Phenotyping Type 2 Diabetes in Terms of Myocardial Insulin Resistance and Its Potential Cardiovascular Consequences: A New Strategy Based on 18F-FDG PET/CT
Background: Systemic insulin resistance is generally postulated as an independent risk factor of cardiovascular events in type 2 diabetes (T2D). However, the role of myocardial insulin resistance (mIR) remains to be clarified. Methods: Two 18F-FDG PET/CT scans were performed on forty-three T2D patie...
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creator | Herance, José Raul Simó, Rafael Velasquez, Mayra Alejandra Paun, Bruno García-Leon, Daniel Aparicio, Carolina Marés, Roso Simó-Servat, Olga Castell-Conesa, Joan Hernández, Cristina Aguadé-Bruix, Santiago |
description | Background: Systemic insulin resistance is generally postulated as an independent risk factor of cardiovascular events in type 2 diabetes (T2D). However, the role of myocardial insulin resistance (mIR) remains to be clarified. Methods: Two 18F-FDG PET/CT scans were performed on forty-three T2D patients at baseline and after hyperinsulinemic–euglycemic clamp (HEC). Myocardial insulin sensitivity (mIS) was determined by measuring the increment in myocardial 18F-FDG uptake after HEC. Coronary artery calcium scoring (CACs) and myocardial radiodensity (mRD) were assessed by CT. Results: After HEC, seventeen patients exhibited a strikingly enhancement of myocardial 18F-FDG uptake and twenty-six a marginal increase, thus revealing mIS and mIR, respectively. Patients with mIR showed higher mRD (HU: 38.95 [33.81–44.06] vs. 30.82 [21.48–38.02]; p = 0.03) and CACs > 400 (AU: 52% vs. 29%; p = 0.002) than patients with mIS. In addition, HOMA-IR and mIS only showed a correlation in those patients with mIR. Conclusions: 18F-FDG PET combined with HEC is a reliable method for identifying patients with mIR. This subgroup of patients was found to be specifically at high risk of developing cardiovascular events and showed myocardial structural changes. Moreover, the gold-standard HOMA-IR index was only associated with mIR in this subgroup of patients. Our results open up a new avenue for stratifying patients with cardiovascular risk in T2D. |
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However, the role of myocardial insulin resistance (mIR) remains to be clarified. Methods: Two 18F-FDG PET/CT scans were performed on forty-three T2D patients at baseline and after hyperinsulinemic–euglycemic clamp (HEC). Myocardial insulin sensitivity (mIS) was determined by measuring the increment in myocardial 18F-FDG uptake after HEC. Coronary artery calcium scoring (CACs) and myocardial radiodensity (mRD) were assessed by CT. Results: After HEC, seventeen patients exhibited a strikingly enhancement of myocardial 18F-FDG uptake and twenty-six a marginal increase, thus revealing mIS and mIR, respectively. Patients with mIR showed higher mRD (HU: 38.95 [33.81–44.06] vs. 30.82 [21.48–38.02]; p = 0.03) and CACs > 400 (AU: 52% vs. 29%; p = 0.002) than patients with mIS. In addition, HOMA-IR and mIS only showed a correlation in those patients with mIR. Conclusions: 18F-FDG PET combined with HEC is a reliable method for identifying patients with mIR. This subgroup of patients was found to be specifically at high risk of developing cardiovascular events and showed myocardial structural changes. Moreover, the gold-standard HOMA-IR index was only associated with mIR in this subgroup of patients. Our results open up a new avenue for stratifying patients with cardiovascular risk in T2D.