Experimental hyperhomocysteinemia impairs coronary flow velocity reserve
Hyperhomocysteinemia has been identified as an independent risk factor for coronary artery disease. One mechanism is considered to be deteriorated endothelial function that is recovered by vitamin C. However, its direct action on coronary circulation has yet to be examined. This study was designed t...
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| Veröffentlicht in: | International journal of cardiology 2005-09, Vol.104 (2), p.163-169 |
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| container_title | International journal of cardiology |
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| creator | Yamashita, Kazuhito Tasaki, Hiromi Nagai, Yoshitaka Suzuka, Hiroshi Nihei, Shun-ichi Kobayashi, Kengo Horiuchi, Masataka Nakashima, Yasuhide Adachi, Tetsuo |
| description | Hyperhomocysteinemia has been identified as an independent risk factor for coronary artery disease. One mechanism is considered to be deteriorated endothelial function that is recovered by vitamin C. However, its direct action on coronary circulation has yet to be examined. This study was designed to test the hypothesis that experimental acute hyperhomocysteinemia would impair coronary flow velocity reserve (CFR) by increasing oxidative stress.
Eleven healthy male volunteers (aged 23.3±0.9 years) were enrolled. CFR induced by intravenous 5′-adenosine triphosphate infusion was measured by transthoracic-Doppler echocardiography. Measurements were taken before and 4 h after administration of a placebo, oral methionine (L-methionine 0.1 g/kg) or oral methionine plus vitamin C (2 g) on 3 separate days.
The baseline average diastolic peak velocity (APV) was similar in all 3 groups. In the methionine group, plasma homocysteine increased (12.9±7.0 to 32.1±9.4 nmol/ml,
p |
| doi_str_mv | 10.1016/j.ijcard.2004.10.026 |
| format | Article |
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Eleven healthy male volunteers (aged 23.3±0.9 years) were enrolled. CFR induced by intravenous 5′-adenosine triphosphate infusion was measured by transthoracic-Doppler echocardiography. Measurements were taken before and 4 h after administration of a placebo, oral methionine (L-methionine 0.1 g/kg) or oral methionine plus vitamin C (2 g) on 3 separate days.
The baseline average diastolic peak velocity (APV) was similar in all 3 groups. In the methionine group, plasma homocysteine increased (12.9±7.0 to 32.1±9.4 nmol/ml,
p<0.0001), while APV under hyperemic conditions (APV-hyp) and CFR significantly decreased (87.2±11.4 cm/sec and 4.02±0.70 to 73.2±10.2 cm/sec and 3.35±0.52,
p=0.0022 and 0.0030, respectively). Moreover, there was a significant inverse correlation between the plasma homocysteine and CFR (
r=-0.620,
p=0.0021). However, upon simultaneous administration of vitamin C, APV-hyp and CVR did not decrease despite an elevation in plasma homocysteine.
