Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data?

Abstract Poorly controlled diabetes is characterized by premature cardiovascular mortality and morbidity. The mechanisms linking hyperglycemia with accelerated atherosclerotic disease have not been fully elucidated; however, are thought to be mediated through vascular inflammation, oxidative stress...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Strain, W. David [verfasserIn] Smith, Christine

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Cardiovascular outcomes DPP-4 inhibition Endothelial function GLP-1 receptor agonists Incretin

Anmerkung:	© The Author(s) 2016

Übergeordnetes Werk:	Enthalten in: Diabetes therapy - New York, NY [u.a.] : Springer Healthcare Communications, 2010, 7(2016), 2 vom: 24. März, Seite 175-185
Übergeordnetes Werk:	volume:7 ; year:2016 ; number:2 ; day:24 ; month:03 ; pages:175-185

Links:	Volltext

DOI / URN:	10.1007/s13300-016-0165-z

Katalog-ID:	SPR031250513

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spelling	10.1007/s13300-016-0165-z doi (DE-627)SPR031250513 (SPR)s13300-016-0165-z-e DE-627 ger DE-627 rakwb eng Strain, W. David verfasserin aut Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data? 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Abstract Poorly controlled diabetes is characterized by premature cardiovascular mortality and morbidity. The mechanisms linking hyperglycemia with accelerated atherosclerotic disease have not been fully elucidated; however, are thought to be mediated through vascular inflammation, oxidative stress and endothelial dysfunction. The advent of incretin-based therapy, whether by increasing endogenous glucagon-like peptide (GLP)-1 and glucose-dependent inhibitory polypeptide by inhibition of their breakdown using di-peptidyl peptidase 4 inhibitors, or augmenting GLP-1 activity using either exendin-4-based drugs or synthetic GLP-1 analogs promised not just improvements in glycemic control, but improvements in endothelial function, lipid profiles and markers of vascular inflammation. As such, it was anticipated they would demonstrate cardiovascular benefit in those with diabetes, indeed early meta-analyses suggested cardiovascular events would be reduced. To date, however, this benefit has failed to materialize, indeed the cardiovascular outcome trials, whilst meeting their primary endpoint of cardiovascular safety, have failed to demonstrate any improvements in stroke or myocardial infarction. This review will explore the data and attempt to answer the question: what went wrong? Cardiovascular outcomes (dpeaa)DE-He213 DPP-4 inhibition (dpeaa)DE-He213 Endothelial function (dpeaa)DE-He213 GLP-1 receptor agonists (dpeaa)DE-He213 Incretin (dpeaa)DE-He213 Smith, Christine aut Enthalten in Diabetes therapy New York, NY [u.a.] : Springer Healthcare Communications, 2010 7(2016), 2 vom: 24. März, Seite 175-185 (DE-627)632439165 (DE-600)2566702-6 1869-6961 nnns volume:7 year:2016 number:2 day:24 month:03 pages:175-185 https://dx.doi.org/10.1007/s13300-016-0165-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016 2 24 03 175-185
allfields_unstemmed	10.1007/s13300-016-0165-z doi (DE-627)SPR031250513 (SPR)s13300-016-0165-z-e DE-627 ger DE-627 rakwb eng Strain, W. David verfasserin aut Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data? 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Abstract Poorly controlled diabetes is characterized by premature cardiovascular mortality and morbidity. The mechanisms linking hyperglycemia with accelerated atherosclerotic disease have not been fully elucidated; however, are thought to be mediated through vascular inflammation, oxidative stress and endothelial dysfunction. The advent of incretin-based therapy, whether by increasing endogenous glucagon-like peptide (GLP)-1 and glucose-dependent inhibitory polypeptide by inhibition of their breakdown using di-peptidyl peptidase 4 inhibitors, or augmenting GLP-1 activity using either exendin-4-based drugs or synthetic GLP-1 analogs promised not just improvements in glycemic control, but improvements in endothelial function, lipid profiles and markers of vascular inflammation. As such, it was anticipated they would demonstrate cardiovascular benefit in those with diabetes, indeed early meta-analyses suggested cardiovascular events would be reduced. To date, however, this benefit has failed to materialize, indeed the cardiovascular outcome trials, whilst meeting their primary endpoint of cardiovascular safety, have failed to demonstrate any improvements in stroke or myocardial infarction. This review will explore the data and attempt to answer the question: what went wrong? Cardiovascular outcomes (dpeaa)DE-He213 DPP-4 inhibition (dpeaa)DE-He213 Endothelial function (dpeaa)DE-He213 GLP-1 receptor agonists (dpeaa)DE-He213 Incretin (dpeaa)DE-He213 Smith, Christine aut Enthalten in Diabetes therapy New York, NY [u.a.] : Springer Healthcare Communications, 2010 7(2016), 2 vom: 24. März, Seite 175-185 (DE-627)632439165 (DE-600)2566702-6 1869-6961 nnns volume:7 year:2016 number:2 day:24 month:03 pages:175-185 https://dx.doi.org/10.1007/s13300-016-0165-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016 2 24 03 175-185
