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The relationship between endothelial-dependent flow-mediated dilation and diastolic function in type 2 diabetes

Aims Diastolic dysfunction represents the earliest and most common manifestation of diabetic cardiomyopathy. Nitric oxide (NO), a potent vasodilator and anti-inflammatory mediator released from the subendocardial and coronary endothelium, favors left ventricular distensibility and relaxation. In typ...

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Published in:Acta diabetologica 2024-11, Vol.61 (11), p.1475-1482
Main Authors: Cutruzzolà, Antonio, Parise, Martina, Cacia, Michele, Lucà, Stefania, Irace, Concetta, Gnasso, Agostino
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container_start_page 1475
container_title Acta diabetologica
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creator Cutruzzolà, Antonio
Parise, Martina
Cacia, Michele
Lucà, Stefania
Irace, Concetta
Gnasso, Agostino
description Aims Diastolic dysfunction represents the earliest and most common manifestation of diabetic cardiomyopathy. Nitric oxide (NO), a potent vasodilator and anti-inflammatory mediator released from the subendocardial and coronary endothelium, favors left ventricular distensibility and relaxation. In type 2 diabetes (T2D), the NO bioavailability is reduced due to the oxidative stress and inflammatory state of the endothelium, because of chronic hyperglycemia. The aim of the present research is to evaluate the relationship between endothelial function and diastolic function in subjects with T2D. Method Subjects with T2D and age and sex-matched healthy controls were consecutively recruited. All participants underwent flow-mediated dilation (FMD) to assess endothelial function, and echocardiography to evaluate diastolic function. Results Thirty-five patients (6 women, 29 men) and 35 healthy controls were included in the final analysis. FMD was significantly lower in T2D than controls (4.4 ± 3.4 vs. 8.5 ± 4.3%, p  = 0.001). T2D presented different abnormalities in diastolic function compared to controls: lower E/A (early to late diastolic transmitral flow velocity), lower septal and lateral e′ (early diastolic myocardial tissue velocity at septum and lateral wall), and higher E/e′ (surrogate of filling pressure). In subjects with T2D, we observed a significant correlation between FMD and E/e′ (r = −0.63, p  = 0.001), lateral e′ (r = 0.44, p  = 0.03), and septal e′ (r = 0.39, p  = 0.05). Conclusions Our observational study demonstrated a link between FMD and diastolic dysfunction in subjects with type 2 diabetes.
doi_str_mv 10.1007/s00592-024-02313-1
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Nitric oxide (NO), a potent vasodilator and anti-inflammatory mediator released from the subendocardial and coronary endothelium, favors left ventricular distensibility and relaxation. In type 2 diabetes (T2D), the NO bioavailability is reduced due to the oxidative stress and inflammatory state of the endothelium, because of chronic hyperglycemia. The aim of the present research is to evaluate the relationship between endothelial function and diastolic function in subjects with T2D. Method Subjects with T2D and age and sex-matched healthy controls were consecutively recruited. All participants underwent flow-mediated dilation (FMD) to assess endothelial function, and echocardiography to evaluate diastolic function. Results Thirty-five patients (6 women, 29 men) and 35 healthy controls were included in the final analysis. FMD was significantly lower in T2D than controls (4.4 ± 3.4 vs. 8.5 ± 4.3%, p  = 0.001). T2D presented different abnormalities in diastolic function compared to controls: lower E/A (early to late diastolic transmitral flow velocity), lower septal and lateral e′ (early diastolic myocardial tissue velocity at septum and lateral wall), and higher E/e′ (surrogate of filling pressure). In subjects with T2D, we observed a significant correlation between FMD and E/e′ (r = −0.63, p  = 0.001), lateral e′ (r = 0.44, p  = 0.03), and septal e′ (r = 0.39, p  = 0.05). Conclusions Our observational study demonstrated a link between FMD and diastolic dysfunction in subjects with type 2 diabetes.