Obesity and statins are both independent predictors of enhanced coronary arteriolar dilation in patients undergoing heart surgery
A paradoxical inverse relationship between body mass index, morbidity and mortality in patients with ischemic heart disease has been noted; but the underlying mechanisms remain unclear. Given that coronary resistance arteries are the primary regulators of myocardial blood flow, we examined the effec...
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| Veröffentlicht in: | Journal of cardiothoracic surgery 2013-04, Vol.8 (1), p.117-117, Article 117 |
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| creator | Cassuto, James Feher, Attila Lan, Ling Patel, Vijay S Kamath, Vinayak Anthony, Daniel C Bagi, Zsolt |
| description | A paradoxical inverse relationship between body mass index, morbidity and mortality in patients with ischemic heart disease has been noted; but the underlying mechanisms remain unclear. Given that coronary resistance arteries are the primary regulators of myocardial blood flow, we examined the effects of obesity and medication on dilator function in coronary microvessels.
Bradykinin-induced coronary dilation was assessed by videomicroscopy in ex vivo coronary arterioles obtained from 64 consecutive patients undergoing heart surgery. Multi-variable linear regression and logistic regression were used to investigate the effects of obesity (BMI ≥ 30 kg/M2) and the influences of medications on vessel responses.
In isolated, pressurized (80 mmHg) coronary arterioles of obese and non-obese patient the active (73±4 vs. 79±13 μm) and passive (111 ± 5.5 vs. 118 ± 5.0 μm) diameters were similar. Bradykinin elicited substantial dilation in coronary arterioles, with a similar magnitude in obese and non-obese patients (to 10-8 M: 55 ± 5% vs. 46 ± 5%, P = 0.20), but with significantly enhanced sensitivity in obesity (EC50: 8.2x10-9 M vs. 1.9x10-8 M, respectively, P = 0.03). When adjusted for other risk factors and medications, obesity and statins were determined to be the only positive predictors of enhanced dilation, as assessed with multiple regression analysis. Moreover, obese patients with or without statin exhibited significantly increased coronary dilation to bradykinin, when compared to non-obese patients without statin therapy.
Obesity and statin therapy are independently associated with an enhanced dilator function of coronary arterioles in patients undergoing heart surgery, which may offer a potential mechanism for the better cardiovascular outcome described earlier as the obesity paradox. |
| doi_str_mv | 10.1186/1749-8090-8-117 |
| format | Article |
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Bradykinin-induced coronary dilation was assessed by videomicroscopy in ex vivo coronary arterioles obtained from 64 consecutive patients undergoing heart surgery. Multi-variable linear regression and logistic regression were used to investigate the effects of obesity (BMI ≥ 30 kg/M2) and the influences of medications on vessel responses.
In isolated, pressurized (80 mmHg) coronary arterioles of obese and non-obese patient the active (73±4 vs. 79±13 μm) and passive (111 ± 5.5 vs. 118 ± 5.0 μm) diameters were similar. Bradykinin elicited substantial dilation in coronary arterioles, with a similar magnitude in obese and non-obese patients (to 10-8 M: 55 ± 5% vs. 46 ± 5%, P = 0.20), but with significantly enhanced sensitivity in obesity (EC50: 8.2x10-9 M vs. 1.9x10-8 M, respectively, P = 0.03). When adjusted for other risk factors and medications, obesity and statins were determined to be the only positive predictors of enhanced dilation, as assessed with multiple regression analysis. Moreover, obese patients with or without statin exhibited significantly increased coronary dilation to bradykinin, when compared to non-obese patients without statin therapy.
