Iron Metabolism, Hepcidin, and Mortality (the Ludwigshafen Risk and Cardiovascular Health Study)
Anemia has been shown to be a risk factor for coronary artery disease (CAD) and mortality, whereas the role of iron metabolism remains controversial. We analyzed iron metabolism and its associations with cardiovascular death and total mortality in patients undergoing coronary angiography with a medi...
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| Veröffentlicht in: | Clinical chemistry (Baltimore, Md.) Md.), 2019-07, Vol.65 (7), p.849-861 |
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| creator | Grammer, Tanja B Scharnagl, Hubert Dressel, Alexander Kleber, Marcus E Silbernagel, Günther Pilz, Stefan Tomaschitz, Andreas Koenig, Wolfgang Mueller-Myhsok, Bertram März, Winfried Strnad, Pavel |
| description | Anemia has been shown to be a risk factor for coronary artery disease (CAD) and mortality, whereas the role of iron metabolism remains controversial.
We analyzed iron metabolism and its associations with cardiovascular death and total mortality in patients undergoing coronary angiography with a median follow-up of 9.9 years. Hemoglobin and iron status were determined in 1480 patients with stable CAD and in 682 individuals in whom significant CAD had been excluded by angiography.
Multivariate-adjusted hazard ratios (HRs) for total mortality in the lowest quartiles of iron, transferrin saturation, ferritin, soluble transferrin receptor (sTfR), and hemoglobin were 1.22 (95% CI, 0.96-1.60), 1.23 (95% CI, 0.97-1.56), 1.27 (95% CI, 1.02-1.58), 1.26 (95% CI, 0.97-1.65), and 0.99 (95% CI, 0.79-1.24), respectively, compared to the second or third quartile, which served as reference (1.00) because of a J-shaped association. The corresponding HRs for total mortality in the highest quartiles were 1.44 (95% CI, 1.10-1.87), 1.37 (95% CI, 1.05-1.77), 1.17 (95% CI, 0.92-1.50), 1.76 (95% CI, 1.39-2.22), and 0.83 (95% CI, 0.63-1.09). HRs for cardiovascular death were similar. For hepcidin, the adjusted HRs for total mortality and cardiovascular deaths were 0.62 (95% CI, 0.49-0.78) and 0.70 (95% CI, 0.52-0.90) in the highest quartile compared to the lowest one.
In stable patients undergoing angiography, serum iron, transferrin saturation, sTfR, and ferritin had J-shaped associations and hemoglobin only a marginal association with cardiovascular and total mortality. Hepcidin was continuously and inversely related to mortality. |
| doi_str_mv | 10.1373/clinchem.2018.297242 |
| format | Article |
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We analyzed iron metabolism and its associations with cardiovascular death and total mortality in patients undergoing coronary angiography with a median follow-up of 9.9 years. Hemoglobin and iron status were determined in 1480 patients with stable CAD and in 682 individuals in whom significant CAD had been excluded by angiography.
Multivariate-adjusted hazard ratios (HRs) for total mortality in the lowest quartiles of iron, transferrin saturation, ferritin, soluble transferrin receptor (sTfR), and hemoglobin were 1.22 (95% CI, 0.96-1.60), 1.23 (95% CI, 0.97-1.56), 1.27 (95% CI, 1.02-1.58), 1.26 (95% CI, 0.97-1.65), and 0.99 (95% CI, 0.79-1.24), respectively, compared to the second or third quartile, which served as reference (1.00) because of a J-shaped association. The corresponding HRs for total mortality in the highest quartiles were 1.44 (95% CI, 1.10-1.87), 1.37 (95% CI, 1.05-1.77), 1.17 (95% CI, 0.92-1.50), 1.76 (95% CI, 1.39-2.22), and 0.83 (95% CI, 0.63-1.09). HRs for cardiovascular death were similar. For hepcidin, the adjusted HRs for total mortality and cardiovascular deaths were 0.62 (95% CI, 0.49-0.78) and 0.70 (95% CI, 0.52-0.90) in the highest quartile compared to the lowest one.
