Heart failure in the patient with diabetes: Epidemiology, aetiology, prognosis, therapy and the effect of glucose‐lowering medications
In people with type 2 diabetes the frequency of heart failure (HF) is increased and mortality from HF is higher than with non‐diabetic HF. The increased frequency of HF is attributable to the cardiotoxic tetrad of ischaemic heart disease, left ventricular hypertrophy, diabetic cardiomyopathy and an...
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Veröffentlicht in: | Diabetes, obesity & metabolism obesity & metabolism, 2019-06, Vol.21 (6), p.1277-1290 |
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description | In people with type 2 diabetes the frequency of heart failure (HF) is increased and mortality from HF is higher than with non‐diabetic HF. The increased frequency of HF is attributable to the cardiotoxic tetrad of ischaemic heart disease, left ventricular hypertrophy, diabetic cardiomyopathy and an extracellular volume expansion resistant to atrial natriuretic peptides. Activation of the renin‐angiotensin‐aldosterone system and sympathetic nervous systems results in cardiac remodelling, which worsens cardiac function. Reversal of remodelling can be achieved, and cardiac function improved in people with HF with reduced ejection fraction (HFrEF) by treatment with angiotensin‐converting enzyme inhibitors and β‐blockers. However, with HF with preserved ejection fraction (HFpEF), only therapy for the underlying risk factors helps. Blockers of mineralocorticoid receptors may be beneficial in both HFrEF and HFpEF. Glucose‐lowering drugs can have a negative effect (insulin, sulphonylureas, dipeptidyl peptidase‐4 inhibitors and thiazolidinediones), a neutral effect (α‐glucosidase inhibitors and glucagon‐like peptide‐1 receptor agonists) or a positive effect (sodium‐glucose co‐transporter‐2 inhibitors and metformin). |
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H. ; Goncalves, Edison</creator><creatorcontrib>Bell, David S. H. ; Goncalves, Edison</creatorcontrib><description>In people with type 2 diabetes the frequency of heart failure (HF) is increased and mortality from HF is higher than with non‐diabetic HF. The increased frequency of HF is attributable to the cardiotoxic tetrad of ischaemic heart disease, left ventricular hypertrophy, diabetic cardiomyopathy and an extracellular volume expansion resistant to atrial natriuretic peptides. Activation of the renin‐angiotensin‐aldosterone system and sympathetic nervous systems results in cardiac remodelling, which worsens cardiac function. Reversal of remodelling can be achieved, and cardiac function improved in people with HF with reduced ejection fraction (HFrEF) by treatment with angiotensin‐converting enzyme inhibitors and β‐blockers. However, with HF with preserved ejection fraction (HFpEF), only therapy for the underlying risk factors helps. Blockers of mineralocorticoid receptors may be beneficial in both HFrEF and HFpEF. Glucose‐lowering drugs can have a negative effect (insulin, sulphonylureas, dipeptidyl peptidase‐4 inhibitors and thiazolidinediones), a neutral effect (α‐glucosidase inhibitors and glucagon‐like peptide‐1 receptor agonists) or a positive effect (sodium‐glucose co‐transporter‐2 inhibitors and metformin).</description><identifier>ISSN: 1462-8902</identifier><identifier>EISSN: 1463-1326</identifier><identifier>DOI: 10.1111/dom.13652</identifier><identifier>PMID: 30724013</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Aldosterone ; Angiotensin ; antidiabetic drug ; Antidiabetics ; Blood Glucose - drug effects ; Cardiac function ; Cardiomyopathy ; Congestive heart failure ; Coronary artery disease ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - drug therapy ; Dipeptidyl-peptidase IV ; Epidemiology ; GLP-1 receptor agonists ; GLP‐1 analogue ; Glucagon ; Glucose ; Glucose transporter ; Heart failure ; Heart Failure - complications ; Heart Failure - diagnosis ; Humans ; Hypertrophy ; Hypoglycemic Agents - adverse effects ; Hypoglycemic Agents - pharmacology ; Hypoglycemic Agents - therapeutic use ; Insulin ; insulin therapy ; Medical prognosis ; Metformin ; Mineralocorticoid receptors ; Peptidase ; Prognosis ; Renin ; Risk factors ; SGLT2 inhibitor ; Sodium ; Thiazolidinediones ; Ventricle ; Ventricular Remodeling - drug effects ; α-Glucosidase</subject><ispartof>Diabetes, obesity & metabolism, 2019-06, Vol.21 (6), p.1277-1290</ispartof><rights>2019 John Wiley & Sons Ltd</rights><rights>2019 John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3532-1ee35eaf85411ea26d64bf10f97d06cba6ab6214320a2c5b25a1c258ee7906213</citedby><cites>FETCH-LOGICAL-c3532-1ee35eaf85411ea26d64bf10f97d06cba6ab6214320a2c5b25a1c258ee7906213</cites><orcidid>0000-0002-3035-6126 ; 0000-0002-7887-1231</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fdom.13652$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fdom.13652$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30724013$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bell, David S. H.