A Metabolic Approach to the Management of Ischemic Heart Disease
Abstract Myocardial ischemia occurs when there is a supply and demand imbalance between the delivery of oxygenated blood to the myocardium and the needs of the myocardium to maintain normal cardiac function at any level of activity. The commonest cause of the imbalance is obstructive coronary artery...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Jackson, Graham [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2003 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: American journal of cardiovascular drugs - Cham : Springer, 2001, 3(2003), Suppl 1 vom: Dez., Seite 27-33 |
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| Übergeordnetes Werk: |
volume:3 ; year:2003 ; number:Suppl 1 ; month:12 ; pages:27-33 |
| Links: |
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| DOI / URN: |
10.2165/00129784-200303001-00004 |
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SPR032945574 |
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| 520 | |a Abstract Myocardial ischemia occurs when there is a supply and demand imbalance between the delivery of oxygenated blood to the myocardium and the needs of the myocardium to maintain normal cardiac function at any level of activity. The commonest cause of the imbalance is obstructive coronary artery disease. A pharmacologic hemodynamic approach to therapy principally focuses on reducing demand (slowing heart rate, lowering blood pressure, reducing contractility and increasing peripheral venous and arterial vasodilatation), with a variable effect on supply (coronary vasodilatation). This is a proven and highly effective approach indirectly improving myocardial metabolism. An alternative and complementary strategy avoids any effect on hemodynamics, but by direct action at the cellular level minimizes the ischemic disruption of cardiac metabolism. Trimetazidine inhibits the fatty acid oxidation enzyme long-chain 3-ketoacyl-coenzyme A thiolase (3-KAT), thereby decreasing fatty acid oxidation and increasing the combustion of glucose and lactate. This switch back from ischemia-induced fatty acid oxidation to glucose oxidation has been shown to be of significant clinical benefit, both subjectively and objectively, independent of or in combination with conventional hemodynamic agents. | ||
| 650 | 4 | |a Stable Angina |7 (dpeaa)DE-He213 | |
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| 650 | 4 | |a Chronic Stable Angina |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Isosorbide Dinitrate |7 (dpeaa)DE-He213 | |
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10.2165/00129784-200303001-00004 doi (DE-627)SPR032945574 (SPR)00129784-200303001-00004-e DE-627 ger DE-627 rakwb eng 610 ASE Jackson, Graham verfasserin aut A Metabolic Approach to the Management of Ischemic Heart Disease 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Myocardial ischemia occurs when there is a supply and demand imbalance between the delivery of oxygenated blood to the myocardium and the needs of the myocardium to maintain normal cardiac function at any level of activity. The commonest cause of the imbalance is obstructive coronary artery disease. A pharmacologic hemodynamic approach to therapy principally focuses on reducing demand (slowing heart rate, lowering blood pressure, reducing contractility and increasing peripheral venous and arterial vasodilatation), with a variable effect on supply (coronary vasodilatation). This is a proven and highly effective approach indirectly improving myocardial metabolism. An alternative and complementary strategy avoids any effect on hemodynamics, but by direct action at the cellular level minimizes the ischemic disruption of cardiac metabolism. Trimetazidine inhibits the fatty acid oxidation enzyme long-chain 3-ketoacyl-coenzyme A thiolase (3-KAT), thereby decreasing fatty acid oxidation and increasing the combustion of glucose and lactate. This switch back from ischemia-induced fatty acid oxidation to glucose oxidation has been shown to be of significant clinical benefit, both subjectively and objectively, independent of or in combination with conventional hemodynamic agents. Stable Angina (dpeaa)DE-He213 Obstructive Coronary Artery Disease (dpeaa)DE-He213 Trimetazidine (dpeaa)DE-He213 Chronic Stable Angina (dpeaa)DE-He213 Isosorbide Dinitrate (dpeaa)DE-He213 Enthalten in American journal of cardiovascular drugs Cham : Springer, 2001 3(2003), Suppl 1 vom: Dez., Seite 27-33 (DE-627)327643943 (DE-600)2043647-6 1179-187X nnns volume:3 year:2003 number:Suppl 1 month:12 pages:27-33 https://dx.doi.org/10.2165/00129784-200303001-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE 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_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 3 2003 Suppl 1 12 27-33 |
