Sildenafil and phosphodiesterase-5 inhibitors for heart failure
Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nit...
Ausführliche Beschreibung
Autor*in: |
Guazzi, Marco [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2008 |
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Schlagwörter: |
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Übergeordnetes Werk: |
Enthalten in: Current heart failure reports - Philadelphia, Pa. : Current Science, 2004, 5(2008), 2 vom: Juni, Seite 110-114 |
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Übergeordnetes Werk: |
volume:5 ; year:2008 ; number:2 ; month:06 ; pages:110-114 |
Links: |
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DOI / URN: |
10.1007/s11897-008-0018-9 |
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Katalog-ID: |
SPR022919759 |
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520 | |a Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nitric oxide signaling by increasing the availability of cyclic guanosine monophosphate (cGMP). A number of background studies support the use of PDE5 inhibitors in HF. Treatment of pulmonary hypertension secondary to left ventricular dysfunction appears to be a primary target by virtue of the high PDE5 selectivity for the pulmonary circulation. Basic studies suggest that increased cGMP activity by PDE5 inhibition has potentially favorable direct myocardial effects that may block adrenergic, hypertrophic, and proapoptotic signaling. Furthermore, studies in humans have underscored the benefits of acute PDE5 inhibition on lung diffusion capacity, systemic endothelial function, muscle perfusion, and exercise performance. Despite promising initial data, larger controlled trials are necessary to define the safety, tolerability, and potential impact of PDE5 inhibitors on morbidity and mortality across the wide spectrum of patients with HF. | ||
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10.1007/s11897-008-0018-9 doi (DE-627)SPR022919759 (SPR)s11897-008-0018-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Guazzi, Marco verfasserin aut Sildenafil and phosphodiesterase-5 inhibitors for heart failure 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nitric oxide signaling by increasing the availability of cyclic guanosine monophosphate (cGMP). A number of background studies support the use of PDE5 inhibitors in HF. Treatment of pulmonary hypertension secondary to left ventricular dysfunction appears to be a primary target by virtue of the high PDE5 selectivity for the pulmonary circulation. Basic studies suggest that increased cGMP activity by PDE5 inhibition has potentially favorable direct myocardial effects that may block adrenergic, hypertrophic, and proapoptotic signaling. Furthermore, studies in humans have underscored the benefits of acute PDE5 inhibition on lung diffusion capacity, systemic endothelial function, muscle perfusion, and exercise performance. Despite promising initial data, larger controlled trials are necessary to define the safety, tolerability, and potential impact of PDE5 inhibitors on morbidity and mortality across the wide spectrum of patients with HF. Pulmonary Hypertension (dpeaa)DE-He213 Chronic Heart Failure (dpeaa)DE-He213 PDE5 Inhibition (dpeaa)DE-He213 Systolic Heart Failure (dpeaa)DE-He213 Congestive Heart Failure Patient (dpeaa)DE-He213 Enthalten in Current heart failure reports Philadelphia, Pa. : Current Science, 2004 5(2008), 2 vom: Juni, Seite 110-114 (DE-627)479466890 (DE-600)2177075-X 1546-9549 nnns volume:5 year:2008 number:2 month:06 pages:110-114 https://dx.doi.org/10.1007/s11897-008-0018-9 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_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 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_2070 GBV_ILN_2086 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_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 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 44.85 ASE AR 5 2008 2 06 110-114 |
spelling |
10.1007/s11897-008-0018-9 doi (DE-627)SPR022919759 (SPR)s11897-008-0018-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Guazzi, Marco verfasserin aut Sildenafil and phosphodiesterase-5 inhibitors for heart failure 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nitric oxide signaling by increasing the availability of cyclic guanosine monophosphate (cGMP). A number of background studies support the use of PDE5 inhibitors in HF. Treatment of pulmonary hypertension secondary to left ventricular dysfunction appears to be a primary target by virtue of the high PDE5 selectivity for the pulmonary circulation. Basic studies suggest that increased cGMP activity by PDE5 inhibition has potentially favorable direct myocardial effects that may block adrenergic, hypertrophic, and proapoptotic signaling. Furthermore, studies in humans have underscored the benefits of acute PDE5 inhibition on lung diffusion capacity, systemic endothelial function, muscle perfusion, and exercise