In stable patients undergoing angiography, serum iron, transferrin saturation, sTfR, and ferritin had J-shaped associations and hemoglobin only a marginal association with cardiovascular and total mortality. Hepcidin was continuously and inversely related to mortality.</description><identifier>ISSN: 0009-9147</identifier><identifier>EISSN: 1530-8561</identifier><identifier>DOI: 10.1373/clinchem.2018.297242</identifier><identifier>PMID: 30917972</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Acute coronary syndromes ; Aged ; Anemia ; Angiography ; C-Reactive Protein - metabolism ; Cardiovascular disease ; Cardiovascular diseases ; Coronary artery ; Coronary artery disease ; Coronary Artery Disease - metabolism ; Coronary Artery Disease - mortality ; Coronary vessels ; Diabetes ; Female ; Ferritin ; Ferritins - metabolism ; Follow-Up Studies ; Health risk assessment ; Heart diseases ; Heart failure ; Hemoglobin ; Hepcidin ; Hepcidins - metabolism ; Humans ; Iron ; Iron - metabolism ; Kidney diseases ; Laboratories ; Male ; Medical imaging ; Metabolism ; Middle Aged ; Mortality ; Proportional Hazards Models ; Prospective Studies ; Quartiles ; Risk analysis ; Risk Factors ; Saturation ; Systematic review ; Transferrin ; Transferrin - metabolism ; Transferrins ; Womens health</subject><ispartof>Clinical chemistry (Baltimore, Md.), 2019-07, Vol.65 (7), p.849-861</ispartof><rights>2019 American Association for Clinical Chemistry.</rights><rights>Copyright American Association for Clinical Chemistry Jul 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-450401b731bc3693ce25c2f512ef96c0f95dde694b9942ef0ed5e557c5cf3b6d3</citedby><cites>FETCH-LOGICAL-c381t-450401b731bc3693ce25c2f512ef96c0f95dde694b9942ef0ed5e557c5cf3b6d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30917972$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Grammer, Tanja B</creatorcontrib><creatorcontrib>Scharnagl, Hubert</creatorcontrib><creatorcontrib>Dressel, Alexander</creatorcontrib><creatorcontrib>Kleber, Marcus E</creatorcontrib><creatorcontrib>Silbernagel, Günther</creatorcontrib><creatorcontrib>Pilz, Stefan</creatorcontrib><creatorcontrib>Tomaschitz, Andreas</creatorcontrib><creatorcontrib>Koenig, Wolfgang</creatorcontrib><creatorcontrib>Mueller-Myhsok, Bertram</creatorcontrib><creatorcontrib>März, Winfried</creatorcontrib><creatorcontrib>Strnad, Pavel</creatorcontrib><title>Iron Metabolism, Hepcidin, and Mortality (the Ludwigshafen Risk and Cardiovascular Health Study)</title><title>Clinical chemistry (Baltimore, Md.)</title><addtitle>Clin Chem</addtitle><description>Anemia has been shown to be a risk factor for coronary artery disease (CAD) and mortality, whereas the role of iron metabolism remains controversial.
We analyzed iron metabolism and its associations with cardiovascular death and total mortality in patients undergoing coronary angiography with a median follow-up of 9.9 years. Hemoglobin and iron status were determined in 1480 patients with stable CAD and in 682 individuals in whom significant CAD had been excluded by angiography.
Multivariate-adjusted hazard ratios (HRs) for total mortality in the lowest quartiles of iron, transferrin saturation, ferritin, soluble transferrin receptor (sTfR), and hemoglobin were 1.22 (95% CI, 0.96-1.60), 1.23 (95% CI, 0.97-1.56), 1.27 (95% CI, 1.02-1.58), 1.26 (95% CI, 0.97-1.65), and 0.99 (95% CI, 0.79-1.24), respectively, compared to the second or third quartile, which served as reference (1.00) because of a J-shaped association. The corresponding HRs for total mortality in the highest quartiles were 1.44 (95% CI, 1.10-1.87), 1.37 (95% CI, 1.05-1.77), 1.17 (95% CI, 0.92-1.50), 1.76 (95% CI, 1.39-2.22), and 0.83 (95% CI, 0.63-1.09). HRs for cardiovascular death were similar. For hepcidin, the adjusted HRs for total mortality and cardiovascular deaths were 0.62 (95% CI, 0.49-0.78) and 0.70 (95% CI, 0.52-0.90) in the highest quartile compared to the lowest one.