Experimentally induced acute hyperhomocysteinemia significantly decreased CFR, and this decrease was significantly reversed by vitamin C administration. Oxidative stress is suggested to play a major role in the deleterious effects of homocysteine on the coronary microcirculation.</description><identifier>ISSN: 0167-5273</identifier><identifier>EISSN: 1874-1754</identifier><identifier>DOI: 10.1016/j.ijcard.2004.10.026</identifier><identifier>PMID: 16168809</identifier><identifier>CODEN: IJCDD5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Adenosine Triphosphate - administration & dosage ; Administration, Oral ; Adult ; Antioxidant ; Antioxidants - administration & dosage ; Ascorbic Acid - administration & dosage ; Biological and medical sciences ; Biomarkers - blood ; Blood Flow Velocity ; Cardiology. Vascular system ; Coronary artery disease ; Coronary Circulation ; Coronary flow velocity reserve ; Coronary heart disease ; Endothelium ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Heart ; Homocysteine ; Homocysteine - blood ; Homocysteine - drug effects ; Homocysteine - metabolism ; Humans ; Hyperhomocysteinemia - metabolism ; Hyperhomocysteinemia - physiopathology ; Male ; Medical sciences ; Methionine - administration & dosage ; Oxidative Stress - drug effects ; Reference Values ; Research Design ; Superoxide Dismutase - drug effects ; Superoxide Dismutase - metabolism ; Time Factors</subject><ispartof>International journal of cardiology, 2005-09, Vol.104 (2), p.163-169</ispartof><rights>2005 Elsevier Ireland Ltd</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-c05f8c53167ca4e3acc8949ed77cbe27fd7d6972d37ee6a779a26b91aae995503</citedby><cites>FETCH-LOGICAL-c456t-c05f8c53167ca4e3acc8949ed77cbe27fd7d6972d37ee6a779a26b91aae995503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0167527305001592$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17117539$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16168809$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yamashita, Kazuhito</creatorcontrib><creatorcontrib>Tasaki, Hiromi</creatorcontrib><creatorcontrib>Nagai, Yoshitaka</creatorcontrib><creatorcontrib>Suzuka, Hiroshi</creatorcontrib><creatorcontrib>Nihei, Shun-ichi</creatorcontrib><creatorcontrib>Kobayashi, Kengo</creatorcontrib><creatorcontrib>Horiuchi, Masataka</creatorcontrib><creatorcontrib>Nakashima, Yasuhide</creatorcontrib><creatorcontrib>Adachi, Tetsuo</creatorcontrib><title>Experimental hyperhomocysteinemia impairs coronary flow velocity reserve</title><title>International journal of cardiology</title><addtitle>Int J Cardiol</addtitle><description>Hyperhomocysteinemia has been identified as an independent risk factor for coronary artery disease. One mechanism is considered to be deteriorated endothelial function that is recovered by vitamin C. However, its direct action on coronary circulation has yet to be examined. This study was designed to test the hypothesis that experimental acute hyperhomocysteinemia would impair coronary flow velocity reserve (CFR) by increasing oxidative stress.
Eleven healthy male volunteers (aged 23.3±0.9 years) were enrolled. CFR induced by intravenous 5′-adenosine triphosphate infusion was measured by transthoracic-Doppler echocardiography. Measurements were taken before and 4 h after administration of a placebo, oral methionine (L-methionine 0.1 g/kg) or oral methionine plus vitamin C (2 g) on 3 separate days.
The baseline average diastolic peak velocity (APV) was similar in all 3 groups. In the methionine group, plasma homocysteine increased (12.9±7.0 to 32.1±9.4 nmol/ml,
p<0.0001), while APV under hyperemic conditions (APV-hyp) and CFR significantly decreased (87.2±11.4 cm/sec and 4.02±0.70 to 73.2±10.2 cm/sec and 3.35±0.52,
p=0.0022 and 0.0030, respectively). Moreover, there was a significant inverse correlation between the plasma homocysteine and CFR (
r=-0.620,
p=0.0021). However, upon simultaneous administration of vitamin C, APV-hyp and CVR did not decrease despite an elevation in plasma homocysteine.