| spelling |
10.2165/00129784-200303001-00004 doi (DE-627)SPR032945574 (SPR)00129784-200303001-00004-e DE-627 ger DE-627 rakwb eng 610 ASE Jackson, Graham verfasserin aut A Metabolic Approach to the Management of Ischemic Heart Disease 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Myocardial ischemia occurs when there is a supply and demand imbalance between the delivery of oxygenated blood to the myocardium and the needs of the myocardium to maintain normal cardiac function at any level of activity. The commonest cause of the imbalance is obstructive coronary artery disease. A pharmacologic hemodynamic approach to therapy principally focuses on reducing demand (slowing heart rate, lowering blood pressure, reducing contractility and increasing peripheral venous and arterial vasodilatation), with a variable effect on supply (coronary vasodilatation). This is a proven and highly effective approach indirectly improving myocardial metabolism. An alternative and complementary strategy avoids any effect on hemodynamics, but by direct action at the cellular level minimizes the ischemic disruption of cardiac metabolism. Trimetazidine inhibits the fatty acid oxidation enzyme long-chain 3-ketoacyl-coenzyme A thiolase (3-KAT), thereby decreasing fatty acid oxidation and increasing the combustion of glucose and lactate. This switch back from ischemia-induced fatty acid oxidation to glucose oxidation has been shown to be of significant clinical benefit, both subjectively and objectively, independent of or in combination with conventional hemodynamic agents. Stable Angina (dpeaa)DE-He213 Obstructive Coronary Artery Disease (dpeaa)DE-He213 Trimetazidine (dpeaa)DE-He213 Chronic Stable Angina (dpeaa)DE-He213 Isosorbide Dinitrate (dpeaa)DE-He213 Enthalten in American journal of cardiovascular drugs Cham : Springer, 2001 3(2003), Suppl 1 vom: Dez., Seite 27-33 (DE-627)327643943 (DE-600)2043647-6 1179-187X nnns volume:3 year:2003 number:Suppl 1 month:12 pages:27-33 https://dx.doi.org/10.2165/00129784-200303001-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE 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_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 3 2003 Suppl 1 12 27-33 |
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10.2165/00129784-200303001-00004 doi (DE-627)SPR032945574 (SPR)00129784-200303001-00004-e DE-627 ger DE-627 rakwb eng 610 ASE Jackson, Graham verfasserin aut A Metabolic Approach to the Management of Ischemic Heart Disease 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Myocardial ischemia occurs when there is a supply and demand imbalance between the delivery of oxygenated blood to the myocardium and the needs of the myocardium to maintain normal cardiac function at any level of activity. The commonest cause of the imbalance is obstructive coronary artery disease. A pharmacologic hemodynamic approach to therapy principally focuses on reducing demand (slowing heart rate, lowering blood pressure, reducing contractility and increasing peripheral venous and arterial vasodilatation), with a variable effect on supply (coronary vasodilatation). This is a proven and highly effective approach indirectly improving myocardial metabolism. An alternative and complementary strategy avoids any effect on hemodynamics, but by direct action at the cellular level minimizes the ischemic disruption of cardiac metabolism. Trimetazidine inhibits the fatty acid oxidation enzyme long-chain 3-ketoacyl-coenzyme A thiolase (3-KAT), thereby decreasing fatty acid oxidation and increasing the combustion of glucose and lactate. This switch back from ischemia-induced fatty acid oxidation to glucose oxidation has been shown to be of significant clinical benefit, both subjectively and objectively, independent of or in combination with conventional hemodynamic agents. Stable Angina (dpeaa)DE-He213 Obstructive Coronary Artery Disease (dpeaa)DE-He213 Trimetazidine (dpeaa)DE-He213 Chronic Stable Angina (dpeaa)DE-He213 Isosorbide Dinitrate (dpeaa)DE-He213 Enthalten in American journal of cardiovascular drugs Cham : Springer, 2001 3(2003), Suppl 1 vom: Dez., Seite 27-33 (DE-627)327643943 (DE-600)2043647-6 1179-187X nnns volume:3 year:2003 number:Suppl 1 month:12 pages:27-33 https://dx.doi.org/10.2165/00129784-200303001-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE 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_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 3 2003 Suppl 1 12 27-33 |