</description><identifier>ISSN: 2075-4426</identifier><identifier>EISSN: 2075-4426</identifier><identifier>DOI: 10.3390/jpm12010030</identifier><identifier>PMID: 35055345</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Arteriosclerosis ; Calcification (ectopic) ; Cardiovascular diseases ; Clinical trials ; Communication ; Coronary artery ; Diabetes ; Diabetes mellitus (non-insulin dependent) ; Disease ; Drug dosages ; Endocrinology ; Glucose ; Heart failure ; Insulin ; Insulin resistance ; Medical imaging ; Metabolism ; Nuclear medicine ; Patients ; Phenotyping ; Physiology ; Positron emission tomography ; Precision medicine ; Risk factors ; Software ; Tomography</subject><ispartof>Journal of personalized medicine, 2022-01, Vol.12 (1), p.30</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c316t-bb6497354facf5752794cb07071437d378f947353376b08cc8d018bf61a0753f3</citedby><cites>FETCH-LOGICAL-c316t-bb6497354facf5752794cb07071437d378f947353376b08cc8d018bf61a0753f3</cites><orcidid>0000-0001-7178-3290 ; 0000-0002-3109-1721 ; 0000-0001-8617-6274 ; 0000-0003-0475-3096 ; 0000-0002-7339-0172</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8778238/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8778238/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53770,53772</link.rule.ids></links><search><creatorcontrib>Herance, José Raul</creatorcontrib><creatorcontrib>Simó, Rafael</creatorcontrib><creatorcontrib>Velasquez, Mayra Alejandra</creatorcontrib><creatorcontrib>Paun, Bruno</creatorcontrib><creatorcontrib>García-Leon, Daniel</creatorcontrib><creatorcontrib>Aparicio, Carolina</creatorcontrib><creatorcontrib>Marés, Roso</creatorcontrib><creatorcontrib>Simó-Servat, Olga</creatorcontrib><creatorcontrib>Castell-Conesa, Joan</creatorcontrib><creatorcontrib>Hernández, Cristina</creatorcontrib><creatorcontrib>Aguadé-Bruix, Santiago</creatorcontrib><title>Phenotyping Type 2 Diabetes in Terms of Myocardial Insulin Resistance and Its Potential Cardiovascular Consequences: A New Strategy Based on 18F-FDG PET/CT</title><title>Journal of personalized medicine</title><description>Background: Systemic insulin resistance is generally postulated as an independent risk factor of cardiovascular events in type 2 diabetes (T2D). However, the role of myocardial insulin resistance (mIR) remains to be clarified. Methods: Two 18F-FDG PET/CT scans were performed on forty-three T2D patients at baseline and after hyperinsulinemic–euglycemic clamp (HEC). Myocardial insulin sensitivity (mIS) was determined by measuring the increment in myocardial 18F-FDG uptake after HEC. Coronary artery calcium scoring (CACs) and myocardial radiodensity (mRD) were assessed by CT. Results: After HEC, seventeen patients exhibited a strikingly enhancement of myocardial 18F-FDG uptake and twenty-six a marginal increase, thus revealing mIS and mIR, respectively. Patients with mIR showed higher mRD (HU: 38.95 [33.81–44.06] vs. 30.82 [21.48–38.02]; p = 0.03) and CACs > 400 (AU: 52% vs. 29%; p = 0.002) than patients with mIS. In addition, HOMA-IR and mIS only showed a correlation in those patients with mIR. Conclusions: 18F-FDG PET combined with HEC is a reliable method for identifying patients with mIR. This subgroup of patients was found to be specifically at high risk of developing cardiovascular events and showed myocardial structural changes. Moreover, the gold-standard HOMA-IR index was only associated with mIR in this subgroup of patients. Our results open up a new avenue for stratifying patients with cardiovascular risk in T2D.</description><subject>Arteriosclerosis</subject><subject>Calcification (ectopic)</subject><subject>Cardiovascular diseases</subject><subject>Clinical trials</subject><subject>Communication</subject><subject>Coronary artery</subject><subject>Diabetes</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Disease</subject><subject>Drug dosages</subject><subject>Endocrinology</subject><subject>Glucose</subject><subject>Heart failure</subject><subject>Insulin</subject><subject>Insulin resistance</subject><subject>Medical imaging</subject><subject>Metabolism</subject><subject>Nuclear medicine</subject><subject>Patients</subject><subject>Phenotyping</subject><subject>Physiology</subject><subject>Positron emission tomography</subject><subject>Precision medicine</subject><subject>Risk