Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has resulted in a better control of CV disease. The renin-angiotensin system (RAS) is involved in many pathophysiological processes underlying the development of major CV and renal diseases and, thus, it represents an ‘ideal’ target for the pharmacological treatment of these clinical conditions. Recently, in addition to the traditional therapeutic approaches, mostly based on the use of ACE inhibitors and/or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), the scientific and medical community have focused on a new therapeutic possibility to interfere with RAS activity. Indeed, the first compound of the new drug class of direct renin inhibitors, aliskiren, has been made available for clinical use. The therapeutic properties of aliskiren are of particular interest, since it interferes with the enzymatic activities of renin, the key rate-limiting step of the RAS cascade. This unique mechanism of action, e.g. occupation of the renin active site, provides an ‘upstream’ modulation in the RAS enzymatic-proteic cascade. This results in an inhibition of the biological properties of renin to promote the cleavage of the angiotensin I peptide from the angiotensinogen substrate. Clinical studies have demonstrated that the use of aliskiren provides antihypertensive efficacy comparable with, or even superior to, that observed with other classes of antihypertensive drugs. Also, the addition of aliskiren to different antihypertensive strategies results in a further significant increase in blood pressure (BP) reduction than those achieved with monotherapy based on diuretics, calcium-channel antagonists, ACE inhibitors and ARBs. The overall safety and tolerability of aliskiren are comparable with other classes of antihypertensive drugs and almost overlap with placebo. Recent evidence also demonstrates that aliskiren is effective in promoting the regression of organ damage (e.g. microalbuminuria and left ventricular hypertrophy), beyond its BP-lowering properties and in addition to standard therapies, including ARBs. An ambitious programme of clinical development of this modern antihypertensive drug will investigate whether aliskiren may further limit the incidence of major CV and renal events in hypertensive patients with co-morbidities, treated with the available therapeutic strategies, including ACE inhibitors and ARBs. Enthalten in High blood pressure & cardiovascular prevention [S.l.] : Springer International, 2003 15(2008), 4 vom: Okt., Seite 255-268 (DE-627)490226264 (DE-600)2192466-1 1179-1985 nnns volume:15 year:2008 number:4 month:10 pages:255-268 https://dx.doi.org/10.2165/0151642-200815040-00005 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 15 2008 4 10 255-268 |
spelling |
10.2165/0151642-200815040-00005 doi (DE-627)SPR036366129 (SPR)0151642-200815040-00005-e DE-627 ger DE-627 rakwb eng Volpe, Massimo verfasserin aut Cardiovascular Risk in Hypertension - Can We Ask for More? 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Adis Data Information BV 2008 Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has resulted in a better control of CV disease. The renin-angiotensin system (RAS) is involved in many pathophysiological processes underlying the development of major CV and renal diseases and, thus, it represents an ‘ideal’ target for the pharmacological treatment of these clinical conditions. Recently, in addition to the traditional therapeutic approaches, mostly based on the use of ACE inhibitors and/or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), the scientific and medical community have focused on a new therapeutic possibility to interfere with RAS activity. Indeed, the first compound of the new drug class of direct renin inhibitors, aliskiren, has been made available for clinical use. The therapeutic properties of aliskiren are of particular interest, since it interferes with the enzymatic activities of renin, the key rate-limiting step of the RAS cascade. This unique mechanism of action, e.g. occupation of the renin active site, provides an ‘upstream’ modulation in the RAS enzymatic-proteic cascade. This results in an inhibition of the biological properties of renin to promote the cleavage of the angiotensin I peptide from the angiotensinogen substrate. Clinical studies have demonstrated that the use of aliskiren provides antihypertensive efficacy comparable with, or even superior to, that observed with other classes of antihypertensive drugs. Also, the addition of aliskiren to different antihypertensive strategies results in a further significant increase in blood pressure (BP) reduction than those achieved with monotherapy based on diuretics, calcium-channel antagonists, ACE inhibitors and ARBs. The overall safety and tolerability of aliskiren are comparable with other classes of antihypertensive drugs and almost overlap with placebo. Recent evidence also demonstrates that aliskiren is effective in promoting the regression of organ damage (e.g. microalbuminuria and left ventricular hypertrophy), beyond its BP-lowering properties and in addition to standard therapies, including ARBs. An ambitious programme of clinical development of this modern antihypertensive drug will investigate whether aliskiren may further limit the incidence of major CV and renal events in hypertensive patients with co-morbidities, treated with the available therapeutic strategies, including ACE inhibitors and ARBs. Enthalten in High blood pressure & cardiovascular prevention [S.l.] : Springer International, 2003 15(2008), 4 vom: Okt., Seite 255-268 (DE-627)490226264 (DE-600)2192466-1 1179-1985 nnns volume:15 year:2008 number:4 month:10 pages:255-268 https://dx.doi.org/10.2165/0151642-200815040-00005 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 15 2008 4 10 255-268 |