In stable patients undergoing angiography, serum iron, transferrin saturation, sTfR, and ferritin had J-shaped associations and hemoglobin only a marginal association with cardiovascular and total mortality. Hepcidin was continuously and inversely related to mortality.</description><subject>Acute coronary syndromes</subject><subject>Aged</subject><subject>Anemia</subject><subject>Angiography</subject><subject>C-Reactive Protein - metabolism</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Coronary artery</subject><subject>Coronary artery disease</subject><subject>Coronary Artery Disease - metabolism</subject><subject>Coronary Artery Disease - mortality</subject><subject>Coronary vessels</subject><subject>Diabetes</subject><subject>Female</subject><subject>Ferritin</subject><subject>Ferritins - metabolism</subject><subject>Follow-Up Studies</subject><subject>Health risk assessment</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Hemoglobin</subject><subject>Hepcidin</subject><subject>Hepcidins - metabolism</subject><subject>Humans</subject><subject>Iron</subject><subject>Iron - metabolism</subject><subject>Kidney diseases</subject><subject>Laboratories</subject><subject>Male</subject><subject>Medical imaging</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Mortality</subject><subject>Proportional Hazards Models</subject><subject>Prospective Studies</subject><subject>Quartiles</subject><subject>Risk analysis</subject><subject>Risk Factors</subject><subject>Saturation</subject><subject>Systematic review</subject><subject>Transferrin</subject><subject>Transferrin - metabolism</subject><subject>Transferrins</subject><subject>Womens health</subject><issn>0009-9147</issn><issn>1530-8561</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkctKAzEUhoMotlbfQGTATYVOzXVmspSitlARvKxjJsnY1LnUJKP07Z3a1oWrcML3_xzOB8A5gmNEUnKtSlurhanGGKJsjHmKKT4AfcQIjDOWoEPQhxDymCOa9sCJ98tupGmWHIMegRylXaIP3mauqaMHE2TelNZXo2hqVspqW48iWevooXFBljaso2FYmGje6m_77heyMHX0ZP3HLzSRTtvmS3rVltJ1DbIMi-g5tHp9dQqOCll6c7Z7B-D17vZlMo3nj_ezyc08ViRDIaYMUojylKBckYQTZTBTuGAIm4InChacaW0STnPOafcHjWaGsVQxVZA80WQAhtvelWs-W-ODqKxXpixlbZrWC4w4RxlNKO3Qy3_osmld3W0nMGYkwxlluKPollKu8d6ZQqycraRbCwTFxoDYGxAbA2JroItd7MrbvDL6L7Q_OfkB9fmDGA</recordid><startdate>20190701</startdate><enddate>20190701</enddate><creator>Grammer, Tanja B</creator><creator>Scharnagl, Hubert</creator><creator>Dressel, Alexander</creator><creator>Kleber, Marcus E</creator><creator>Silbernagel, Günther</creator><creator>Pilz, Stefan</creator><creator>Tomaschitz, Andreas</creator><creator>Koenig, Wolfgang</creator><creator>Mueller-Myhsok, Bertram</creator><creator>März, Winfried</creator><creator>Strnad, Pavel</creator><general>Oxford University Press</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>4U-</scope><scope>7QO</scope><scope>7RV</scope><scope>7TM</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PCBAR</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>20190701</creationdate><title>Iron Metabolism, Hepcidin, and Mortality (the Ludwigshafen Risk and Cardiovascular Health Study)</title><author>Grammer, Tanja B ; Scharnagl, Hubert ; Dressel, Alexander ; Kleber, Marcus E ; Silbernagel, Günther ; Pilz, Stefan ; Tomaschitz, Andreas ; Koenig, Wolfgang ; Mueller-Myhsok, Bertram ; März, Winfried ; Strnad, Pavel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-450401b731bc3693ce25c2f512ef96c0f95dde694b9942ef0ed5e557c5cf3b6d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Acute coronary syndromes</topic><topic>Aged</topic><topic>Anemia</topic><topic>Angiography</topic><topic>C-Reactive Protein - metabolism</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Coronary artery</topic><topic>Coronary artery disease</topic><topic>Coronary Artery Disease - metabolism</topic><topic>Coronary Artery Disease - mortality</topic><topic>Coronary vessels</topic><topic>Diabetes</topic><topic>Female</topic><topic>Ferritin</topic><topic>Ferritins - metabolism</topic><topic>Follow-Up Studies</topic><topic>Health risk assessment</topic><topic>Heart diseases</topic><topic>Heart