allfieldsGer	10.1007/s13300-016-0165-z doi (DE-627)SPR031250513 (SPR)s13300-016-0165-z-e DE-627 ger DE-627 rakwb eng Strain, W. David verfasserin aut Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data? 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Abstract Poorly controlled diabetes is characterized by premature cardiovascular mortality and morbidity. The mechanisms linking hyperglycemia with accelerated atherosclerotic disease have not been fully elucidated; however, are thought to be mediated through vascular inflammation, oxidative stress and endothelial dysfunction. The advent of incretin-based therapy, whether by increasing endogenous glucagon-like peptide (GLP)-1 and glucose-dependent inhibitory polypeptide by inhibition of their breakdown using di-peptidyl peptidase 4 inhibitors, or augmenting GLP-1 activity using either exendin-4-based drugs or synthetic GLP-1 analogs promised not just improvements in glycemic control, but improvements in endothelial function, lipid profiles and markers of vascular inflammation. As such, it was anticipated they would demonstrate cardiovascular benefit in those with diabetes, indeed early meta-analyses suggested cardiovascular events would be reduced. To date, however, this benefit has failed to materialize, indeed the cardiovascular outcome trials, whilst meeting their primary endpoint of cardiovascular safety, have failed to demonstrate any improvements in stroke or myocardial infarction. This review will explore the data and attempt to answer the question: what went wrong? Cardiovascular outcomes (dpeaa)DE-He213 DPP-4 inhibition (dpeaa)DE-He213 Endothelial function (dpeaa)DE-He213 GLP-1 receptor agonists (dpeaa)DE-He213 Incretin (dpeaa)DE-He213 Smith, Christine aut Enthalten in Diabetes therapy New York, NY [u.a.] : Springer Healthcare Communications, 2010 7(2016), 2 vom: 24. März, Seite 175-185 (DE-627)632439165 (DE-600)2566702-6 1869-6961 nnns volume:7 year:2016 number:2 day:24 month:03 pages:175-185 https://dx.doi.org/10.1007/s13300-016-0165-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016 2 24 03 175-185
allfieldsSound	10.1007/s13300-016-0165-z doi (DE-627)SPR031250513 (SPR)s13300-016-0165-z-e DE-627 ger DE-627 rakwb eng Strain, W. David verfasserin aut Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data? 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2016 Abstract Poorly controlled diabetes is characterized by premature cardiovascular mortality and morbidity. The mechanisms linking hyperglycemia with accelerated atherosclerotic disease have not been fully elucidated; however, are thought to be mediated through vascular inflammation, oxidative stress and endothelial dysfunction. The advent of incretin-based therapy, whether by increasing endogenous glucagon-like peptide (GLP)-1 and glucose-dependent inhibitory polypeptide by inhibition of their breakdown using di-peptidyl peptidase 4 inhibitors, or augmenting GLP-1 activity using either exendin-4-based drugs or synthetic GLP-1 analogs promised not just improvements in glycemic control, but improvements in endothelial function, lipid profiles and markers of vascular inflammation. As such, it was anticipated they would demonstrate cardiovascular benefit in those with diabetes, indeed early meta-analyses suggested cardiovascular events would be reduced. To date, however, this benefit has failed to materialize, indeed the cardiovascular outcome trials, whilst meeting their primary endpoint of cardiovascular safety, have failed to demonstrate any improvements in stroke or myocardial infarction. This review will explore the data and attempt to answer the question: what went wrong? Cardiovascular outcomes (dpeaa)DE-He213 DPP-4 inhibition (dpeaa)DE-He213 Endothelial function (dpeaa)DE-He213 GLP-1 receptor agonists (dpeaa)DE-He213 Incretin (dpeaa)DE-He213 Smith, Christine aut Enthalten in Diabetes therapy New York, NY [u.a.] : Springer Healthcare Communications, 2010 7(2016), 2 vom: 24. März, Seite 175-185 (DE-627)632439165 (DE-600)2566702-6 1869-6961 nnns volume:7 year:2016 number:2 day:24 month:03 pages:175-185 https://dx.doi.org/10.1007/s13300-016-0165-z kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 7 2016 2 24 03 175-185
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source	Enthalten in Diabetes therapy 7(2016), 2 vom: 24. März, Seite 175-185 volume:7 year:2016 number:2 day:24 month:03 pages:175-185
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author	Strain, W. David
spellingShingle	Strain, W. David misc Cardiovascular outcomes misc DPP-4 inhibition misc Endothelial function misc GLP-1 receptor agonists misc Incretin Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data?