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10.2165/00129784-200303001-00004 doi (DE-627)SPR032945574 (SPR)00129784-200303001-00004-e DE-627 ger DE-627 rakwb eng 610 ASE Jackson, Graham verfasserin aut A Metabolic Approach to the Management of Ischemic Heart Disease 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Myocardial ischemia occurs when there is a supply and demand imbalance between the delivery of oxygenated blood to the myocardium and the needs of the myocardium to maintain normal cardiac function at any level of activity. The commonest cause of the imbalance is obstructive coronary artery disease. A pharmacologic hemodynamic approach to therapy principally focuses on reducing demand (slowing heart rate, lowering blood pressure, reducing contractility and increasing peripheral venous and arterial vasodilatation), with a variable effect on supply (coronary vasodilatation). This is a proven and highly effective approach indirectly improving myocardial metabolism. An alternative and complementary strategy avoids any effect on hemodynamics, but by direct action at the cellular level minimizes the ischemic disruption of cardiac metabolism. Trimetazidine inhibits the fatty acid oxidation enzyme long-chain 3-ketoacyl-coenzyme A thiolase (3-KAT), thereby decreasing fatty acid oxidation and increasing the combustion of glucose and lactate. This switch back from ischemia-induced fatty acid oxidation to glucose oxidation has been shown to be of significant clinical benefit, both subjectively and objectively, independent of or in combination with conventional hemodynamic agents. Stable Angina (dpeaa)DE-He213 Obstructive Coronary Artery Disease (dpeaa)DE-He213 Trimetazidine (dpeaa)DE-He213 Chronic Stable Angina (dpeaa)DE-He213 Isosorbide Dinitrate (dpeaa)DE-He213 Enthalten in American journal of cardiovascular drugs Cham : Springer, 2001 3(2003), Suppl 1 vom: Dez., Seite 27-33 (DE-627)327643943 (DE-600)2043647-6 1179-187X nnns volume:3 year:2003 number:Suppl 1 month:12 pages:27-33 https://dx.doi.org/10.2165/00129784-200303001-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE 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_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 3 2003 Suppl 1 12 27-33 |
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10.2165/00129784-200303001-00004 doi (DE-627)SPR032945574 (SPR)00129784-200303001-00004-e DE-627 ger DE-627 rakwb eng 610 ASE Jackson, Graham verfasserin aut A Metabolic Approach to the Management of Ischemic Heart Disease 2003 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Myocardial ischemia occurs when there is a supply and demand imbalance between the delivery of oxygenated blood to the myocardium and the needs of the myocardium to maintain normal cardiac function at any level of activity. The commonest cause of the imbalance is obstructive coronary artery disease. A pharmacologic hemodynamic approach to therapy principally focuses on reducing demand (slowing heart rate, lowering blood pressure, reducing contractility and increasing peripheral venous and arterial vasodilatation), with a variable effect on supply (coronary vasodilatation). This is a proven and highly effective approach indirectly improving myocardial metabolism. An alternative and complementary strategy avoids any effect on hemodynamics, but by direct action at the cellular level minimizes the ischemic disruption of cardiac metabolism. Trimetazidine inhibits the fatty acid oxidation enzyme long-chain 3-ketoacyl-coenzyme A thiolase (3-KAT), thereby decreasing fatty acid oxidation and increasing the combustion of glucose and lactate. This switch back from ischemia-induced fatty acid oxidation to glucose oxidation has been shown to be of significant clinical benefit, both subjectively and objectively, independent of or in combination with conventional hemodynamic agents. Stable Angina (dpeaa)DE-He213 Obstructive Coronary Artery Disease (dpeaa)DE-He213 Trimetazidine (dpeaa)DE-He213 Chronic Stable Angina (dpeaa)DE-He213 Isosorbide Dinitrate (dpeaa)DE-He213 Enthalten in American journal of cardiovascular drugs Cham : Springer, 2001 3(2003), Suppl 1 vom: Dez., Seite 27-33 (DE-627)327643943 (DE-600)2043647-6 1179-187X nnns volume:3 year:2003 number:Suppl 1 month:12 pages:27-33 https://dx.doi.org/10.2165/00129784-200303001-00004 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA SSG-OPC-PHA SSG-OPC-ASE 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_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 3 2003 Suppl 1 12 27-33 |
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Enthalten in American journal of cardiovascular drugs 3(2003), Suppl 1 vom: Dez., Seite 27-33 volume:3 year:2003 number:Suppl 1 month:12 pages:27-33 |
