Effects of short-term treatment of hyperlipidemia on coronary vasodilator function and myocardial perfusion in regions having substantial impairment of baseline dilator reverse
We tested the hypothesis that correction of hyperlipidemia improves coronary vasodilator response and maximal perfusion in myocardial regions having substantial impairment of pretreatment vasodilator capacity. Measurements of myocardial blood flow were made with PET [13N]ammonia in 12 patients with...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 1998-09, Vol.98 (13), p.1291-1296 |
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| container_title | Circulation (New York, N.Y.) |
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| creator | HUGGINS, G. S PASTERNAK, R. C ALPERT, N. M FISCHMAN, A. J GEWIRTZ, H |
| description | We tested the hypothesis that correction of hyperlipidemia improves coronary vasodilator response and maximal perfusion in myocardial regions having substantial impairment of pretreatment vasodilator capacity.
Measurements of myocardial blood flow were made with PET [13N]ammonia in 12 patients with ischemic heart disease (11 men; age, 65+/-8 years [mean+/-SD]) at rest and during adenosine at 70 and then 140 microg . kg-1 . min-1 for 5 minutes each before and approximately 4 months after simvastatin treatment (40 mg daily). Simvastatin reduced LDL (171+/-13 before versus 99+/-18 mg/dL after simvastatin, P |
| doi_str_mv | 10.1161/01.cir.98.13.1291 |
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Measurements of myocardial blood flow were made with PET [13N]ammonia in 12 patients with ischemic heart disease (11 men; age, 65+/-8 years [mean+/-SD]) at rest and during adenosine at 70 and then 140 microg . kg-1 . min-1 for 5 minutes each before and approximately 4 months after simvastatin treatment (40 mg daily). Simvastatin reduced LDL (171+/-13 before versus 99+/-18 mg/dL after simvastatin, P<0.001) and increased HDL (39+/-8 versus 45+/-9 mg/dL, P<0.05). Myocardial segments were classified on the basis of pretreatment blood flow response to 140 microg . kg-1 . min-1 adenosine as normal (flow >/=2 mL . min-1 . g-1) or abnormal (flow <2 mL . min-1 . g-1). In normal segments, baseline myocardial blood flow (0.95+/-0.32) increased (P<0.001) at both low- (1.62+/-0.81) and high- (2.63+/-0.41) dose adenosine and was unchanged both at rest and with adenosine after simvastatin. In abnormal segments, myocardial blood flow at rest (0. 73+/-0.19) increased at low- (1.06+/-0.59, P<0.02) and high- (1. 29+/-0.33, P<0.01) dose adenosine. After simvastatin, myocardial blood flow increased more compared with pretreatment at both low- (1. 37+/-0.66, P<0.05 versus pretreatment) and high- (1.89+/-0.79, P<0. 01 versus pretreatment) dose adenosine.
Short-term lipid-lowering therapy increases stenotic segment maximal myocardial blood flow by approximately 45%. The mechanism involves enhanced, flow-mediated dilation of stenotic epicardial conduit vessels and may account at least in part for the efficacy of lipid lowering in secondary prevention trials and in reducing ischemic episodes in ambulatory patients.]]></description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.cir.98.13.1291</identifier><identifier>PMID: 9751677</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adenosine - pharmacology ; Aged ; Biological and medical sciences ; Coronary Circulation - drug effects ; Coronary Vessels - drug effects ; Coronary Vessels - physiopathology ; Female ; General and cellular metabolism. Vitamins ; Humans ; Hyperlipidemias - drug therapy ; Hyperlipidemias - physiopathology ; Hypolipidemic Agents - pharmacology ; Lipids - blood ; Male ; Medical sciences ; Middle Aged ; Myocardial Ischemia - physiopathology ; Pharmacology. Drug treatments ; Simvastatin - pharmacology ; Simvastatin - therapeutic use ; Vasodilation - drug effects</subject><ispartof>Circulation (New York, N.Y.), 1998-09, Vol.98 (13), p.1291-1296</ispartof><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-70e46918cffabc52da19c1d41859e965b9d7d1e2f5d422c427cf64088a80885c3</citedby><cites>FETCH-LOGICAL-c476t-70e46918cffabc52da19c1d41859e965b9d7d1e2f5d422c427cf64088a80885c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2400230$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9751677$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HUGGINS, G. S</creatorcontrib><creatorcontrib>PASTERNAK, R. C</creatorcontrib><creatorcontrib>ALPERT, N. M</creatorcontrib><creatorcontrib>FISCHMAN, A. J</creatorcontrib><creatorcontrib>GEWIRTZ, H</creatorcontrib><title>Effects of short-term treatment of hyperlipidemia on coronary vasodilator function and myocardial perfusion in regions having substantial impairment of baseline dilator reverse</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description><![CDATA[We tested the hypothesis that correction of hyperlipidemia improves coronary vasodilator response and maximal perfusion in myocardial regions having substantial impairment of pretreatment vasodilator capacity.