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10.2165/0151642-200815040-00005 doi (DE-627)SPR036366129 (SPR)0151642-200815040-00005-e DE-627 ger DE-627 rakwb eng Volpe, Massimo verfasserin aut Cardiovascular Risk in Hypertension - Can We Ask for More? 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Adis Data Information BV 2008 Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has resulted in a better control of CV disease. The renin-angiotensin system (RAS) is involved in many pathophysiological processes underlying the development of major CV and renal diseases and, thus, it represents an ‘ideal’ target for the pharmacological treatment of these clinical conditions. Recently, in addition to the traditional therapeutic approaches, mostly based on the use of ACE inhibitors and/or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), the scientific and medical community have focused on a new therapeutic possibility to interfere with RAS activity. Indeed, the first compound of the new drug class of direct renin inhibitors, aliskiren, has been made available for clinical use. The therapeutic properties of aliskiren are of particular interest, since it interferes with the enzymatic activities of renin, the key rate-limiting step of the RAS cascade. This unique mechanism of action, e.g. occupation of the renin active site, provides an ‘upstream’ modulation in the RAS enzymatic-proteic cascade. This results in an inhibition of the biological properties of renin to promote the cleavage of the angiotensin I peptide from the angiotensinogen substrate. Clinical studies have demonstrated that the use of aliskiren provides antihypertensive efficacy comparable with, or even superior to, that observed with other classes of antihypertensive drugs. Also, the addition of aliskiren to different antihypertensive strategies results in a further significant increase in blood pressure (BP) reduction than those achieved with monotherapy based on diuretics, calcium-channel antagonists, ACE inhibitors and ARBs. The overall safety and tolerability of aliskiren are comparable with other classes of antihypertensive drugs and almost overlap with placebo. Recent evidence also demonstrates that aliskiren is effective in promoting the regression of organ damage (e.g. microalbuminuria and left ventricular hypertrophy), beyond its BP-lowering properties and in addition to standard therapies, including ARBs. An ambitious programme of clinical development of this modern antihypertensive drug will investigate whether aliskiren may further limit the incidence of major CV and renal events in hypertensive patients with co-morbidities, treated with the available therapeutic strategies, including ACE inhibitors and ARBs. Enthalten in High blood pressure & cardiovascular prevention [S.l.] : Springer International, 2003 15(2008), 4 vom: Okt., Seite 255-268 (DE-627)490226264 (DE-600)2192466-1 1179-1985 nnns volume:15 year:2008 number:4 month:10 pages:255-268 https://dx.doi.org/10.2165/0151642-200815040-00005 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 15 2008 4 10 255-268 |
allfieldsGer |
10.2165/0151642-200815040-00005 doi (DE-627)SPR036366129 (SPR)0151642-200815040-00005-e DE-627 ger DE-627 rakwb eng Volpe, Massimo verfasserin aut Cardiovascular Risk in Hypertension - Can We Ask for More? 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Adis Data Information BV 2008 Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has resulted in a better control of CV disease. The renin-angiotensin system (RAS) is involved in many pathophysiological processes underlying the development of major CV and renal diseases and, thus, it represents an ‘ideal’ target for the pharmacological treatment of these clinical conditions. Recently, in addition to the traditional therapeutic approaches, mostly based on the use of ACE inhibitors and/or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), the scientific and medical community have focused on a new therapeutic possibility to interfere with RAS activity. Indeed, the first compound of the new drug class of direct renin inhibitors, aliskiren, has been made available for clinical use. The therapeutic properties of aliskiren are of particular interest, since it interferes with the enzymatic activities of renin, the key rate-limiting step of the RAS cascade. This unique mechanism of action, e.g. occupation of the renin active site, provides an ‘upstream’ modulation in the RAS enzymatic-proteic cascade. This results in an