failure</topic><topic>Hemoglobin</topic><topic>Hepcidin</topic><topic>Hepcidins - metabolism</topic><topic>Humans</topic><topic>Iron</topic><topic>Iron - metabolism</topic><topic>Kidney diseases</topic><topic>Laboratories</topic><topic>Male</topic><topic>Medical imaging</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Mortality</topic><topic>Proportional Hazards Models</topic><topic>Prospective Studies</topic><topic>Quartiles</topic><topic>Risk analysis</topic><topic>Risk Factors</topic><topic>Saturation</topic><topic>Systematic review</topic><topic>Transferrin</topic><topic>Transferrin - 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Academic</collection><jtitle>Clinical chemistry (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Grammer, Tanja B</au><au>Scharnagl, Hubert</au><au>Dressel, Alexander</au><au>Kleber, Marcus E</au><au>Silbernagel, Günther</au><au>Pilz, Stefan</au><au>Tomaschitz, Andreas</au><au>Koenig, Wolfgang</au><au>Mueller-Myhsok, Bertram</au><au>März, Winfried</au><au>Strnad, Pavel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Iron Metabolism, Hepcidin, and Mortality (the Ludwigshafen Risk and Cardiovascular Health Study)</atitle><jtitle>Clinical chemistry (Baltimore, Md.)</jtitle><addtitle>Clin Chem</addtitle><date>2019-07-01</date><risdate>2019</risdate><volume>65</volume><issue>7</issue><spage>849</spage><epage>861</epage><pages>849-861</pages><issn>0009-9147</issn><eissn>1530-8561</eissn><abstract>Anemia has been shown to be a risk factor for coronary artery disease (CAD) and mortality, whereas the role of iron metabolism remains controversial.
We analyzed iron metabolism and its associations with cardiovascular death and total mortality in patients undergoing coronary angiography with a median follow-up of 9.9 years. Hemoglobin and iron status were determined in 1480 patients with stable CAD and in 682 individuals in whom significant CAD had been excluded by angiography.
Multivariate-adjusted hazard ratios (HRs) for total mortality in the lowest quartiles of iron, transferrin saturation, ferritin, soluble transferrin receptor (sTfR), and hemoglobin were 1.22 (95% CI, 0.96-1.60), 1.23 (95% CI, 0.97-1.56), 1.27 (95% CI, 1.02-1.58), 1.26 (95% CI, 0.97-1.65), and 0.99 (95% CI, 0.79-1.24), respectively, compared to the second or third quartile, which served as reference (1.00) because of a J-shaped association. The corresponding HRs for total mortality in the highest quartiles were 1.44 (95% CI, 1.10-1.87), 1.37 (95% CI, 1.05-1.77), 1.17 (95% CI, 0.92-1.50), 1.76 (95% CI, 1.39-2.22), and 0.83 (95% CI, 0.63-1.09). HRs for cardiovascular death were similar. For hepcidin, the adjusted HRs for total mortality and cardiovascular deaths were 0.62 (95% CI, 0.49-0.78) and 0.70 (95% CI, 0.52-0.90) in the highest quartile compared to the lowest one.
In stable patients undergoing angiography, serum iron, transferrin saturation, sTfR, and ferritin had J-shaped associations and hemoglobin only a marginal association with cardiovascular and total mortality. Hepcidin was continuously and inversely related to mortality.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>30917972</pmid><doi>10.1373/clinchem.2018.297242</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute coronary syndromes Aged Anemia Angiography C-Reactive Protein - metabolism Cardiovascular disease Cardiovascular diseases Coronary artery Coronary artery disease Coronary Artery Disease - metabolism Coronary Artery Disease - mortality Coronary vessels Diabetes Female Ferritin Ferritins - metabolism Follow-Up Studies Health risk assessment Heart diseases Heart failure Hemoglobin Hepcidin Hepcidins - metabolism Humans Iron Iron - metabolism Kidney diseases Laboratories Male Medical imaging Metabolism Middle Aged Mortality Proportional Hazards Models Prospective Studies Quartiles Risk analysis Risk Factors Saturation Systematic review Transferrin Transferrin - metabolism Transferrins Womens health |
| title | Iron Metabolism, Hepcidin, and Mortality (the Ludwigshafen Risk and Cardiovascular Health Study) |
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