Does Vascular Calcification Accelerate Inflammation?

Abstract Background Atherosclerosis is an inflammatory condition with calcification apparent late in the disease process. The extent and progression of coronary calcification predict cardiovascular events. Relatively little is known about noncoronary vascular calcification. Objectives This study inv...

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Veröffentlicht in:Journal of the American College of Cardiology 2016-01, Vol.67 (1), p.69-78
Hauptverfasser: Joshi, Francis R., MBBS, Rajani, Nikil K., MA, Abt, Markus, PhD, Woodward, Mark, PhD, Bucerius, Jan, MD, PhD, Mani, Venkatesh, PhD, Tawakol, Ahmed, MD, Kallend, David, MBBS, Fayad, Zahi A., PhD, Rudd, James H.F., MD, PhD
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container_end_page 78
container_issue 1
container_start_page 69
container_title Journal of the American College of Cardiology
container_volume 67
creator Joshi, Francis R., MBBS
Rajani, Nikil K., MA
Abt, Markus, PhD
Woodward, Mark, PhD
Bucerius, Jan, MD, PhD
Mani, Venkatesh, PhD
Tawakol, Ahmed, MD
Kallend, David, MBBS
Fayad, Zahi A., PhD
Rudd, James H.F., MD, PhD
description Abstract Background Atherosclerosis is an inflammatory condition with calcification apparent late in the disease process. The extent and progression of coronary calcification predict cardiovascular events. Relatively little is known about noncoronary vascular calcification. Objectives This study investigated noncoronary vascular calcification and its influence on changes in vascular inflammation. Methods A total of 130 participants in the dal-PLAQUE (Safety and efficacy of dalcetrapib on atherosclerotic disease using novel non-invasive multimodality imaging) study underwent fluorodeoxyglucose positron emission tomography/computed tomography at entry and at 6 months. Calcification of the ascending aorta, arch, carotid, and coronary arteries was quantified. Cardiovascular risk factors were related to arterial calcification. The influences of baseline calcification and drug therapy (dalcetrapib vs. placebo) on progression of calcification were determined. Finally, baseline calcification was related to changes in vascular inflammation. Results Age >65 years old was consistently associated with higher baseline calcium scores. Arch calcification trended to progress more in those with calcification at baseline (p = 0.055). There were no significant differences between progression of vascular calcification with dalcetrapib compared to that with placebo. Average carotid target-to-background ratio indexes declined over 6 months if carotid calcium was absent (single hottest slice [p = 0.037], mean of maximum target-to-background ratio [p = 0.010], and mean most diseased segment [p < 0.001]), but did not significantly change if calcification was present at baseline. Conclusions Across multiple arterial regions, higher age is consistently associated with higher calcium scores. The presence of vascular calcification at baseline is associated with progressive calcification; in the carotid arteries, calcification appears to influence vascular inflammation. Dalcetrapib therapy did not affect vascular calcification.
doi_str_mv 10.1016/j.jacc.2015.10.050
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The extent and progression of coronary calcification predict cardiovascular events. Relatively little is known about noncoronary vascular calcification. Objectives This study investigated noncoronary vascular calcification and its influence on changes in vascular inflammation. Methods A total of 130 participants in the dal-PLAQUE (Safety and efficacy of dalcetrapib on atherosclerotic disease using novel non-invasive multimodality imaging) study underwent fluorodeoxyglucose positron emission tomography/computed tomography at entry and at 6 months. Calcification of the ascending aorta, arch, carotid, and coronary arteries was quantified. Cardiovascular risk factors were related to arterial calcification. The influences of baseline calcification and drug therapy (dalcetrapib vs. placebo) on progression of calcification were determined. Finally, baseline calcification was related to changes in vascular inflammation. Results Age &gt;65 years old was consistently associated with higher baseline calcium scores. Arch calcification trended to progress more in those with calcification at baseline (p = 0.055). There were no significant differences between progression of vascular calcification with dalcetrapib compared to that with placebo. Average carotid target-to-background ratio indexes declined over 6 months if carotid calcium was absent (single hottest slice [p = 0.037], mean of maximum target-to-background ratio [p = 0.010], and mean most diseased segment [p &lt; 0.001]), but did not significantly change if calcification was present at baseline. Conclusions Across multiple arterial regions, higher age is consistently associated with higher calcium scores. The presence of vascular calcification at baseline is associated with progressive calcification; in the carotid arteries, calcification appears to influence vascular inflammation. Dalcetrapib therapy did not affect vascular calcification.