Obesity and statin therapy are independently associated with an enhanced dilator function of coronary arterioles in patients undergoing heart surgery, which may offer a potential mechanism for the better cardiovascular outcome described earlier as the obesity paradox.</description><identifier>ISSN: 1749-8090</identifier><identifier>EISSN: 1749-8090</identifier><identifier>DOI: 10.1186/1749-8090-8-117</identifier><identifier>PMID: 23631400</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Aged ; Analysis ; Body Mass Index ; Bradykinin ; Bradykinin - pharmacology ; Cardiac patients ; Cardiac Surgical Procedures ; Cardiovascular agents ; Cardiovascular disease ; Coronary Artery Disease - complications ; Coronary Artery Disease - drug therapy ; Coronary Artery Disease - physiopathology ; Coronary Vessels - drug effects ; Coronary Vessels - physiopathology ; Evaluation ; Female ; Health aspects ; Heart diseases ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use ; In Vitro Techniques ; Ischemia ; Male ; Microcirculation - drug effects ; Microscopy, Video ; Middle Aged ; Mortality ; Obesity ; Obesity - complications ; Obesity - physiopathology ; Regression Analysis ; Risk Factors ; Statins ; Surgery ; Vasodilation - drug effects ; Vasodilation - physiology ; Weight control</subject><ispartof>Journal of cardiothoracic surgery, 2013-04, Vol.8 (1), p.117-117, Article 117</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Cassuto et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2013 Cassuto et al.; licensee BioMed Central Ltd. 2013 Cassuto et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b547t-c76999331334696ad5c6a431b692b61109a2d8d957c753b8d22339ff3e9b17cc3</citedby><cites>FETCH-LOGICAL-b547t-c76999331334696ad5c6a431b692b61109a2d8d957c753b8d22339ff3e9b17cc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658876/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658876/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,27907,27908,53774,53776</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23631400$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cassuto, James</creatorcontrib><creatorcontrib>Feher, Attila</creatorcontrib><creatorcontrib>Lan, Ling</creatorcontrib><creatorcontrib>Patel, Vijay S</creatorcontrib><creatorcontrib>Kamath, Vinayak</creatorcontrib><creatorcontrib>Anthony, Daniel C</creatorcontrib><creatorcontrib>Bagi, Zsolt</creatorcontrib><title>Obesity and statins are both independent predictors of enhanced coronary arteriolar dilation in patients undergoing heart surgery</title><title>Journal of cardiothoracic surgery</title><addtitle>J Cardiothorac Surg</addtitle><description>A paradoxical inverse relationship between body mass index, morbidity and mortality in patients with ischemic heart disease has been noted; but the underlying mechanisms remain unclear. Given that coronary resistance arteries are the primary regulators of myocardial blood flow, we examined the effects of obesity and medication on dilator function in coronary microvessels.
Bradykinin-induced coronary dilation was assessed by videomicroscopy in ex vivo coronary arterioles obtained from 64 consecutive patients undergoing heart surgery. Multi-variable linear regression and logistic regression were used to investigate the effects of obesity (BMI ≥ 30 kg/M2) and the influences of medications on vessel responses.
In isolated, pressurized (80 mmHg) coronary arterioles of obese and non-obese patient the active (73±4 vs. 79±13 μm) and passive (111 ± 5.5 vs. 118 ± 5.0 μm) diameters were similar. Bradykinin elicited substantial dilation in coronary arterioles, with a similar magnitude in obese and non-obese patients (to 10-8 M: 55 ± 5% vs. 46 ± 5%, P = 0.20), but with significantly enhanced sensitivity in obesity (EC50: 8.2x10-9 M vs. 1.9x10-8 M, respectively, P = 0.03). When adjusted for other risk factors and medications, obesity and statins were determined to be the only positive predictors of enhanced dilation, as assessed with multiple regression analysis. Moreover, obese patients with or without statin exhibited significantly increased coronary dilation to bradykinin, when compared to non-obese patients without statin therapy.