</description><identifier>ISSN: 1432-5233</identifier><identifier>ISSN: 0940-5429</identifier><identifier>EISSN: 1432-5233</identifier><identifier>DOI: 10.1007/s00592-024-02313-1</identifier><identifier>PMID: 38847923</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Adult ; Aged ; Bioavailability ; Blood Flow Velocity - physiology ; Cardiomyopathy ; Case-Control Studies ; Diabetes ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - complications ; Diabetes Mellitus, Type 2 - physiopathology ; Diabetic Cardiomyopathies - diagnostic imaging ; Diabetic Cardiomyopathies - etiology ; Diabetic Cardiomyopathies - physiopathology ; Diastole - physiology ; Echocardiography ; Endothelium ; Endothelium, Vascular - physiopathology ; Female ; Flow velocity ; Heart ; Humans ; Hyperglycemia ; Inflammation ; Internal Medicine ; Male ; Medicine ; Medicine &amp; Public Health ; Metabolic Diseases ; Middle Aged ; Nitric oxide ; Original ; Original Article ; Oxidative stress ; Vasodilation - physiology ; Velocity ; Ventricular Dysfunction, Left - diagnostic imaging ; Ventricular Dysfunction, Left - etiology ; Ventricular Dysfunction, Left - physiopathology ; Ventricular Function, Left - physiology</subject><ispartof>Acta diabetologica, 2024-11, Vol.61 (11), p.1475-1482</ispartof><rights>The Author(s) 2024</rights><rights>2024. The Author(s).</rights><rights>The Author(s) 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2024 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c356t-c83c33d038e1d84385016c7d8f29d5112edf5fcd62282bc2f0bf8731aee480d23</cites><orcidid>0000-0002-6848-4262</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38847923$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cutruzzolà, Antonio</creatorcontrib><creatorcontrib>Parise, Martina</creatorcontrib><creatorcontrib>Cacia, Michele</creatorcontrib><creatorcontrib>Lucà, Stefania</creatorcontrib><creatorcontrib>Irace, Concetta</creatorcontrib><creatorcontrib>Gnasso, Agostino</creatorcontrib><title>The relationship between endothelial-dependent flow-mediated dilation and diastolic function in type 2 diabetes</title><title>Acta diabetologica</title><addtitle>Acta Diabetol</addtitle><addtitle>Acta Diabetol</addtitle><description>Aims Diastolic dysfunction represents the earliest and most common manifestation of diabetic cardiomyopathy. Nitric oxide (NO), a potent vasodilator and anti-inflammatory mediator released from the subendocardial and coronary endothelium, favors left ventricular distensibility and relaxation. In type 2 diabetes (T2D), the NO bioavailability is reduced due to the oxidative stress and inflammatory state of the endothelium, because of chronic hyperglycemia. The aim of the present research is to evaluate the relationship between endothelial function and diastolic function in subjects with T2D. Method Subjects with T2D and age and sex-matched healthy controls were consecutively recruited. All participants underwent flow-mediated dilation (FMD) to assess endothelial function, and echocardiography to evaluate diastolic function. Results Thirty-five patients (6 women, 29 men) and 35 healthy controls were included in the final analysis. FMD was significantly lower in T2D than controls (4.4 ± 3.4 vs. 8.5 ± 4.3%, p  = 0.001). T2D presented different abnormalities in diastolic function compared to controls: lower E/A (early to late diastolic transmitral flow velocity), lower septal and lateral e′ (early diastolic myocardial tissue velocity at septum and lateral wall), and higher E/e′ (surrogate of filling pressure). In subjects with T2D, we observed a significant correlation between FMD and E/e′ (r = −0.63, p  = 0.001), lateral e′ (r = 0.44, p  = 0.03), and septal e′ (r = 0.39, p  = 0.05). Conclusions Our observational study demonstrated a link between FMD and diastolic dysfunction in subjects with type 2 diabetes.