The endothelial nitric oxide synthase T-786c mutation, a treatable etiology of Prinzmetal's angina
We assessed to what degree the endothelial nitric oxide synthase (eNOS) T-786C polymorphism, leading to reduced nitric oxide (NO) production-coronary artery spasm, was reversibly associated with Prinzmetal’s variant angina (PVA). ENOS T-786C PCR analyses were done in 19 women, 8 men, 26 Caucasian, 1...
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| Veröffentlicht in: | Translational research : the journal of laboratory and clinical medicine 2013-07, Vol.162 (1), p.64-66 |
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| creator | Glueck, Charles J Valdes, Alejandro Bowe, Dedrick Munsif, Siddharth Wang, Ping |
| description | We assessed to what degree the endothelial nitric oxide synthase (eNOS) T-786C polymorphism, leading to reduced nitric oxide (NO) production-coronary artery spasm, was reversibly associated with Prinzmetal’s variant angina (PVA). ENOS T-786C PCR analyses were done in 19 women, 8 men, 26 Caucasian, 1 African-American, median age 53, with well-documented PVA and in 72 healthy controls who did not differ by race or gender. Of the 27 cases, 7 (26%) were homozygous for wild-type normal eNOS (CC), 13 (48%) were T-786C heterozygotes (CT), and 7 (26%) were T-786C homozygotes (TT) vs controls, 44 (61%) CC, 27 (38%) TC, and 1 (1%) TT, P |
| doi_str_mv | 10.1016/j.trsl.2013.03.003 |
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ENOS T-786C PCR analyses were done in 19 women, 8 men, 26 Caucasian, 1 African-American, median age 53, with well-documented PVA and in 72 healthy controls who did not differ by race or gender. Of the 27 cases, 7 (26%) were homozygous for wild-type normal eNOS (CC), 13 (48%) were T-786C heterozygotes (CT), and 7 (26%) were T-786C homozygotes (TT) vs controls, 44 (61%) CC, 27 (38%) TC, and 1 (1%) TT, P < 0.0001. The mutant eNOS T-786C allele frequency in PVA patients was 27/54 (50%) vs 29/144 (20%) in controls, P < 0.0001. On oral L-arginine (9.2 g/d) to increase production of NO for a median of 4.7 months in 16 PVA patients with symptomatic angina despite conventional nitrate-calcium channel blockers, using the Seattle Angina Questionnaire, satisfaction with symptom remission rose (median) from 50% to 100% ( P = 0.004), satisfaction with angina frequency reduction rose from 65% to 80% ( P = 0.02), satisfaction with treatment for symptoms rose from 38% to 88% ( P = 0.001), and perception of overall life status rose from 25 to 71% ( P = 0.0002). On L-arginine (median 4.7 months), in 20 patients, none had worsening of angina, and of 7 patients whose angina totally resolved, eNOS T-786C homozygosity was over-represented, P = 0 .04. The eNOS T-786C mutation appears to be a reversible etiology of PVA in patients whose angina may be ameliorated by L-arginine.</description><identifier>ISSN: 1931-5244</identifier><identifier>EISSN: 1878-1810</identifier><identifier>DOI: 10.1016/j.trsl.2013.03.003</identifier><identifier>PMID: 23567331</identifier><language>eng</language><publisher>United States: Mosby, Inc</publisher><subject>Angina Pectoris, Variant - drug therapy ; Angina Pectoris, Variant - enzymology ; Angina Pectoris, Variant - genetics ; Arginine - therapeutic use ; Calcium Channel Blockers - therapeutic use ; Female ; Genetic Predisposition to Disease ; Humans ; Internal Medicine ; Male ; Middle Aged ; Mutation ; Nitrates - therapeutic use ; Nitric Oxide Synthase Type III - genetics ; Surveys and Questionnaires</subject><ispartof>Translational research : the journal of laboratory and clinical medicine, 2013-07, Vol.162 (1), p.64-66</ispartof><rights>Mosby, Inc.</rights><rights>2013 Mosby, Inc.</rights><rights>Copyright © 2013 Mosby, Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c411t-28888b70d00701f072f44271a8ac77d03aa99b398a365e09a55ef3dfcf6af7c53</citedby><cites>FETCH-LOGICAL-c411t-28888b70d00701f072f44271a8ac77d03aa99b398a365e09a55ef3dfcf6af7c53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.trsl.2013.03.