Obesity and statin therapy are independently associated with an enhanced dilator function of coronary arterioles in patients undergoing heart surgery, which may offer a potential mechanism for the better cardiovascular outcome described earlier as the obesity paradox.</description><subject>Aged</subject><subject>Analysis</subject><subject>Body Mass Index</subject><subject>Bradykinin</subject><subject>Bradykinin - pharmacology</subject><subject>Cardiac patients</subject><subject>Cardiac Surgical Procedures</subject><subject>Cardiovascular agents</subject><subject>Cardiovascular disease</subject><subject>Coronary Artery Disease - complications</subject><subject>Coronary Artery Disease - drug therapy</subject><subject>Coronary Artery Disease - physiopathology</subject><subject>Coronary Vessels - drug effects</subject><subject>Coronary Vessels - physiopathology</subject><subject>Evaluation</subject><subject>Female</subject><subject>Health aspects</subject><subject>Heart diseases</subject><subject>Humans</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</subject><subject>In Vitro Techniques</subject><subject>Ischemia</subject><subject>Male</subject><subject>Microcirculation - drug effects</subject><subject>Microscopy, Video</subject><subject>Middle Aged</subject><subject>Mortality</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - physiopathology</subject><subject>Regression Analysis</subject><subject>Risk Factors</subject><subject>Statins</subject><subject>Surgery</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilation - physiology</subject><subject>Weight control</subject><issn>1749-8090</issn><issn>1749-8090</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp1ksFrHSEQxiW0JGmSc29F6HkTXXddvRTS0LSFQC7tWVx19xl2datuIcf8553HSx55kCLoMPPNj09HhD5Sckmp4Fe0a2QliCSVqCjtjtDpPvPuVXyCPuT8QEjTMtIeo5OacUYbQk7R033vsi-PWAeLc9HFh4x1criPZYN9sG5xsIWCl-SsNyWmjOOAXdjoYJzFJqYYdAJAKi75OOmErZ8AFAP04wUiaM94BUwaow8j3jgQ47ym0aXHc_R-0FN2F8_nGfp9--3XzY_q7v77z5vru6pvm65UpuNSSsYoYw2XXNvWcN0w2nNZ95xSInVthZVtZ7qW9cLWNWNyGJiTPe2MYWfoy467rP3srAFTSU9qSX4G-ypqrw4rwW_UGP8qxlshOg6ArztA7-N_AIcVE2e1HYHajkAJBQMCyOdnFyn-WV0u6iGuKcDFFWUtjIcJWHvVqCenfBgiAM3ss1HXLWs6KiQnoLp8QwXLutmbGNzgIX_QcLVrMCnmnNywN0-J2v6nN-x-ev1oe_3LB2L_AKYvyAA</recordid><startdate>20130430</startdate><enddate>20130430</enddate><creator>Cassuto, James</creator><creator>Feher, Attila</creator><creator>Lan, Ling</creator><creator>Patel, Vijay S</creator><creator>Kamath, Vinayak</creator><creator>Anthony, Daniel C</creator><creator>Bagi, Zsolt</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7Z</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20130430</creationdate><title>Obesity and statins are both independent predictors of enhanced coronary arteriolar dilation in patients undergoing heart surgery</title><author>Cassuto, James ; Feher, Attila ; Lan, Ling ; Patel, Vijay S ; Kamath, Vinayak ; Anthony, Daniel C ; Bagi, Zsolt</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b547t-c76999331334696ad5c6a431b692b61109a2d8d957c753b8d22339ff3e9b17cc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Aged</topic><topic>Analysis</topic><topic>Body Mass Index</topic><topic>Bradykinin</topic><topic>Bradykinin - pharmacology</topic><topic>Cardiac patients</topic><topic>Cardiac Surgical Procedures</topic><topic>Cardiovascular agents</topic><topic>Cardiovascular disease</topic><topic>Coronary Artery Disease - complications</topic><topic>Coronary Artery Disease - drug therapy</topic><topic>Coronary Artery Disease - physiopathology</topic><topic>Coronary Vessels - drug effects</topic><topic>Coronary Vessels - physiopathology</topic><topic>Evaluation</topic><topic>Female</topic><topic>Health aspects</topic><topic>Heart diseases</topic><topic>Humans</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use</topic><topic>In Vitro Techniques</topic><topic>Ischemia</topic><topic>Male</topic><topic>Microcirculation - drug effects</topic><topic>Microscopy, Video</topic><topic>Middle Aged</topic><topic>Mortality</topic><topic>Obesity</topic><topic>Obesity - complications</topic><topic>Obesity - physiopathology</topic><topic>Regression Analysis</topic><topic>Risk