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topic_title	Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data? Cardiovascular outcomes (dpeaa)DE-He213 DPP-4 inhibition (dpeaa)DE-He213 Endothelial function (dpeaa)DE-He213 GLP-1 receptor agonists (dpeaa)DE-He213 Incretin (dpeaa)DE-He213
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title	Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data?
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title_full	Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data?
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title_auth	Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data?
abstract	Abstract Poorly controlled diabetes is characterized by premature cardiovascular mortality and morbidity. The mechanisms linking hyperglycemia with accelerated atherosclerotic disease have not been fully elucidated; however, are thought to be mediated through vascular inflammation, oxidative stress and endothelial dysfunction. The advent of incretin-based therapy, whether by increasing endogenous glucagon-like peptide (GLP)-1 and glucose-dependent inhibitory polypeptide by inhibition of their breakdown using di-peptidyl peptidase 4 inhibitors, or augmenting GLP-1 activity using either exendin-4-based drugs or synthetic GLP-1 analogs promised not just improvements in glycemic control, but improvements in endothelial function, lipid profiles and markers of vascular inflammation. As such, it was anticipated they would demonstrate cardiovascular benefit in those with diabetes, indeed early meta-analyses suggested cardiovascular events would be reduced. To date, however, this benefit has failed to materialize, indeed the cardiovascular outcome trials, whilst meeting their primary endpoint of cardiovascular safety, have failed to demonstrate any improvements in stroke or myocardial infarction. This review will explore the data and attempt to answer the question: what went wrong? © The Author(s) 2016
abstractGer	Abstract Poorly controlled diabetes is characterized by premature cardiovascular mortality and morbidity. The mechanisms linking hyperglycemia with accelerated atherosclerotic disease have not been fully elucidated; however, are thought to be mediated through vascular inflammation, oxidative stress and endothelial dysfunction. The advent of incretin-based therapy, whether by increasing endogenous glucagon-like peptide (GLP)-1 and glucose-dependent inhibitory polypeptide by inhibition of their breakdown using di-peptidyl peptidase 4 inhibitors, or augmenting GLP-1 activity using either exendin-4-based drugs or synthetic GLP-1 analogs promised not just improvements in glycemic control, but improvements in endothelial function, lipid profiles and markers of vascular inflammation. As such, it was anticipated they would demonstrate cardiovascular benefit in those with diabetes, indeed early meta-analyses suggested cardiovascular events would be reduced. To date, however, this benefit has failed to materialize, indeed the cardiovascular outcome trials, whilst meeting their primary endpoint of cardiovascular safety, have failed to demonstrate any improvements in stroke or myocardial infarction. This review will explore the data and attempt to answer the question: what went wrong? © The Author(s) 2016
abstract_unstemmed	Abstract Poorly controlled diabetes is characterized by premature cardiovascular mortality and morbidity. The mechanisms linking hyperglycemia with accelerated atherosclerotic disease have not been fully elucidated; however, are thought to be mediated through vascular inflammation, oxidative stress and endothelial dysfunction. The advent of incretin-based therapy, whether by increasing endogenous glucagon-like peptide (GLP)-1 and glucose-dependent inhibitory polypeptide by inhibition of their breakdown using di-peptidyl peptidase 4 inhibitors, or augmenting GLP-1 activity using either exendin-4-based drugs or synthetic GLP-1 analogs promised not just improvements in glycemic control, but improvements in endothelial function, lipid profiles and markers of vascular inflammation. As such, it was anticipated they would demonstrate cardiovascular benefit in those with diabetes, indeed early meta-analyses suggested cardiovascular events would be reduced. To date, however, this benefit has failed to materialize, indeed the cardiovascular outcome trials, whilst meeting their primary endpoint of cardiovascular safety, have failed to demonstrate any improvements in stroke or myocardial infarction. This review will explore the data and attempt to answer the question: what went wrong? © The Author(s) 2016
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title_short	Cardiovascular Outcome Studies in Diabetes: How Do We Make Sense of These New Data?
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