Measurements of myocardial blood flow were made with PET [13N]ammonia in 12 patients with ischemic heart disease (11 men; age, 65+/-8 years [mean+/-SD]) at rest and during adenosine at 70 and then 140 microg . kg-1 . min-1 for 5 minutes each before and approximately 4 months after simvastatin treatment (40 mg daily). Simvastatin reduced LDL (171+/-13 before versus 99+/-18 mg/dL after simvastatin, P<0.001) and increased HDL (39+/-8 versus 45+/-9 mg/dL, P<0.05). Myocardial segments were classified on the basis of pretreatment blood flow response to 140 microg . kg-1 . min-1 adenosine as normal (flow >/=2 mL . min-1 . g-1) or abnormal (flow <2 mL . min-1 . g-1). In normal segments, baseline myocardial blood flow (0.95+/-0.32) increased (P<0.001) at both low- (1.62+/-0.81) and high- (2.63+/-0.41) dose adenosine and was unchanged both at rest and with adenosine after simvastatin. In abnormal segments, myocardial blood flow at rest (0. 73+/-0.19) increased at low- (1.06+/-0.59, P<0.02) and high- (1. 29+/-0.33, P<0.01) dose adenosine. After simvastatin, myocardial blood flow increased more compared with pretreatment at both low- (1. 37+/-0.66, P<0.05 versus pretreatment) and high- (1.89+/-0.79, P<0. 01 versus pretreatment) dose adenosine.
Short-term lipid-lowering therapy increases stenotic segment maximal myocardial blood flow by approximately 45%. The mechanism involves enhanced, flow-mediated dilation of stenotic epicardial conduit vessels and may account at least in part for the efficacy of lipid lowering in secondary prevention trials and in reducing ischemic episodes in ambulatory patients.]]></description><subject>Adenosine - pharmacology</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Coronary Circulation - drug effects</subject><subject>Coronary Vessels - drug effects</subject><subject>Coronary Vessels - physiopathology</subject><subject>Female</subject><subject>General and cellular metabolism. Vitamins</subject><subject>Humans</subject><subject>Hyperlipidemias - drug therapy</subject><subject>Hyperlipidemias - physiopathology</subject><subject>Hypolipidemic Agents - pharmacology</subject><subject>Lipids - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Ischemia - physiopathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Simvastatin - pharmacology</subject><subject>Simvastatin - therapeutic use</subject><subject>Vasodilation - drug effects</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9Ud2K1DAULqKs4-oDeCHkQrxrzUnSprmUYdWFhYVFr0OanuxE2mRM0oF5Kx_Rlp3dm_P3_QTyVdVHoA1AB18pNNanRvUN8AaYglfVDlomatFy9braUUpVLTljb6t3Of9Z147L9qq6UrKFTspd9e_GObQlk-hIPsRU6oJpJiWhKTOGst0P5yOmyR_9iLM3JAZiY4rBpDM5mRxHP5kSE3FLsMWvqAkjmc_RmjR6M5FV7Ja8AT6QhI_rlMnBnHx4JHkZcjGhbDw_H41Pz48OJuPkA5Jn-4QnTBnfV2-cmTJ-uPTr6vf3m1_7n_Xd_Y_b_be72grZlVpSFJ2C3jpnBtuy0YCyMAroW4Wqawc1yhGQuXYUjFnBpHWdoH1v-rW0ll9XX558jyn-XTAXPftscZpMwLhkLbniIECtRHgi2hRzTuj0Mfl5_RwNVG8paQp6f_ugVa-B6y2lVfPpYr4MM44vikssK_75gptszeSSCdbnFxoTlDJO-X-yHqBO</recordid><startdate>19980929</startdate><enddate>19980929</enddate><creator>HUGGINS, G. S</creator><creator>PASTERNAK, R. C</creator><creator>ALPERT, N. M</creator><creator>FISCHMAN, A. J</creator><creator>GEWIRTZ, H</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>19980929</creationdate><title>Effects of short-term treatment of hyperlipidemia on coronary vasodilator function and myocardial perfusion in regions having substantial impairment of baseline dilator reverse</title><author>HUGGINS, G. S ; PASTERNAK, R. C ; ALPERT, N. M ; FISCHMAN, A. J ; GEWIRTZ, H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-70e46918cffabc52da19c1d41859e965b9d7d1e2f5d422c427cf64088a80885c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Adenosine - pharmacology</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Coronary Circulation - drug effects</topic><topic>Coronary Vessels - drug effects</topic><topic>Coronary Vessels - physiopathology</topic><topic>Female</topic><topic>General and cellular metabolism. Vitamins</topic><topic>Humans</topic><topic>Hyperlipidemias - drug therapy</topic><topic>Hyperlipidemias - physiopathology</topic><topic>Hypolipidemic Agents - pharmacology</topic><topic>Lipids - blood</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Ischemia - physiopathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Simvastatin - pharmacology</topic><topic>Simvastatin - therapeutic use</topic><topic>Vasodilation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HUGGINS, G. S</creatorcontrib><creatorcontrib>PASTERNAK, R. C</creatorcontrib><creatorcontrib>ALPERT, N. M</creatorcontrib><creatorcontrib>FISCHMAN, A. J</creatorcontrib><creatorcontrib>GEWIRTZ, H</creatorcontrib><collection>Pascal-Francis</collection><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>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HUGGINS, G. S</au><au>PASTERNAK, R. C</au><au>ALPERT, N. M</au><au>FISCHMAN, A. J</au><au>GEWIRTZ, H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of short-term treatment of hyperlipidemia on coronary vasodilator function and myocardial perfusion in regions having substantial impairment of baseline dilator reverse</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1998-09-29</date><risdate>1998</risdate><volume>98</volume><issue>13</issue><spage>1291</spage><epage>1296</epage><pages>1291-1296</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract><![CDATA[We tested the hypothesis that correction of hyperlipidemia improves coronary vasodilator response and maximal perfusion in myocardial regions having substantial impairment of pretreatment vasodilator capacity.
Measurements of myocardial blood flow were made with PET [13N]ammonia in 12 patients with ischemic heart disease (11 men; age, 65+/-8 years [mean+/-SD]) at rest and during adenosine at 70 and then 140 microg . kg-1 . min-1 for 5 minutes each before and approximately 4 months after simvastatin treatment (40 mg daily). Simvastatin reduced LDL (171+/-13 before versus 99+/-18 mg/dL after simvastatin, P<0.001) and increased HDL (39+/-8 versus 45+/-9 mg/dL, P<0.05). Myocardial segments were classified on the basis of pretreatment blood flow response to 140 microg . kg-1 . min-1 adenosine as normal (flow >/=2 mL . min-1 . g-1) or abnormal (flow <2 mL . min-1 . g-1). In normal segments, baseline myocardial blood flow (0.95+/-0.32) increased (P<0.001) at both low- (1.62+/-0.81) and high- (2.63+/-0.41) dose adenosine and was unchanged both at rest and with adenosine after simvastatin. In abnormal segments, myocardial blood flow at rest (0. 73+/-0.19) increased at low- (1.06+/-0.59, P<0.02) and high- (1. 29+/-0.33, P<0.01) dose adenosine. After simvastatin, myocardial blood flow increased more compared with pretreatment at both low- (1. 37+/-0.66, P<0.05 versus pretreatment) and high- (1.89+/-0.79, P<0. 01 versus pretreatment) dose adenosine.
Short-term lipid-lowering therapy increases stenotic segment maximal myocardial blood flow by approximately 45%. The mechanism involves enhanced, flow-mediated dilation of stenotic epicardial conduit vessels and may account at least in part for the efficacy of lipid lowering in secondary prevention trials and in reducing ischemic episodes in ambulatory patients.]]></abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>9751677</pmid><doi>10.1161/01.cir.98.13.1291</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0009-7322 |
| ispartof | Circulation (New York, N.Y.), 1998-09, Vol.98 (13), p.1291-1296 |
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| source | Electronic Journals Library; MEDLINE; American Heart Association; Journals@Ovid Complete |
| subjects | Adenosine - pharmacology Aged Biological and medical sciences Coronary Circulation - drug effects Coronary Vessels - drug effects Coronary Vessels - physiopathology Female General and cellular metabolism. Vitamins Humans Hyperlipidemias - drug therapy Hyperlipidemias - physiopathology Hypolipidemic Agents - pharmacology Lipids - blood Male Medical sciences Middle Aged Myocardial Ischemia - physiopathology Pharmacology. Drug treatments Simvastatin - pharmacology Simvastatin - therapeutic use Vasodilation - drug effects |
| title | Effects of short-term treatment of hyperlipidemia on coronary vasodilator function and myocardial perfusion in regions having substantial impairment of baseline dilator reverse |
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