performance. Despite promising initial data, larger controlled trials are necessary to define the safety, tolerability, and potential impact of PDE5 inhibitors on morbidity and mortality across the wide spectrum of patients with HF. Pulmonary Hypertension (dpeaa)DE-He213 Chronic Heart Failure (dpeaa)DE-He213 PDE5 Inhibition (dpeaa)DE-He213 Systolic Heart Failure (dpeaa)DE-He213 Congestive Heart Failure Patient (dpeaa)DE-He213 Enthalten in Current heart failure reports Philadelphia, Pa. : Current Science, 2004 5(2008), 2 vom: Juni, Seite 110-114 (DE-627)479466890 (DE-600)2177075-X 1546-9549 nnns volume:5 year:2008 number:2 month:06 pages:110-114 https://dx.doi.org/10.1007/s11897-008-0018-9 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_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 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_2070 GBV_ILN_2086 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_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 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 44.85 ASE AR 5 2008 2 06 110-114 |
allfields_unstemmed |
10.1007/s11897-008-0018-9 doi (DE-627)SPR022919759 (SPR)s11897-008-0018-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Guazzi, Marco verfasserin aut Sildenafil and phosphodiesterase-5 inhibitors for heart failure 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nitric oxide signaling by increasing the availability of cyclic guanosine monophosphate (cGMP). A number of background studies support the use of PDE5 inhibitors in HF. Treatment of pulmonary hypertension secondary to left ventricular dysfunction appears to be a primary target by virtue of the high PDE5 selectivity for the pulmonary circulation. Basic studies suggest that increased cGMP activity by PDE5 inhibition has potentially favorable direct myocardial effects that may block adrenergic, hypertrophic, and proapoptotic signaling. Furthermore, studies in humans have underscored the benefits of acute PDE5 inhibition on lung diffusion capacity, systemic endothelial function, muscle perfusion, and exercise performance. Despite promising initial data, larger controlled trials are necessary to define the safety, tolerability, and potential impact of PDE5 inhibitors on morbidity and mortality across the wide spectrum of patients with HF. Pulmonary Hypertension (dpeaa)DE-He213 Chronic Heart Failure (dpeaa)DE-He213 PDE5 Inhibition (dpeaa)DE-He213 Systolic Heart Failure (dpeaa)DE-He213 Congestive Heart Failure Patient (dpeaa)DE-He213 Enthalten in Current heart failure reports Philadelphia, Pa. : Current Science, 2004 5(2008), 2 vom: Juni, Seite 110-114 (DE-627)479466890 (DE-600)2177075-X 1546-9549 nnns volume:5 year:2008 number:2 month:06 pages:110-114 https://dx.doi.org/10.1007/s11897-008-0018-9 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_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 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_2070 GBV_ILN_2086 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_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 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 44.85 ASE AR 5 2008 2 06 110-114 |
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10.1007/s11897-008-0018-9 doi (DE-627)SPR022919759 (SPR)s11897-008-0018-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Guazzi, Marco verfasserin aut Sildenafil and phosphodiesterase-5 inhibitors for heart failure 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nitric oxide signaling by increasing the availability of cyclic guanosine monophosphate (cGMP). A number of background studies support the use of PDE5 inhibitors in HF. Treatment of pulmonary hypertension secondary to left ventricular dysfunction appears to be a primary target by virtue of the high PDE5 selectivity for the pulmonary circulation. Basic studies suggest that increased cGMP activity by PDE5 inhibition has potentially favorable direct myocardial effects that may block adrenergic, hypertrophic, and proapoptotic signaling. Furthermore, studies in humans have underscored the benefits of acute PDE5 inhibition on lung diffusion capacity, systemic endothelial function, muscle perfusion, and exercise performance. Despite promising initial data, larger controlled trials are necessary to define the safety, tolerability, and potential impact of PDE5 inhibitors on morbidity and mortality across the wide spectrum of patients with HF. Pulmonary Hypertension (dpeaa)DE-He213 Chronic Heart Failure (dpeaa)DE-He213 PDE5 Inhibition (dpeaa)DE-He213 Systolic Heart Failure (dpeaa)DE-He213 Congestive Heart Failure Patient (dpeaa)DE-He213 Enthalten in Current heart failure reports Philadelphia, Pa. : Current Science, 2004 5(2008), 2 vom: Juni, Seite 110-114 (DE-627)479466890 (DE-600)2177075-X 1546-9549 nnns volume:5 year:2008 number:2 month:06 pages:110-114 https://dx.doi.org/10.1007/s11897-008-0018-9 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_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 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_2070 GBV_ILN_2086 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_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 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 44.85 ASE AR 5 2008 2 06 110-114 |