Factors</topic><topic>Statins</topic><topic>Surgery</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilation - physiology</topic><topic>Weight control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cassuto, James</creatorcontrib><creatorcontrib>Feher, Attila</creatorcontrib><creatorcontrib>Lan, Ling</creatorcontrib><creatorcontrib>Patel, Vijay S</creatorcontrib><creatorcontrib>Kamath, Vinayak</creatorcontrib><creatorcontrib>Anthony, Daniel C</creatorcontrib><creatorcontrib>Bagi, Zsolt</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biochemistry Abstracts 1</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cardiothoracic surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cassuto, James</au><au>Feher, Attila</au><au>Lan, Ling</au><au>Patel, Vijay S</au><au>Kamath, Vinayak</au><au>Anthony, Daniel C</au><au>Bagi, Zsolt</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Obesity and statins are both independent predictors of enhanced coronary arteriolar dilation in patients undergoing heart surgery</atitle><jtitle>Journal of cardiothoracic surgery</jtitle><addtitle>J Cardiothorac Surg</addtitle><date>2013-04-30</date><risdate>2013</risdate><volume>8</volume><issue>1</issue><spage>117</spage><epage>117</epage><pages>117-117</pages><artnum>117</artnum><issn>1749-8090</issn><eissn>1749-8090</eissn><abstract>A paradoxical inverse relationship between body mass index, morbidity and mortality in patients with ischemic heart disease has been noted; but the underlying mechanisms remain unclear. Given that coronary resistance arteries are the primary regulators of myocardial blood flow, we examined the effects of obesity and medication on dilator function in coronary microvessels.
Bradykinin-induced coronary dilation was assessed by videomicroscopy in ex vivo coronary arterioles obtained from 64 consecutive patients undergoing heart surgery. Multi-variable linear regression and logistic regression were used to investigate the effects of obesity (BMI ≥ 30 kg/M2) and the influences of medications on vessel responses.
In isolated, pressurized (80 mmHg) coronary arterioles of obese and non-obese patient the active (73±4 vs. 79±13 μm) and passive (111 ± 5.5 vs. 118 ± 5.0 μm) diameters were similar. Bradykinin elicited substantial dilation in coronary arterioles, with a similar magnitude in obese and non-obese patients (to 10-8 M: 55 ± 5% vs. 46 ± 5%, P = 0.20), but with significantly enhanced sensitivity in obesity (EC50: 8.2x10-9 M vs. 1.9x10-8 M, respectively, P = 0.03). When adjusted for other risk factors and medications, obesity and statins were determined to be the only positive predictors of enhanced dilation, as assessed with multiple regression analysis. Moreover, obese patients with or without statin exhibited significantly increased coronary dilation to bradykinin, when compared to non-obese patients without statin therapy.
Obesity and statin therapy are independently associated with an enhanced dilator function of coronary arterioles in patients undergoing heart surgery, which may offer a potential mechanism for the better cardiovascular outcome described earlier as the obesity paradox.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23631400</pmid><doi>10.1186/1749-8090-8-117</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Analysis Body Mass Index Bradykinin Bradykinin - pharmacology Cardiac patients Cardiac Surgical Procedures Cardiovascular agents Cardiovascular disease Coronary Artery Disease - complications Coronary Artery Disease - drug therapy Coronary Artery Disease - physiopathology Coronary Vessels - drug effects Coronary Vessels - physiopathology Evaluation Female Health aspects Heart diseases Humans Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use In Vitro Techniques Ischemia Male Microcirculation - drug effects Microscopy, Video Middle Aged Mortality Obesity Obesity - complications Obesity - physiopathology Regression Analysis Risk Factors Statins Surgery Vasodilation - drug effects Vasodilation - physiology Weight control |
| title | Obesity and statins are both independent predictors of enhanced coronary arteriolar dilation in patients undergoing heart surgery |
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