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23567331$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Glueck, Charles J</creatorcontrib><creatorcontrib>Valdes, Alejandro</creatorcontrib><creatorcontrib>Bowe, Dedrick</creatorcontrib><creatorcontrib>Munsif, Siddharth</creatorcontrib><creatorcontrib>Wang, Ping</creatorcontrib><title>The endothelial nitric oxide synthase T-786c mutation, a treatable etiology of Prinzmetal's angina</title><title>Translational research : the journal of laboratory and clinical medicine</title><addtitle>Transl Res</addtitle><description>We assessed to what degree the endothelial nitric oxide synthase (eNOS) T-786C polymorphism, leading to reduced nitric oxide (NO) production-coronary artery spasm, was reversibly associated with Prinzmetal’s variant angina (PVA). ENOS T-786C PCR analyses were done in 19 women, 8 men, 26 Caucasian, 1 African-American, median age 53, with well-documented PVA and in 72 healthy controls who did not differ by race or gender. Of the 27 cases, 7 (26%) were homozygous for wild-type normal eNOS (CC), 13 (48%) were T-786C heterozygotes (CT), and 7 (26%) were T-786C homozygotes (TT) vs controls, 44 (61%) CC, 27 (38%) TC, and 1 (1%) TT, P < 0.0001. The mutant eNOS T-786C allele frequency in PVA patients was 27/54 (50%) vs 29/144 (20%) in controls, P < 0.0001. On oral L-arginine (9.2 g/d) to increase production of NO for a median of 4.7 months in 16 PVA patients with symptomatic angina despite conventional nitrate-calcium channel blockers, using the Seattle Angina Questionnaire, satisfaction with symptom remission rose (median) from 50% to 100% ( P = 0.004), satisfaction with angina frequency reduction rose from 65% to 80% ( P = 0.02), satisfaction with treatment for symptoms rose from 38% to 88% ( P = 0.001), and perception of overall life status rose from 25 to 71% ( P = 0.0002). On L-arginine (median 4.7 months), in 20 patients, none had worsening of angina, and of 7 patients whose angina totally resolved, eNOS T-786C homozygosity was over-represented, P = 0 .04. The eNOS T-786C mutation appears to be a reversible etiology of PVA in patients whose angina may be ameliorated by L-arginine.</description><subject>Angina Pectoris, Variant - drug therapy</subject><subject>Angina Pectoris, Variant - enzymology</subject><subject>Angina Pectoris, Variant - genetics</subject><subject>Arginine - therapeutic use</subject><subject>Calcium Channel Blockers - therapeutic use</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Nitrates - therapeutic use</subject><subject>Nitric Oxide Synthase Type III - genetics</subject><subject>Surveys and Questionnaires</subject><issn>1931-5244</issn><issn>1878-1810</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU-LFDEQxRtR3HX1C3iQ3PRgj5Wku9MNsiCL_2BBwfEcqtPVOxkzyZqkxfHTm2ZWDx4sCiqE9x7Ur6rqKYcNB9692m9yTG4jgMsNlAZ5rzrnvepr3nO4X96D5HUrmuasepTSHqDpBmgeVmdCtp2Skp9X43ZHjPwU8o6cRce8zdEaFn7aiVg6-rzDRGxbq74z7LBkzDb4lwxZjoQZR1fs5cuFmyMLM_scrf91oIzueWLob6zHx9WDGV2iJ3fzovr67u326kN9_en9x6s317VpOM-16EuNCiYABXwGJeamEYpjj0apCSTiMIxy6FF2LcGAbUuznGYzdzgr08qL6sUp9zaG7wulrA82GXIOPYUlaS4VF0rwHopUnKQmhpQizfo22gPGo-agV7Z6r1e2emWroTTIYnp2l7-MB5r-Wv7ALILXJwGVLX9YijoZS97QZCOZrKdg_59_-Y_dOOutQfeNjpT2YYm-8NNcJ6FBf1mvux6XSyjIulb-BqBNn1I</recordid><startdate>20130701</startdate><enddate>20130701</enddate><creator>Glueck, Charles J</creator><creator>Valdes, Alejandro</creator><creator>Bowe, Dedrick</creator><creator>Munsif, Siddharth</creator><creator>Wang, Ping</creator><general>Mosby, 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>7X8</scope></search><sort><creationdate>20130701</creationdate><title>The endothelial nitric oxide synthase T-786c mutation, a treatable etiology of Prinzmetal's angina</title><author>Glueck, Charles J ; Valdes, Alejandro ; Bowe, Dedrick ; Munsif, Siddharth ; Wang, Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c411t-28888b70d00701f072f44271a8ac77d03aa99b398a365e09a55ef3dfcf6af7c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Angina Pectoris, Variant - drug therapy</topic><topic>Angina Pectoris, Variant - enzymology</topic><topic>Angina Pectoris, Variant - genetics</topic><topic>Arginine - therapeutic use</topic><topic>Calcium Channel Blockers - therapeutic use</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Nitrates - therapeutic use</topic><topic>Nitric Oxide Synthase Type III - genetics</topic><topic>Surveys and Questionnaires</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Glueck, Charles J</creatorcontrib><creatorcontrib>Valdes, Alejandro</creatorcontrib><creatorcontrib>Bowe, Dedrick</creatorcontrib><creatorcontrib>Munsif, Siddharth</creatorcontrib><creatorcontrib>Wang, Ping</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Translational research : the journal of laboratory and clinical medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Glueck, Charles J</au><au>Valdes, Alejandro</au><au>Bowe, Dedrick</au><au>Munsif, Siddharth</au><au>Wang, Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The endothelial nitric oxide synthase T-786c mutation, a treatable etiology of Prinzmetal's angina</atitle><jtitle>Translational research : the journal of laboratory and clinical medicine</jtitle><addtitle>Transl Res</addtitle><date>2013-07-01</date><risdate>2013</risdate><volume>162</volume><issue>1</issue><spage>64</spage><epage>66</epage><pages>64-66</pages><issn>1931-5244</issn><eissn>1878-1810</eissn><abstract>We assessed to what degree the endothelial nitric oxide synthase (eNOS) T-786C polymorphism, leading to reduced nitric oxide (NO) production-coronary artery spasm, was reversibly associated with Prinzmetal’s variant angina (PVA). ENOS T-786C PCR analyses were done in 19 women, 8 men, 26 Caucasian, 1 African-American, median age 53, with well-documented PVA and in 72 healthy controls who did not differ by race or gender. Of the 27 cases, 7 (26%) were homozygous for wild-type normal eNOS (CC), 13 (48%) were T-786C heterozygotes (CT), and 7 (26%) were T-786C homozygotes (TT) vs controls, 44 (61%) CC, 27 (38%) TC, and 1 (1%) TT, P < 0.0001. The mutant eNOS T-786C allele frequency in PVA patients was 27/54 (50%) vs 29/144 (20%) in controls, P < 0.0001. On oral L-arginine (9.2 g/d) to increase production of NO for a median of 4.7 months in 16 PVA patients with symptomatic angina despite conventional nitrate-calcium channel blockers, using the Seattle Angina Questionnaire, satisfaction with symptom remission rose (median) from 50% to 100% ( P = 0.004), satisfaction with angina frequency reduction rose from 65% to 80% ( P = 0.02), satisfaction with treatment for symptoms rose from 38% to 88% ( P = 0.001), and perception of overall life status rose from 25 to 71% ( P = 0.0002). On L-arginine (median 4.7 months), in 20 patients, none had worsening of angina, and of 7 patients whose angina totally resolved, eNOS T-786C homozygosity was over-represented, P = 0 .04. The eNOS T-786C mutation appears to be a reversible etiology of PVA in patients whose angina may be ameliorated by L-arginine.</abstract><cop>United States</cop><pub>Mosby, Inc</pub><pmid>23567331</pmid><doi>10.1016/j.trsl.2013.03.003</doi><tpages>3</tpages></addata></record> |
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| subjects | Angina Pectoris, Variant - drug therapy Angina Pectoris, Variant - enzymology Angina Pectoris, Variant - genetics Arginine - therapeutic use Calcium Channel Blockers - therapeutic use Female Genetic Predisposition to Disease Humans Internal Medicine Male Middle Aged Mutation Nitrates - therapeutic use Nitric Oxide Synthase Type III - genetics Surveys and Questionnaires |
| title | The endothelial nitric oxide synthase T-786c mutation, a treatable etiology of Prinzmetal's angina |
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