allfieldsSound |
10.1007/s11897-008-0018-9 doi (DE-627)SPR022919759 (SPR)s11897-008-0018-9-e DE-627 ger DE-627 rakwb eng 610 ASE 44.85 bkl Guazzi, Marco verfasserin aut Sildenafil and phosphodiesterase-5 inhibitors for heart failure 2008 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nitric oxide signaling by increasing the availability of cyclic guanosine monophosphate (cGMP). A number of background studies support the use of PDE5 inhibitors in HF. Treatment of pulmonary hypertension secondary to left ventricular dysfunction appears to be a primary target by virtue of the high PDE5 selectivity for the pulmonary circulation. Basic studies suggest that increased cGMP activity by PDE5 inhibition has potentially favorable direct myocardial effects that may block adrenergic, hypertrophic, and proapoptotic signaling. Furthermore, studies in humans have underscored the benefits of acute PDE5 inhibition on lung diffusion capacity, systemic endothelial function, muscle perfusion, and exercise performance. Despite promising initial data, larger controlled trials are necessary to define the safety, tolerability, and potential impact of PDE5 inhibitors on morbidity and mortality across the wide spectrum of patients with HF. Pulmonary Hypertension (dpeaa)DE-He213 Chronic Heart Failure (dpeaa)DE-He213 PDE5 Inhibition (dpeaa)DE-He213 Systolic Heart Failure (dpeaa)DE-He213 Congestive Heart Failure Patient (dpeaa)DE-He213 Enthalten in Current heart failure reports Philadelphia, Pa. : Current Science, 2004 5(2008), 2 vom: Juni, Seite 110-114 (DE-627)479466890 (DE-600)2177075-X 1546-9549 nnns volume:5 year:2008 number:2 month:06 pages:110-114 https://dx.doi.org/10.1007/s11897-008-0018-9 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_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 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_2070 GBV_ILN_2086 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_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 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 44.85 ASE AR 5 2008 2 06 110-114 |
language |
English |
source |
Enthalten in Current heart failure reports 5(2008), 2 vom: Juni, Seite 110-114 volume:5 year:2008 number:2 month:06 pages:110-114 |
sourceStr |
Enthalten in Current heart failure reports 5(2008), 2 vom: Juni, Seite 110-114 volume:5 year:2008 number:2 month:06 pages:110-114 |
format_phy_str_mv |
Article |
institution |
findex.gbv.de |
topic_facet |
Pulmonary Hypertension Chronic Heart Failure PDE5 Inhibition Systolic Heart Failure Congestive Heart Failure Patient |
dewey-raw |
610 |
isfreeaccess_bool |
false |
container_title |
Current heart failure reports |
authorswithroles_txt_mv |
Guazzi, Marco @@aut@@ |
publishDateDaySort_date |
2008-06-01T00:00:00Z |
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479466890 |
dewey-sort |
3610 |
id |
SPR022919759 |
language_de |
englisch |
fullrecord |
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Guazzi, Marco |
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Guazzi, Marco ddc 610 bkl 44.85 misc Pulmonary Hypertension misc Chronic Heart Failure misc PDE5 Inhibition misc Systolic Heart Failure misc Congestive Heart Failure Patient Sildenafil and phosphodiesterase-5 inhibitors for heart failure |
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610 ASE 44.85 bkl Sildenafil and phosphodiesterase-5 inhibitors for heart failure Pulmonary Hypertension (dpeaa)DE-He213 Chronic Heart Failure (dpeaa)DE-He213 PDE5 Inhibition (dpeaa)DE-He213 Systolic Heart Failure (dpeaa)DE-He213 Congestive Heart Failure Patient (dpeaa)DE-He213 |
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Sildenafil and phosphodiesterase-5 inhibitors for heart failure |
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sildenafil and phosphodiesterase-5 inhibitors for heart failure |
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Sildenafil and phosphodiesterase-5 inhibitors for heart failure |
abstract |
Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nitric oxide signaling by increasing the availability of cyclic guanosine monophosphate (cGMP). A number of background studies support the use of PDE5 inhibitors in HF. Treatment of pulmonary hypertension secondary to left ventricular dysfunction appears to be a primary target by virtue of the high PDE5 selectivity for the pulmonary circulation. Basic studies suggest that increased cGMP activity by PDE5 inhibition has potentially favorable direct myocardial effects that may block adrenergic, hypertrophic, and proapoptotic signaling. Furthermore, studies in humans have underscored the benefits of acute PDE5 inhibition on lung diffusion capacity, systemic endothelial function, muscle perfusion, and exercise performance. Despite promising initial data, larger controlled trials are necessary to define the safety, tolerability, and potential impact of PDE5 inhibitors on morbidity and mortality across the wide spectrum of patients with HF. |