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2015.10.050</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>Atherosclerosis ; Calcification ; Cardiology ; Cardiovascular ; Cardiovascular disease ; Carotid arteries ; carotid arteries ; Cholesterol ; Coronary vessels ; dalcetrapib ; fluorine-18 ; fluorodeoxyglucose ; Internal Medicine ; Lipoproteins ; Medical imaging ; Methods ; Mortality ; positron emission tomography ; Pulmonary arteries ; Studies ; Veins &amp; arteries</subject><ispartof>Journal of the American College of Cardiology, 2016-01, Vol.67 (1), p.69-78</ispartof><rights>American College of Cardiology Foundation</rights><rights>2016 American College of Cardiology Foundation</rights><rights>Copyright Elsevier Limited Jan 5, 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2720-9c27e53a4cb258ce627a3dac96a04cee542d0b0488f574d8f625ad284d8cc2cb3</citedby><cites>FETCH-LOGICAL-c2720-9c27e53a4cb258ce627a3dac96a04cee542d0b0488f574d8f625ad284d8cc2cb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0735109715071405$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids></links><search><creatorcontrib>Joshi, Francis R., MBBS</creatorcontrib><creatorcontrib>Rajani, Nikil K., MA</creatorcontrib><creatorcontrib>Abt, Markus, PhD</creatorcontrib><creatorcontrib>Woodward, Mark, PhD</creatorcontrib><creatorcontrib>Bucerius, Jan, MD, PhD</creatorcontrib><creatorcontrib>Mani, Venkatesh, PhD</creatorcontrib><creatorcontrib>Tawakol, Ahmed, MD</creatorcontrib><creatorcontrib>Kallend, David, MBBS</creatorcontrib><creatorcontrib>Fayad, Zahi A., PhD</creatorcontrib><creatorcontrib>Rudd, James H.F., MD, PhD</creatorcontrib><title>Does Vascular Calcification Accelerate Inflammation?</title><title>Journal of the American College of Cardiology</title><description>Abstract Background Atherosclerosis is an inflammatory condition with calcification apparent late in the disease process. The extent and progression of coronary calcification predict cardiovascular events. Relatively little is known about noncoronary vascular calcification. Objectives This study investigated noncoronary vascular calcification and its influence on changes in vascular inflammation. Methods A total of 130 participants in the dal-PLAQUE (Safety and efficacy of dalcetrapib on atherosclerotic disease using novel non-invasive multimodality imaging) study underwent fluorodeoxyglucose positron emission tomography/computed tomography at entry and at 6 months. Calcification of the ascending aorta, arch, carotid, and coronary arteries was quantified. Cardiovascular risk factors were related to arterial calcification. The influences of baseline calcification and drug therapy (dalcetrapib vs. placebo) on progression of calcification were determined. Finally, baseline calcification was related to changes in vascular inflammation. Results Age &gt;65 years old was consistently associated with higher baseline calcium scores. Arch calcification trended to progress more in those with calcification at baseline (p = 0.055). There were no significant differences between progression of vascular calcification with dalcetrapib compared to that with placebo. Average carotid target-to-background ratio indexes declined over 6 months if carotid calcium was absent (single hottest slice [p = 0.037], mean of maximum target-to-background ratio [p = 0.010], and mean most diseased segment [p &lt; 0.001]), but did not significantly change if calcification was present at baseline. Conclusions Across multiple arterial regions, higher age is consistently associated with higher calcium scores. The presence of vascular calcification at baseline is associated with progressive calcification; in the carotid arteries, calcification appears to influence vascular inflammation. Dalcetrapib therapy did not affect vascular calcification.</description><subject>Atherosclerosis</subject><subject>Calcification</subject><subject>Cardiology</subject><subject>Cardiovascular</subject><subject>Cardiovascular disease</subject><subject>Carotid arteries</subject><subject>carotid arteries</subject><subject>Cholesterol</subject><subject>Coronary vessels</subject><subject>dalcetrapib</subject><subject>fluorine-18</subject><subject>fluorodeoxyglucose</subject><subject>Internal Medicine</subject><subject>Lipoproteins</subject><subject>Medical imaging</subject><subject>Methods</subject><subject>Mortality</subject><subject>positron emission tomography</subject><subject>Pulmonary arteries</subject><subject>Studies</subject><subject>Veins &amp; arteries</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNp9kN1Kw0AQhRdRsFZfwKuC14mzm2yyAVFK_SsUvPDndtlOJrAxTepuKvRtfBafzI0VBC-8OsOZOTPDx9gph5gDz87ruDaIsQAugxGDhD024lKqKJFFvs9GkCcy4lDkh-zI-xoAMsWLEZPXHfnJi_G4aYybzEyDtrJoetu1kykiNeRMT58f87ZqzGr13bg6ZgeVaTyd_OiYPd_ePM3uo8XD3Xw2XUQocgFREYRkYlJcCqmQMpGbpDRYZAZSJJKpKGEJqVKVzNNSVZmQphQqlIgCl8mYne32rl33tiHf67rbuDac1DyXBYBQPAtTYjeFrvPeUaXXzq6M22oOesCjaz3g0QOewQt4QuhiF6Lw_7slpz1aapFK6wh7XXb2__jlnzg2tg3gmlfakv99U3uhQT8O_Af8XELOU5DJFxmXgm8</recordid><startdate>20160105</startdate><enddate>20160105</enddate><creator>Joshi, Francis R., MBBS</creator><creator>Rajani, Nikil K., MA</creator><creator>Abt, Markus, PhD</creator><creator>Woodward, Mark, PhD</creator><creator>Bucerius, Jan, MD, PhD</creator><creator>Mani, Venkatesh, PhD</creator><creator>Tawakol, Ahmed, MD</creator><creator>Kallend, David, MBBS</creator><creator>Fayad, Zahi A., PhD</creator><creator>Rudd, James H.F., MD, PhD</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>20160105</creationdate><title>Does Vascular Calcification Accelerate Inflammation?