</description><subject>Adult</subject><subject>Aged</subject><subject>Bioavailability</subject><subject>Blood Flow Velocity - physiology</subject><subject>Cardiomyopathy</subject><subject>Case-Control Studies</subject><subject>Diabetes</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - complications</subject><subject>Diabetes Mellitus, Type 2 - physiopathology</subject><subject>Diabetic Cardiomyopathies - diagnostic imaging</subject><subject>Diabetic Cardiomyopathies - etiology</subject><subject>Diabetic Cardiomyopathies - physiopathology</subject><subject>Diastole - physiology</subject><subject>Echocardiography</subject><subject>Endothelium</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Female</subject><subject>Flow velocity</subject><subject>Heart</subject><subject>Humans</subject><subject>Hyperglycemia</subject><subject>Inflammation</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine &amp; Public Health</subject><subject>Metabolic Diseases</subject><subject>Middle Aged</subject><subject>Nitric oxide</subject><subject>Original</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Vasodilation - physiology</subject><subject>Velocity</subject><subject>Ventricular Dysfunction, Left - diagnostic imaging</subject><subject>Ventricular Dysfunction, Left - etiology</subject><subject>Ventricular Dysfunction, Left - physiopathology</subject><subject>Ventricular Function, Left - physiology</subject><issn>1432-5233</issn><issn>0940-5429</issn><issn>1432-5233</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9UU1v1DAQjRAVLYU_wAFZ4sIl1OOJE-eEUAW0UqVeytny2pOuq6wd7ISq_x5vU0rh0INlj9_HzOhV1Tvgn4Dz7iRzLntRc9GUg4A1vKiOoEFRS4H48sn7sHqd8w3nIDpUr6pDVKrpeoFHVbzaEks0mtnHkLd-Yhuab4kCo-DivKXRm7F2NJWSwsyGMd7WO3LezOSY86uQmbAvTJ7j6C0blmDvv31g891ETOzBYkz5TXUwmDHT24f7uPrx7evV6Vl9cfn9_PTLRW1RtnNtFVpEx1ERONWgkhxa2zk1iN5JAEFukIN1rRBKbKwY-GZQHYIhahR3Ao-rz6vvtGzKuLbMnsyop-R3Jt3paLz-Fwl-q6_jLw0gERrA4vDxwSHFnwvlWe98tjSOJlBcskbeyl5xofpC_fAf9SYuKZT9NIJA2TRdKwtLrCybYs6JhsdpgOt9oHoNVJdA9X2gGoro_dM9HiV_EiwEXAm5QOGa0t_ez9j-BjtArYY</recordid><startdate>20241101</startdate><enddate>20241101</enddate><creator>Cutruzzolà, Antonio</creator><creator>Parise, Martina</creator><creator>Cacia, Michele</creator><creator>Lucà, Stefania</creator><creator>Irace, Concetta</creator><creator>Gnasso, Agostino</creator><general>Springer Milan</general><general>Springer Nature B.V</general><scope>C6C</scope><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>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6848-4262</orcidid></search><sort><creationdate>20241101</creationdate><title>The relationship between endothelial-dependent flow-mediated dilation and diastolic function in type 2 diabetes</title><author>Cutruzzolà, Antonio ; Parise, Martina ; Cacia, Michele ; Lucà, Stefania ; Irace, Concetta ; Gnasso, Agostino</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-c83c33d038e1d84385016c7d8f29d5112edf5fcd62282bc2f0bf8731aee480d23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Bioavailability</topic><topic>Blood Flow Velocity - physiology</topic><topic>Cardiomyopathy</topic><topic>Case-Control Studies</topic><topic>Diabetes</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - complications</topic><topic>Diabetes Mellitus, Type 2 - physiopathology</topic><topic>Diabetic Cardiomyopathies - diagnostic imaging</topic><topic>Diabetic Cardiomyopathies - etiology</topic><topic>Diabetic Cardiomyopathies - physiopathology</topic><topic>Diastole - physiology</topic><topic>Echocardiography</topic><topic>Endothelium</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Female</topic><topic>Flow velocity</topic><topic>Heart</topic><topic>Humans</topic><topic>Hyperglycemia</topic><topic>Inflammation</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine &amp; Public Health</topic><topic>Metabolic Diseases</topic><topic>Middle Aged</topic><topic>Nitric oxide</topic><topic>Original</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Vasodilation - physiology</topic><topic>Velocity</topic><topic>Ventricular Dysfunction, Left - diagnostic imaging</topic><topic>Ventricular Dysfunction, Left - etiology</topic><topic>Ventricular Dysfunction, Left - physiopathology</topic><topic>Ventricular