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Stable Angina Obstructive Coronary Artery Disease Trimetazidine Chronic Stable Angina Isosorbide Dinitrate |
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Jackson, Graham @@aut@@ |
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Jackson, Graham |
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metabolic approach to the management of ischemic heart disease |
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A Metabolic Approach to the Management of Ischemic Heart Disease |
| abstract |
Abstract Myocardial ischemia occurs when there is a supply and demand imbalance between the delivery of oxygenated blood to the myocardium and the needs of the myocardium to maintain normal cardiac function at any level of activity. The commonest cause of the imbalance is obstructive coronary artery disease. A pharmacologic hemodynamic approach to therapy principally focuses on reducing demand (slowing heart rate, lowering blood pressure, reducing contractility and increasing peripheral venous and arterial vasodilatation), with a variable effect on supply (coronary vasodilatation). This is a proven and highly effective approach indirectly improving myocardial metabolism. An alternative and complementary strategy avoids any effect on hemodynamics, but by direct action at the cellular level minimizes the ischemic disruption of cardiac metabolism. Trimetazidine inhibits the fatty acid oxidation enzyme long-chain 3-ketoacyl-coenzyme A thiolase (3-KAT), thereby decreasing fatty acid oxidation and increasing the combustion of glucose and lactate. This switch back from ischemia-induced fatty acid oxidation to glucose oxidation has been shown to be of significant clinical benefit, both subjectively and objectively, independent of or in combination with conventional hemodynamic agents. |
| abstractGer |
Abstract Myocardial ischemia occurs when there is a supply and demand imbalance between the delivery of oxygenated blood to the myocardium and the needs of the myocardium to maintain normal cardiac function at any level of activity. The commonest cause of the imbalance is obstructive coronary artery disease. A pharmacologic hemodynamic approach to therapy principally focuses on reducing demand (slowing heart rate, lowering blood pressure, reducing contractility and increasing peripheral venous and arterial vasodilatation), with a variable effect on supply (coronary vasodilatation). This is a proven and highly effective approach indirectly improving myocardial metabolism. An alternative and complementary strategy avoids any effect on hemodynamics, but by direct action at the cellular level minimizes the ischemic disruption of cardiac metabolism. Trimetazidine inhibits the fatty acid oxidation enzyme long-chain 3-ketoacyl-coenzyme A thiolase (3-KAT), thereby decreasing fatty acid oxidation and increasing the combustion of glucose and lactate. This switch back from ischemia-induced fatty acid oxidation to glucose oxidation has been shown to be of significant clinical benefit, both subjectively and objectively, independent of or in combination with conventional hemodynamic agents. |
| abstract_unstemmed |
Abstract Myocardial ischemia occurs when there is a supply and demand imbalance between the delivery of oxygenated blood to the myocardium and the needs of the myocardium to maintain normal cardiac function at any level of activity. The commonest cause of the imbalance is obstructive coronary artery disease. A pharmacologic hemodynamic approach to therapy principally focuses on reducing demand (slowing heart rate, lowering blood pressure, reducing contractility and increasing peripheral venous and arterial vasodilatation), with a variable effect on supply (coronary vasodilatation). This is a proven and highly effective approach indirectly improving myocardial metabolism. An alternative and complementary strategy avoids any effect on hemodynamics, but by direct action at the cellular level minimizes the ischemic disruption of cardiac metabolism. Trimetazidine inhibits the fatty acid oxidation enzyme long-chain 3-ketoacyl-coenzyme A thiolase (3-KAT), thereby decreasing fatty acid oxidation and increasing the combustion of glucose and lactate. This switch back from ischemia-induced fatty acid oxidation to glucose oxidation has been shown to be of significant clinical benefit, both subjectively and objectively, independent of or in combination with conventional hemodynamic agents. |
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A Metabolic Approach to the Management of Ischemic Heart Disease |
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