</title><author>Joshi, Francis R., MBBS ; Rajani, Nikil K., MA ; Abt, Markus, PhD ; Woodward, Mark, PhD ; Bucerius, Jan, MD, PhD ; Mani, Venkatesh, PhD ; Tawakol, Ahmed, MD ; Kallend, David, MBBS ; Fayad, Zahi A., PhD ; Rudd, James H.F., MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2720-9c27e53a4cb258ce627a3dac96a04cee542d0b0488f574d8f625ad284d8cc2cb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Atherosclerosis</topic><topic>Calcification</topic><topic>Cardiology</topic><topic>Cardiovascular</topic><topic>Cardiovascular disease</topic><topic>Carotid arteries</topic><topic>carotid arteries</topic><topic>Cholesterol</topic><topic>Coronary vessels</topic><topic>dalcetrapib</topic><topic>fluorine-18</topic><topic>fluorodeoxyglucose</topic><topic>Internal Medicine</topic><topic>Lipoproteins</topic><topic>Medical imaging</topic><topic>Methods</topic><topic>Mortality</topic><topic>positron emission tomography</topic><topic>Pulmonary arteries</topic><topic>Studies</topic><topic>Veins &amp; arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Joshi, Francis R., MBBS</creatorcontrib><creatorcontrib>Rajani, Nikil K., MA</creatorcontrib><creatorcontrib>Abt, Markus, PhD</creatorcontrib><creatorcontrib>Woodward, Mark, PhD</creatorcontrib><creatorcontrib>Bucerius, Jan, MD, PhD</creatorcontrib><creatorcontrib>Mani, Venkatesh, PhD</creatorcontrib><creatorcontrib>Tawakol, Ahmed, MD</creatorcontrib><creatorcontrib>Kallend, David, MBBS</creatorcontrib><creatorcontrib>Fayad, Zahi A., PhD</creatorcontrib><creatorcontrib>Rudd, James H.F., MD, PhD</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Premium</collection><jtitle>Journal of the American College of Cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Joshi, Francis R., MBBS</au><au>Rajani, Nikil K., MA</au><au>Abt, Markus, PhD</au><au>Woodward, Mark, PhD</au><au>Bucerius, Jan, MD, PhD</au><au>Mani, Venkatesh, PhD</au><au>Tawakol, Ahmed, MD</au><au>Kallend, David, MBBS</au><au>Fayad, Zahi A., PhD</au><au>Rudd, James H.F., MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Does Vascular Calcification Accelerate Inflammation?</atitle><jtitle>Journal of the American College of Cardiology</jtitle><date>2016-01-05</date><risdate>2016</risdate><volume>67</volume><issue>1</issue><spage>69</spage><epage>78</epage><pages>69-78</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><abstract>Abstract Background Atherosclerosis is an inflammatory condition with calcification apparent late in the disease process. The extent and progression of coronary calcification predict cardiovascular events. Relatively little is known about noncoronary vascular calcification. Objectives This study investigated noncoronary vascular calcification and its influence on changes in vascular inflammation. Methods A total of 130 participants in the dal-PLAQUE (Safety and efficacy of dalcetrapib on atherosclerotic disease using novel non-invasive multimodality imaging) study underwent fluorodeoxyglucose positron emission tomography/computed tomography at entry and at 6 months. Calcification of the ascending aorta, arch, carotid, and coronary arteries was quantified. Cardiovascular risk factors were related to arterial calcification. The influences of baseline calcification and drug therapy (dalcetrapib vs. placebo) on progression of calcification were determined. Finally, baseline calcification was related to changes in vascular inflammation. Results Age &gt;65 years old was consistently associated with higher baseline calcium scores. Arch calcification trended to progress more in those with calcification at baseline (p = 0.055). There were no significant differences between progression of vascular calcification with dalcetrapib compared to that with placebo. Average carotid target-to-background ratio indexes declined over 6 months if carotid calcium was absent (single hottest slice [p = 0.037], mean of maximum target-to-background ratio [p = 0.010], and mean most diseased segment [p &lt; 0.001]), but did not significantly change if calcification was present at baseline. Conclusions Across multiple arterial regions, higher age is consistently associated with higher calcium scores. The presence of vascular calcification at baseline is associated with progressive calcification; in the carotid arteries, calcification appears to influence vascular inflammation. Dalcetrapib therapy did not affect vascular calcification.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><doi>10.1016/j.jacc.2015.10.050</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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source Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Atherosclerosis
Calcification
Cardiology
Cardiovascular
Cardiovascular disease
Carotid arteries
carotid arteries
Cholesterol
Coronary vessels
dalcetrapib
fluorine-18
fluorodeoxyglucose
Internal Medicine
Lipoproteins
Medical imaging
Methods
Mortality
positron emission tomography
Pulmonary arteries
Studies
Veins & arteries
title Does Vascular Calcification Accelerate Inflammation?
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