Function, Left - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cutruzzolà, Antonio</creatorcontrib><creatorcontrib>Parise, Martina</creatorcontrib><creatorcontrib>Cacia, Michele</creatorcontrib><creatorcontrib>Lucà, Stefania</creatorcontrib><creatorcontrib>Irace, Concetta</creatorcontrib><creatorcontrib>Gnasso, Agostino</creatorcontrib><collection>SpringerOpen</collection><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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta diabetologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cutruzzolà, Antonio</au><au>Parise, Martina</au><au>Cacia, Michele</au><au>Lucà, Stefania</au><au>Irace, Concetta</au><au>Gnasso, Agostino</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The relationship between endothelial-dependent flow-mediated dilation and diastolic function in type 2 diabetes</atitle><jtitle>Acta diabetologica</jtitle><stitle>Acta Diabetol</stitle><addtitle>Acta Diabetol</addtitle><date>2024-11-01</date><risdate>2024</risdate><volume>61</volume><issue>11</issue><spage>1475</spage><epage>1482</epage><pages>1475-1482</pages><issn>1432-5233</issn><issn>0940-5429</issn><eissn>1432-5233</eissn><abstract>Aims Diastolic dysfunction represents the earliest and most common manifestation of diabetic cardiomyopathy. Nitric oxide (NO), a potent vasodilator and anti-inflammatory mediator released from the subendocardial and coronary endothelium, favors left ventricular distensibility and relaxation. In type 2 diabetes (T2D), the NO bioavailability is reduced due to the oxidative stress and inflammatory state of the endothelium, because of chronic hyperglycemia. The aim of the present research is to evaluate the relationship between endothelial function and diastolic function in subjects with T2D. Method Subjects with T2D and age and sex-matched healthy controls were consecutively recruited. All participants underwent flow-mediated dilation (FMD) to assess endothelial function, and echocardiography to evaluate diastolic function. Results Thirty-five patients (6 women, 29 men) and 35 healthy controls were included in the final analysis. FMD was significantly lower in T2D than controls (4.4 ± 3.4 vs. 8.5 ± 4.3%, p  = 0.001). T2D presented different abnormalities in diastolic function compared to controls: lower E/A (early to late diastolic transmitral flow velocity), lower septal and lateral e′ (early diastolic myocardial tissue velocity at septum and lateral wall), and higher E/e′ (surrogate of filling pressure). In subjects with T2D, we observed a significant correlation between FMD and E/e′ (r = −0.63, p  = 0.001), lateral e′ (r = 0.44, p  = 0.03), and septal e′ (r = 0.39, p  = 0.05). Conclusions Our observational study demonstrated a link between FMD and diastolic dysfunction in subjects with type 2 diabetes.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>38847923</pmid><doi>10.1007/s00592-024-02313-1</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-6848-4262</orcidid><oa>free_for_read</oa></addata></record>
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source Springer Nature
subjects Adult
Aged
Bioavailability
Blood Flow Velocity - physiology
Cardiomyopathy
Case-Control Studies
Diabetes
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - physiopathology
Diabetic Cardiomyopathies - diagnostic imaging
Diabetic Cardiomyopathies - etiology
Diabetic Cardiomyopathies - physiopathology
Diastole - physiology
Echocardiography
Endothelium
Endothelium, Vascular - physiopathology
Female
Flow velocity
Heart
Humans
Hyperglycemia
Inflammation
Internal Medicine
Male
Medicine
Medicine & Public Health
Metabolic Diseases
Middle Aged
Nitric oxide
Original
Original Article
Oxidative stress
Vasodilation - physiology
Velocity
Ventricular Dysfunction, Left - diagnostic imaging
Ventricular Dysfunction, Left - etiology
Ventricular Dysfunction, Left - physiopathology
Ventricular Function, Left - physiology
title The relationship between endothelial-dependent flow-mediated dilation and diastolic function in type 2 diabetes
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