</creatorcontrib><creatorcontrib>Goncalves, Edison</creatorcontrib><title>Heart failure in the patient with diabetes: Epidemiology, aetiology, prognosis, therapy and the effect of glucose‐lowering medications</title><title>Diabetes, obesity & metabolism</title><addtitle>Diabetes Obes Metab</addtitle><description>In people with type 2 diabetes the frequency of heart failure (HF) is increased and mortality from HF is higher than with non‐diabetic HF. The increased frequency of HF is attributable to the cardiotoxic tetrad of ischaemic heart disease, left ventricular hypertrophy, diabetic cardiomyopathy and an extracellular volume expansion resistant to atrial natriuretic peptides. Activation of the renin‐angiotensin‐aldosterone system and sympathetic nervous systems results in cardiac remodelling, which worsens cardiac function. Reversal of remodelling can be achieved, and cardiac function improved in people with HF with reduced ejection fraction (HFrEF) by treatment with angiotensin‐converting enzyme inhibitors and β‐blockers. However, with HF with preserved ejection fraction (HFpEF), only therapy for the underlying risk factors helps. Blockers of mineralocorticoid receptors may be beneficial in both HFrEF and HFpEF. Glucose‐lowering drugs can have a negative effect (insulin, sulphonylureas, dipeptidyl peptidase‐4 inhibitors and thiazolidinediones), a neutral effect (α‐glucosidase inhibitors and glucagon‐like peptide‐1 receptor agonists) or a positive effect (sodium‐glucose co‐transporter‐2 inhibitors and metformin).</description><subject>Aldosterone</subject><subject>Angiotensin</subject><subject>antidiabetic drug</subject><subject>Antidiabetics</subject><subject>Blood Glucose - drug effects</subject><subject>Cardiac function</subject><subject>Cardiomyopathy</subject><subject>Congestive heart failure</subject><subject>Coronary artery disease</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Dipeptidyl-peptidase IV</subject><subject>Epidemiology</subject><subject>GLP-1 receptor agonists</subject><subject>GLP‐1 analogue</subject><subject>Glucagon</subject><subject>Glucose</subject><subject>Glucose transporter</subject><subject>Heart failure</subject><subject>Heart Failure - complications</subject><subject>Heart Failure - diagnosis</subject><subject>Humans</subject><subject>Hypertrophy</subject><subject>Hypoglycemic Agents - adverse effects</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Insulin</subject><subject>insulin therapy</subject><subject>Medical prognosis</subject><subject>Metformin</subject><subject>Mineralocorticoid receptors</subject><subject>Peptidase</subject><subject>Prognosis</subject><subject>Renin</subject><subject>Risk factors</subject><subject>SGLT2 inhibitor</subject><subject>Sodium</subject><subject>Thiazolidinediones</subject><subject>Ventricle</subject><subject>Ventricular Remodeling - drug effects</subject><subject>α-Glucosidase</subject><issn>1462-8902</issn><issn>1463-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kL9OwzAQhy0EoqUw8ALIEhMSaf0vacuGoFAkUBeYIyc5t67SONiOqm6MjDwjT4LbFDa83En-_J3vh9A5JX0azqAwqz7lScwOUJeKhEeUs-Rw17NoNCasg06cWxJCBB8Nj1GHkyEThPIu-pyCtB4rqcvGAtYV9gvAtfQaKo_X2i9woWUGHtwNntS6gJU2pZlvrrEE_9vW1swr47S73j63st5gWRU7FSgFucdG4XnZ5MbB98dXadZgdTXHKyh0HmaZyp2iIyVLB2f72kNvD5PXu2n0PHt8urt9jnIecxZRAB6DVKNYUAqSJUUiMkWJGg8LkuSZTGSWMCo4I5LlccZiSXMWjwCGYxIueA9dtt7w5_cGnE-XprFVGJkyxkjMiBAiUFctlVvjnAWV1lavpN2klKTbzNOQebrLPLAXe2OThYX-yN-QAzBogbUuYfO_Kb2fvbTKH0nnjYM</recordid><startdate>201906</startdate><enddate>201906</enddate><creator>Bell, David S. H.