inhibition of the biological properties of renin to promote the cleavage of the angiotensin I peptide from the angiotensinogen substrate. Clinical studies have demonstrated that the use of aliskiren provides antihypertensive efficacy comparable with, or even superior to, that observed with other classes of antihypertensive drugs. Also, the addition of aliskiren to different antihypertensive strategies results in a further significant increase in blood pressure (BP) reduction than those achieved with monotherapy based on diuretics, calcium-channel antagonists, ACE inhibitors and ARBs. The overall safety and tolerability of aliskiren are comparable with other classes of antihypertensive drugs and almost overlap with placebo. Recent evidence also demonstrates that aliskiren is effective in promoting the regression of organ damage (e.g. microalbuminuria and left ventricular hypertrophy), beyond its BP-lowering properties and in addition to standard therapies, including ARBs. An ambitious programme of clinical development of this modern antihypertensive drug will investigate whether aliskiren may further limit the incidence of major CV and renal events in hypertensive patients with co-morbidities, treated with the available therapeutic strategies, including ACE inhibitors and ARBs. Enthalten in High blood pressure & cardiovascular prevention [S.l.] : Springer International, 2003 15(2008), 4 vom: Okt., Seite 255-268 (DE-627)490226264 (DE-600)2192466-1 1179-1985 nnns volume:15 year:2008 number:4 month:10 pages:255-268 https://dx.doi.org/10.2165/0151642-200815040-00005 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 15 2008 4 10 255-268 |
allfieldsSound |
10.2165/0151642-200815040-00005 doi (DE-627)SPR036366129 (SPR)0151642-200815040-00005-e DE-627 ger DE-627 rakwb eng Volpe, Massimo verfasserin aut Cardiovascular Risk in Hypertension - Can We Ask for More? 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Adis Data Information BV 2008 Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has resulted in a better control of CV disease. The renin-angiotensin system (RAS) is involved in many pathophysiological processes underlying the development of major CV and renal diseases and, thus, it represents an ‘ideal’ target for the pharmacological treatment of these clinical conditions. Recently, in addition to the traditional therapeutic approaches, mostly based on the use of ACE inhibitors and/or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), the scientific and medical community have focused on a new therapeutic possibility to interfere with RAS activity. Indeed, the first compound of the new drug class of direct renin inhibitors, aliskiren, has been made available for clinical use. The therapeutic properties of aliskiren are of particular interest, since it interferes with the enzymatic activities of renin, the key rate-limiting step of the RAS cascade. This unique mechanism of action, e.g. occupation of the renin active site, provides an ‘upstream’ modulation in the RAS enzymatic-proteic cascade. This results in an inhibition of the biological properties of renin to promote the cleavage of the angiotensin I peptide from the angiotensinogen substrate. Clinical studies have demonstrated that the use of aliskiren provides antihypertensive efficacy comparable with, or even superior to, that observed with other classes of antihypertensive drugs. Also, the addition of aliskiren to different antihypertensive strategies results in a further significant increase in blood pressure (BP) reduction than those achieved with monotherapy based on diuretics, calcium-channel antagonists, ACE inhibitors and ARBs. The overall safety and tolerability of aliskiren are comparable with other classes of antihypertensive drugs and almost overlap with placebo. Recent evidence also demonstrates that aliskiren is effective in promoting the regression of organ damage (e.g. microalbuminuria and left ventricular hypertrophy), beyond its BP-lowering properties and in addition to standard therapies, including ARBs. An ambitious programme of clinical development of this modern antihypertensive drug will investigate whether aliskiren may further limit the incidence of major CV and renal events in hypertensive patients with co-morbidities, treated with the available therapeutic strategies, including ACE inhibitors and ARBs. Enthalten in High blood pressure & cardiovascular prevention [S.l.] : Springer International, 2003 15(2008), 4 vom: Okt., Seite 255-268 (DE-627)490226264 (DE-600)2192466-1 1179-1985 nnns volume:15 year:2008 number:4 month:10 pages:255-268 https://dx.doi.org/10.2165/0151642-200815040-00005 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_266 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 15 2008 4 10 255-268 |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR036366129</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519212532.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2008 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.2165/0151642-200815040-00005</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR036366129</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)0151642-200815040-00005-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Volpe, Massimo</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Cardiovascular Risk in Hypertension - Can We Ask for More?