factors</subject><subject>Software</subject><subject>Tomography</subject><issn>2075-4426</issn><issn>2075-4426</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkd1u1DAQhSMEolXpFS8wEjdIKNS_sZcLpJJ2y0oFVhCuI8dxtlkldrCdojxLX7ZeWqHC3MxI59PRnJkse43Re0pX6Gw_jZggjBBFz7JjggTPGSPF8yfzUXYawh6lkpyQAr3MjihHnFPGj7O77Y2xLi5Tb3dQLZMBAhe9akw0AXoLlfFjANfBl8Vp5dteDbCxYR6S9t2EPkRltQFlW9jEAFsXjY0HqDzA7lYFPQ_KQ-lsML9mk-DwAc7hq_kNP6JX0ewW-KSCacFZwHKdry-uYHtZnZXVq-xFp4ZgTh_7SfZzfVmVn_Prb1eb8vw61xQXMW-agq0E5axTuuOCE7FiukECCcyoaKmQ3YolnVJRNEhqLVuEZdMVWKUT0Y6eZB8ffKe5GU2rUwKvhnry_aj8UjvV1_8qtr-pd-62lkJIQmUyePto4F3KGGI99kGbYVDWuDnUpCCECIY5Seib_9C9m71N8Q4UpliKP9S7B0p7F4I33d9lMKoPf6-f_J3eA6hWnaY</recordid><startdate>20220102</startdate><enddate>20220102</enddate><creator>Herance, José Raul</creator><creator>Simó, Rafael</creator><creator>Velasquez, Mayra Alejandra</creator><creator>Paun, Bruno</creator><creator>García-Leon, Daniel</creator><creator>Aparicio, Carolina</creator><creator>Marés, Roso</creator><creator>Simó-Servat, Olga</creator><creator>Castell-Conesa, Joan</creator><creator>Hernández, Cristina</creator><creator>Aguadé-Bruix, Santiago</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7178-3290</orcidid><orcidid>https://orcid.org/0000-0002-3109-1721</orcidid><orcidid>https://orcid.org/0000-0001-8617-6274</orcidid><orcidid>https://orcid.org/0000-0003-0475-3096</orcidid><orcidid>https://orcid.org/0000-0002-7339-0172</orcidid></search><sort><creationdate>20220102</creationdate><title>Phenotyping Type 2 Diabetes in Terms of Myocardial Insulin Resistance and Its Potential Cardiovascular Consequences: A New Strategy Based on 18F-FDG PET/CT</title><author>Herance, José Raul ; 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However, the role of myocardial insulin resistance (mIR) remains to be clarified. Methods: Two 18F-FDG PET/CT scans were performed on forty-three T2D patients at baseline and after hyperinsulinemic–euglycemic clamp (HEC). Myocardial insulin sensitivity (mIS) was determined by measuring the increment in myocardial 18F-FDG uptake after HEC. Coronary artery calcium scoring (CACs) and myocardial radiodensity (mRD) were assessed by CT. Results: After HEC, seventeen patients exhibited a strikingly enhancement of myocardial 18F-FDG uptake and twenty-six a marginal increase, thus revealing mIS and mIR, respectively. Patients with mIR showed higher mRD (HU: 38.95 [33.81–44.06] vs. 30.82 [21.48–38.02]; p = 0.03) and CACs > 400 (AU: 52% vs. 29%; p = 0.002) than patients with mIS. In addition, HOMA-IR and mIS only showed a correlation in those patients with mIR. Conclusions: 18F-FDG PET combined with HEC is a reliable method for identifying patients with mIR. This subgroup of patients was found to be specifically at high risk of developing cardiovascular events and showed myocardial structural changes. Moreover, the gold-standard HOMA-IR index was only associated with mIR in this subgroup of patients. Our results open up a new avenue for stratifying patients with cardiovascular risk in T2D.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>35055345</pmid><doi>10.3390/jpm12010030</doi><orcidid>https://orcid.org/0000-0001-7178-3290</orcidid><orcidid>https://orcid.org/0000-0002-3109-1721</orcidid><orcidid>https://orcid.org/0000-0001-8617-6274</orcidid><orcidid>https://orcid.org/0000-0003-0475-3096</orcidid><orcidid>https://orcid.org/0000-0002-7339-0172</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Arteriosclerosis Calcification (ectopic) Cardiovascular diseases Clinical trials Communication Coronary artery Diabetes Diabetes mellitus (non-insulin dependent) Disease Drug dosages Endocrinology Glucose Heart failure Insulin Insulin resistance Medical imaging Metabolism Nuclear medicine Patients Phenotyping Physiology Positron emission tomography Precision medicine Risk factors Software Tomography |
title | Phenotyping Type 2 Diabetes in Terms of Myocardial Insulin Resistance and Its Potential Cardiovascular Consequences: A New Strategy Based on 18F-FDG PET/CT |
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