</creator><creator>Goncalves, Edison</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><orcidid>https://orcid.org/0000-0002-3035-6126</orcidid><orcidid>https://orcid.org/0000-0002-7887-1231</orcidid></search><sort><creationdate>201906</creationdate><title>Heart failure in the patient with diabetes: Epidemiology, aetiology, prognosis, therapy and the effect of glucose‐lowering medications</title><author>Bell, David S. H. ; Goncalves, Edison</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3532-1ee35eaf85411ea26d64bf10f97d06cba6ab6214320a2c5b25a1c258ee7906213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aldosterone</topic><topic>Angiotensin</topic><topic>antidiabetic drug</topic><topic>Antidiabetics</topic><topic>Blood Glucose - drug effects</topic><topic>Cardiac function</topic><topic>Cardiomyopathy</topic><topic>Congestive heart failure</topic><topic>Coronary artery disease</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Dipeptidyl-peptidase IV</topic><topic>Epidemiology</topic><topic>GLP-1 receptor agonists</topic><topic>GLP‐1 analogue</topic><topic>Glucagon</topic><topic>Glucose</topic><topic>Glucose transporter</topic><topic>Heart failure</topic><topic>Heart Failure - complications</topic><topic>Heart Failure - diagnosis</topic><topic>Humans</topic><topic>Hypertrophy</topic><topic>Hypoglycemic Agents - adverse effects</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Insulin</topic><topic>insulin therapy</topic><topic>Medical prognosis</topic><topic>Metformin</topic><topic>Mineralocorticoid receptors</topic><topic>Peptidase</topic><topic>Prognosis</topic><topic>Renin</topic><topic>Risk factors</topic><topic>SGLT2 inhibitor</topic><topic>Sodium</topic><topic>Thiazolidinediones</topic><topic>Ventricle</topic><topic>Ventricular Remodeling - drug effects</topic><topic>α-Glucosidase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bell, David S. H.</creatorcontrib><creatorcontrib>Goncalves, Edison</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Diabetes, obesity & metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bell, David S. H.</au><au>Goncalves, Edison</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heart failure in the patient with diabetes: Epidemiology, aetiology, prognosis, therapy and the effect of glucose‐lowering medications</atitle><jtitle>Diabetes, obesity & metabolism</jtitle><addtitle>Diabetes Obes Metab</addtitle><date>2019-06</date><risdate>2019</risdate><volume>21</volume><issue>6</issue><spage>1277</spage><epage>1290</epage><pages>1277-1290</pages><issn>1462-8902</issn><eissn>1463-1326</eissn><abstract>In people with type 2 diabetes the frequency of heart failure (HF) is increased and mortality from HF is higher than with non‐diabetic HF. The increased frequency of HF is attributable to the cardiotoxic tetrad of ischaemic heart disease, left ventricular hypertrophy, diabetic cardiomyopathy and an extracellular volume expansion resistant to atrial natriuretic peptides. Activation of the renin‐angiotensin‐aldosterone system and sympathetic nervous systems results in cardiac remodelling, which worsens cardiac function. Reversal of remodelling can be achieved, and cardiac function improved in people with HF with reduced ejection fraction (HFrEF) by treatment with angiotensin‐converting enzyme inhibitors and β‐blockers. However, with HF with preserved ejection fraction (HFpEF), only therapy for the underlying risk factors helps. Blockers of mineralocorticoid receptors may be beneficial in both HFrEF and HFpEF. Glucose‐lowering drugs can have a negative effect (insulin, sulphonylureas, dipeptidyl peptidase‐4 inhibitors and thiazolidinediones), a neutral effect (α‐glucosidase inhibitors and glucagon‐like peptide‐1 receptor agonists) or a positive effect (sodium‐glucose co‐transporter‐2 inhibitors and metformin).</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>30724013</pmid><doi>10.1111/dom.13652</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-3035-6126</orcidid><orcidid>https://orcid.org/0000-0002-7887-1231</orcidid></addata></record> |
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subjects | Aldosterone Angiotensin antidiabetic drug Antidiabetics Blood Glucose - drug effects Cardiac function Cardiomyopathy Congestive heart failure Coronary artery disease Diabetes Diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - drug therapy Dipeptidyl-peptidase IV Epidemiology GLP-1 receptor agonists GLP‐1 analogue Glucagon Glucose Glucose transporter Heart failure Heart Failure - complications Heart Failure - diagnosis Humans Hypertrophy Hypoglycemic Agents - adverse effects Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use Insulin insulin therapy Medical prognosis Metformin Mineralocorticoid receptors Peptidase Prognosis Renin Risk factors SGLT2 inhibitor Sodium Thiazolidinediones Ventricle Ventricular Remodeling - drug effects α-Glucosidase |
title | Heart failure in the patient with diabetes: Epidemiology, aetiology, prognosis, therapy and the effect of glucose‐lowering medications |
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