</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2008</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Adis Data Information BV 2008</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has resulted in a better control of CV disease. The renin-angiotensin system (RAS) is involved in many pathophysiological processes underlying the development of major CV and renal diseases and, thus, it represents an ‘ideal’ target for the pharmacological treatment of these clinical conditions. Recently, in addition to the traditional therapeutic approaches, mostly based on the use of ACE inhibitors and/or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), the scientific and medical community have focused on a new therapeutic possibility to interfere with RAS activity. Indeed, the first compound of the new drug class of direct renin inhibitors, aliskiren, has been made available for clinical use. 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The overall safety and tolerability of aliskiren are comparable with other classes of antihypertensive drugs and almost overlap with placebo. Recent evidence also demonstrates that aliskiren is effective in promoting the regression of organ damage (e.g. microalbuminuria and left ventricular hypertrophy), beyond its BP-lowering properties and in addition to standard therapies, including ARBs. An ambitious programme of clinical development of this modern antihypertensive drug will investigate whether aliskiren may further limit the incidence of major CV and renal events in hypertensive patients with co-morbidities, treated with the available therapeutic strategies, including ACE inhibitors and ARBs.</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">High blood pressure & cardiovascular prevention</subfield><subfield code="d">[S.l.] : Springer International, 2003</subfield><subfield code="g">15(2008), 4 vom: Okt., Seite 255-268</subfield><subfield code="w">(DE-627)490226264</subfield><subfield code="w">(DE-600)2192466-1</subfield><subfield code="x">1179-1985</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:15</subfield><subfield code="g">year:2008</subfield><subfield code="g">number:4</subfield><subfield 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Cardiovascular Risk in Hypertension - Can We Ask for More? |
abstract |
Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has resulted in a better control of CV disease. The renin-angiotensin system (RAS) is involved in many pathophysiological processes underlying the development of major CV and renal diseases and, thus, it represents an ‘ideal’ target for the pharmacological treatment of these clinical conditions. Recently, in addition to the traditional therapeutic approaches, mostly based on the use of ACE inhibitors and/or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), the scientific and medical community have focused on a new therapeutic possibility to interfere with RAS activity. Indeed, the first compound of the new drug class of direct renin inhibitors, aliskiren, has been made available for clinical use. The therapeutic properties of aliskiren are of particular interest, since it interferes with the enzymatic activities of renin, the key rate-limiting step of the RAS cascade. This unique mechanism of action, e.g. occupation of the renin active site, provides an ‘upstream’ modulation in the RAS enzymatic-proteic cascade. This results in an inhibition of the biological properties of renin to promote the cleavage of the angiotensin I peptide from the angiotensinogen substrate. Clinical studies have demonstrated that the use of aliskiren provides antihypertensive efficacy comparable with, or even superior to, that observed with other classes of antihypertensive drugs. Also, the addition of aliskiren to different antihypertensive strategies results in a further significant increase in blood pressure (BP) reduction than those achieved with monotherapy based on diuretics, calcium-channel antagonists, ACE inhibitors and ARBs. The overall safety and tolerability of aliskiren are comparable with other classes of antihypertensive drugs and almost overlap with placebo. Recent evidence also demonstrates that aliskiren is effective in promoting the regression of organ damage (e.g. microalbuminuria and left ventricular hypertrophy), beyond its BP-lowering properties and in addition to standard therapies, including ARBs. An ambitious programme of clinical development of this modern antihypertensive drug will investigate whether aliskiren may further limit the incidence of major CV and renal events in hypertensive patients with co-morbidities, treated with the available therapeutic strategies, including ACE inhibitors and ARBs. © Adis Data Information BV 2008 |
abstractGer |
Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has resulted in a better control of CV disease. The renin-angiotensin system (RAS) is involved in many pathophysiological processes underlying the development of major CV and renal diseases and, thus, it represents an ‘ideal’ target for the pharmacological treatment of these clinical conditions. Recently, in addition to the traditional therapeutic approaches, mostly based on the use of ACE inhibitors and/or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), the scientific and medical community have focused on a new therapeutic possibility to interfere with RAS activity. Indeed, the first compound of the new drug class of direct renin inhibitors, aliskiren, has been made available for clinical use. The therapeutic properties of aliskiren are of particular interest, since it interferes with the enzymatic activities of renin, the key rate-limiting step of the RAS cascade. This unique mechanism of action, e.g. occupation of the renin active site, provides an ‘upstream’ modulation in the RAS enzymatic-proteic cascade. This results in an inhibition of the biological properties of renin to promote the cleavage of the angiotensin I peptide from the angiotensinogen substrate. Clinical studies have demonstrated that the use of aliskiren provides antihypertensive efficacy comparable with, or even superior to, that observed with other classes of antihypertensive drugs. Also, the addition of aliskiren to different antihypertensive strategies results in a further significant increase in blood pressure (BP) reduction than those achieved with monotherapy based on diuretics, calcium-channel antagonists, ACE inhibitors and ARBs. The overall safety and tolerability of aliskiren are comparable with other classes of antihypertensive drugs and almost overlap with placebo. Recent evidence also demonstrates that aliskiren is effective in promoting the regression of organ damage (e.g. microalbuminuria and left ventricular hypertrophy), beyond its BP-lowering properties and in addition to standard therapies, including ARBs. An ambitious programme of clinical development of this modern antihypertensive drug will investigate whether aliskiren may further limit the incidence of major CV and renal events in hypertensive patients with co-morbidities, treated with the available therapeutic strategies, including ACE inhibitors and ARBs. © Adis Data Information BV 2008 |
abstract_unstemmed |
Abstract The burden of cardiovascular (CV) disease remains high nowadays, despite the tremendous development in the therapeutic strategies that has occurred during the last 30 years. The growing focus on pharmacological strategies capable of interacting with key pathophysiological mechanisms has resulted in a better control of CV disease. The renin-angiotensin system (RAS) is involved in many pathophysiological processes underlying the development of major CV and renal diseases and, thus, it represents an ‘ideal’ target for the pharmacological treatment of these clinical conditions. Recently, in addition to the traditional therapeutic approaches, mostly based on the use of ACE inhibitors and/or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), the scientific and medical community have focused on a new therapeutic possibility to interfere with RAS activity. Indeed, the first compound of the new drug class of direct renin inhibitors, aliskiren, has been made available for clinical use. The therapeutic properties of aliskiren are of particular interest, since it interferes with the enzymatic activities of renin, the key rate-limiting step of the RAS cascade. This unique mechanism of action, e.g. occupation of the renin active site, provides an ‘upstream’ modulation in the RAS enzymatic-proteic cascade. This results in an inhibition of the biological properties of renin to promote the cleavage of the angiotensin I peptide from the angiotensinogen substrate. Clinical studies have demonstrated that the use of aliskiren provides antihypertensive efficacy comparable with, or even superior to, that observed with other classes of antihypertensive drugs. Also, the addition of aliskiren to different antihypertensive strategies results in a further significant increase in blood pressure (BP) reduction than those achieved with monotherapy based on diuretics, calcium-channel antagonists, ACE inhibitors and ARBs. The overall safety and tolerability of aliskiren are comparable with other classes of antihypertensive drugs and almost overlap with placebo. Recent evidence also demonstrates that aliskiren is effective in promoting the regression of organ damage (e.g. microalbuminuria and left ventricular hypertrophy), beyond its BP-lowering properties and in addition to standard therapies, including ARBs. An ambitious programme of clinical development of this modern antihypertensive drug will investigate whether aliskiren may further limit the incidence of major CV and renal events in hypertensive patients with co-morbidities, treated with the available therapeutic strategies, including ACE inhibitors and ARBs. © Adis Data Information BV 2008 |
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title_short |
Cardiovascular Risk in Hypertension - Can We Ask for More? |
url |
https://dx.doi.org/10.2165/0151642-200815040-00005 |
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score |
7.3985224 |