abstractGer |
Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nitric oxide signaling by increasing the availability of cyclic guanosine monophosphate (cGMP). A number of background studies support the use of PDE5 inhibitors in HF. Treatment of pulmonary hypertension secondary to left ventricular dysfunction appears to be a primary target by virtue of the high PDE5 selectivity for the pulmonary circulation. Basic studies suggest that increased cGMP activity by PDE5 inhibition has potentially favorable direct myocardial effects that may block adrenergic, hypertrophic, and proapoptotic signaling. Furthermore, studies in humans have underscored the benefits of acute PDE5 inhibition on lung diffusion capacity, systemic endothelial function, muscle perfusion, and exercise performance. Despite promising initial data, larger controlled trials are necessary to define the safety, tolerability, and potential impact of PDE5 inhibitors on morbidity and mortality across the wide spectrum of patients with HF. |
abstract_unstemmed |
Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nitric oxide signaling by increasing the availability of cyclic guanosine monophosphate (cGMP). A number of background studies support the use of PDE5 inhibitors in HF. Treatment of pulmonary hypertension secondary to left ventricular dysfunction appears to be a primary target by virtue of the high PDE5 selectivity for the pulmonary circulation. Basic studies suggest that increased cGMP activity by PDE5 inhibition has potentially favorable direct myocardial effects that may block adrenergic, hypertrophic, and proapoptotic signaling. Furthermore, studies in humans have underscored the benefits of acute PDE5 inhibition on lung diffusion capacity, systemic endothelial function, muscle perfusion, and exercise performance. Despite promising initial data, larger controlled trials are necessary to define the safety, tolerability, and potential impact of PDE5 inhibitors on morbidity and mortality across the wide spectrum of patients with HF. |
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Sildenafil and phosphodiesterase-5 inhibitors for heart failure |
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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">SPR022919759</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519163436.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201006s2008 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s11897-008-0018-9</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR022919759</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s11897-008-0018-9-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="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.85</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Guazzi, Marco</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Sildenafil and phosphodiesterase-5 inhibitors for heart failure</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="520" ind1=" " ind2=" "><subfield code="a">Abstract Treatment of heart failure (HF) is a challenging task. An impaired nitric oxide pathway contributes to several abnormal cardiac and vascular phenotypes typical of the failing cardiovascular system. Inhibition of phosphodiesterase-5 (PDE5) is a new therapeutic strategy for overexpressing nitric oxide signaling by increasing the availability of cyclic guanosine monophosphate (cGMP). A number of background studies support the use of PDE5 inhibitors in HF. Treatment of pulmonary hypertension secondary to left ventricular dysfunction appears to be a primary target by virtue of the high PDE5 selectivity for the pulmonary circulation. Basic studies suggest that increased cGMP activity by PDE5 inhibition has potentially favorable direct myocardial effects that may block adrenergic, hypertrophic, and proapoptotic signaling. Furthermore, studies in humans have underscored the benefits of acute PDE5 inhibition on lung diffusion capacity, systemic endothelial function, muscle perfusion, and exercise performance. Despite promising initial data, larger controlled trials are necessary to define the safety, tolerability, and potential impact of PDE5 inhibitors on morbidity and mortality across the wide spectrum of patients with HF.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Pulmonary Hypertension</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Chronic Heart Failure</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">PDE5 Inhibition</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Systolic Heart Failure</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Congestive Heart Failure Patient</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield 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