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
Hauptverfasser: Bell, David S. H., Goncalves, Edison
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Goncalves, Edison
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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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 &amp; metabolism, 2019-06, Vol.21 (6), p.1277-1290</ispartof><rights>2019 John Wiley &amp; Sons Ltd</rights><rights>2019 John Wiley &amp; 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 &amp; 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. 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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. 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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 &amp; 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. 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source MEDLINE; Wiley Online Library Journals Frontfile Complete
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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