Experimentally induced acute hyperhomocysteinemia significantly decreased CFR, and this decrease was significantly reversed by vitamin C administration. Oxidative stress is suggested to play a major role in the deleterious effects of homocysteine on the coronary microcirculation.</description><subject>Adenosine Triphosphate - administration & dosage</subject><subject>Administration, Oral</subject><subject>Adult</subject><subject>Antioxidant</subject><subject>Antioxidants - administration & dosage</subject><subject>Ascorbic Acid - administration & dosage</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Blood Flow Velocity</subject><subject>Cardiology. Vascular system</subject><subject>Coronary artery disease</subject><subject>Coronary Circulation</subject><subject>Coronary flow velocity reserve</subject><subject>Coronary heart disease</subject><subject>Endothelium</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Heart</subject><subject>Homocysteine</subject><subject>Homocysteine - blood</subject><subject>Homocysteine - drug effects</subject><subject>Homocysteine - metabolism</subject><subject>Humans</subject><subject>Hyperhomocysteinemia - metabolism</subject><subject>Hyperhomocysteinemia - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methionine - administration & dosage</subject><subject>Oxidative Stress - drug effects</subject><subject>Reference Values</subject><subject>Research Design</subject><subject>Superoxide Dismutase - drug effects</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Time Factors</subject><issn>0167-5273</issn><issn>1874-1754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1LAzEQhoMotlb_gche9LZrsh_J5iJIqR9Q8KLnkM7O0pTdTU221f33pmyhNw9DmOGZ4c1DyC2jCaOMP24SswHtqiSlNA-jhKb8jExZKfKYiSI_J9OAibhIRTYhV95vaAClLC_JhHHGy5LKKXlb_G7RmRa7XjfRegjN2rYWBt-j6bA1OjLtVhvnI7DOdtoNUd3Yn2iPjQXTD5FDj26P1-Si1o3Hm-M7I18vi8_5W7z8eH2fPy9jyAvex0CLuoQiC8lA55hpgFLmEishYIWpqCtRcSnSKhOIXAshdcpXkmmNUhYFzWbkYby7dfZ7h75XrfGATaM7tDuveFnITIaakXwEwVnvHdZqG_4Z8itG1cGg2qjRoDoYPEyDwbB2d7y_W7VYnZaOygJwfwS0B93UTndg_IkTLNjPDtzTyGGwsTfolAeDHWBlHEKvKmv-T_IH89GSmQ</recordid><startdate>20050930</startdate><enddate>20050930</enddate><creator>Yamashita, Kazuhito</creator><creator>Tasaki, Hiromi</creator><creator>Nagai, Yoshitaka</creator><creator>Suzuka, Hiroshi</creator><creator>Nihei, Shun-ichi</creator><creator>Kobayashi, Kengo</creator><creator>Horiuchi, Masataka</creator><creator>Nakashima, Yasuhide</creator><creator>Adachi, Tetsuo</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Science</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>20050930</creationdate><title>Experimental hyperhomocysteinemia impairs coronary flow velocity reserve</title><author>Yamashita, Kazuhito ; Tasaki, Hiromi ; Nagai, Yoshitaka ; Suzuka, Hiroshi ; Nihei, Shun-ichi ; Kobayashi, Kengo ; Horiuchi, Masataka ; Nakashima, Yasuhide ; Adachi, Tetsuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-c05f8c53167ca4e3acc8949ed77cbe27fd7d6972d37ee6a779a26b91aae995503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adenosine Triphosphate - administration & dosage</topic><topic>Administration, Oral</topic><topic>Adult</topic><topic>Antioxidant</topic><topic>Antioxidants - administration & dosage</topic><topic>Ascorbic Acid - administration & dosage</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>Blood Flow Velocity</topic><topic>Cardiology. Vascular system</topic><topic>Coronary artery disease</topic><topic>Coronary Circulation</topic><topic>Coronary flow velocity reserve</topic><topic>Coronary heart disease</topic><topic>Endothelium</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Heart</topic><topic>Homocysteine</topic><topic>Homocysteine - blood</topic><topic>Homocysteine - drug effects</topic><topic>Homocysteine - metabolism</topic><topic>Humans</topic><topic>Hyperhomocysteinemia - metabolism</topic><topic>Hyperhomocysteinemia - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methionine - administration & dosage</topic><topic>Oxidative Stress - drug effects</topic><topic>Reference Values</topic><topic>Research Design</topic><topic>Superoxide Dismutase - drug effects</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yamashita, Kazuhito</creatorcontrib><creatorcontrib>Tasaki, Hiromi</creatorcontrib><creatorcontrib>Nagai, Yoshitaka</creatorcontrib><creatorcontrib>Suzuka, Hiroshi</creatorcontrib><creatorcontrib>Nihei, Shun-ichi</creatorcontrib><creatorcontrib>Kobayashi, Kengo</creatorcontrib><creatorcontrib>Horiuchi, Masataka</creatorcontrib><creatorcontrib>Nakashima, Yasuhide</creatorcontrib><creatorcontrib>Adachi, Tetsuo</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>International journal of cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yamashita, Kazuhito</au><au>Tasaki, Hiromi</au><au>Nagai, Yoshitaka</au><au>Suzuka, Hiroshi</au><au>Nihei, Shun-ichi</au><au>Kobayashi, Kengo</au><au>Horiuchi, Masataka</au><au>Nakashima, Yasuhide</au><au>Adachi, Tetsuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Experimental hyperhomocysteinemia impairs coronary flow velocity reserve</atitle><jtitle>International journal of cardiology</jtitle><addtitle>Int J Cardiol</addtitle><date>2005-09-30</date><risdate>2005</risdate><volume>104</volume><issue>2</issue><spage>163</spage><epage>169</epage><pages>163-169</pages><issn>0167-5273</issn><eissn>1874-1754</eissn><coden>IJCDD5</coden><abstract>Hyperhomocysteinemia has been identified as an independent risk factor for coronary artery disease. One mechanism is considered to be deteriorated endothelial function that is recovered by vitamin C. However, its direct action on coronary circulation has yet to be examined. This study was designed to test the hypothesis that experimental acute hyperhomocysteinemia would impair coronary flow velocity reserve (CFR) by increasing oxidative stress.
Eleven healthy male volunteers (aged 23.3±0.9 years) were enrolled. CFR induced by intravenous 5′-adenosine triphosphate infusion was measured by transthoracic-Doppler echocardiography. Measurements were taken before and 4 h after administration of a placebo, oral methionine (L-methionine 0.1 g/kg) or oral methionine plus vitamin C (2 g) on 3 separate days.
The baseline average diastolic peak velocity (APV) was similar in all 3 groups. In the methionine group, plasma homocysteine increased (12.9±7.0 to 32.1±9.4 nmol/ml,
p<0.0001), while APV under hyperemic conditions (APV-hyp) and CFR significantly decreased (87.2±11.4 cm/sec and 4.02±0.70 to 73.2±10.2 cm/sec and 3.35±0.52,
p=0.0022 and 0.0030, respectively). Moreover, there was a significant inverse correlation between the plasma homocysteine and CFR (
r=-0.620,
p=0.0021). However, upon simultaneous administration of vitamin C, APV-hyp and CVR did not decrease despite an elevation in plasma homocysteine.
Experimentally induced acute hyperhomocysteinemia significantly decreased CFR, and this decrease was significantly reversed by vitamin C administration. Oxidative stress is suggested to play a major role in the deleterious effects of homocysteine on the coronary microcirculation.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>16168809</pmid><doi>10.1016/j.ijcard.2004.10.026</doi><tpages>7</tpages></addata></record> |
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| subjects | Adenosine Triphosphate - administration & dosage Administration, Oral Adult Antioxidant Antioxidants - administration & dosage Ascorbic Acid - administration & dosage Biological and medical sciences Biomarkers - blood Blood Flow Velocity Cardiology. Vascular system Coronary artery disease Coronary Circulation Coronary flow velocity reserve Coronary heart disease Endothelium Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Heart Homocysteine Homocysteine - blood Homocysteine - drug effects Homocysteine - metabolism Humans Hyperhomocysteinemia - metabolism Hyperhomocysteinemia - physiopathology Male Medical sciences Methionine - administration & dosage Oxidative Stress - drug effects Reference Values Research Design Superoxide Dismutase - drug effects Superoxide Dismutase - metabolism Time Factors |
| title | Experimental hyperhomocysteinemia impairs coronary flow velocity reserve |
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