<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT03821090</url>
  </required_header>
  <id_info>
    <org_study_id>cardiac affection in RA</org_study_id>
    <nct_id>NCT03821090</nct_id>
  </id_info>
  <brief_title>Rheumatoid Arthritis Disease Activity and Sub Clinical Atherosclerosis</brief_title>
  <official_title>A Study in Subclinical Atherosclerosis in Patients With Rheumatoid Arthritis</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Assiut University</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Assiut University</source>
  <oversight_info>
    <is_fda_regulated_drug>No</is_fda_regulated_drug>
    <is_fda_regulated_device>No</is_fda_regulated_device>
  </oversight_info>
  <brief_summary>
    <textblock>
      RA is associated with traditional cerebrovascular risk factors as subclinical&#xD;
      atherosclerosis.&#xD;
&#xD;
      Chronic inflammation and high disease activity are associated with atherosclerotic burden,&#xD;
      higher incidence of cerebrovascular disease ,chronic heart failure , and mortality of&#xD;
      patients with RA .&#xD;
&#xD;
      High-sensitivity cardiac troponin I (hs-cTnI) predicted a greater risk coronary heart&#xD;
      disease, heart failure hospitalization and overall mortality in the general population .&#xD;
&#xD;
      So the aim of the study is to correlate between high sensitive cardiac troponin I , TNF-α to&#xD;
      disease activity and presence of subclinical atherosclerosis in RA patients&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterized by&#xD;
      progressive joint destruction, associated with extra-articular manifestations, affecting&#xD;
      different internal organs .&#xD;
&#xD;
      Interestingly, these patients show an increased risk of mortality when compared to general&#xD;
      population and recent evidence clearly confirmed that this risk is largely due to&#xD;
      cerebro-cardiovascular events (CV Es), this may be explained by the greater prevalence,&#xD;
      severity, burden and different composition of occult coronary lesions in RA compared with&#xD;
      age- and gender-matched controls.&#xD;
&#xD;
      RA is associated with traditional CV risk factors ,subclinical atherosclerosis,arrhythmias ,&#xD;
      and coronary calcifications .&#xD;
&#xD;
      Increased subclinical atherosclerosis, mainly carotid artery plaques, may be observed in RA&#xD;
      patients, the increased carotid intima-media thickness (cIMT) and presence of plaques are&#xD;
      accepted as strong predictors of generalized atherosclerosis and major CVEs in both non-RA&#xD;
      and RA subjects.&#xD;
&#xD;
      The evidence of traditional CV risk factors and subclinical atherosclerosis does not fully&#xD;
      explain the increased incidence of CVEs in these patients; suggesting that the CV risk may be&#xD;
      independently associated with RA and in fact, this risk has been shown to be associated with&#xD;
      additional features specific of RA, such as the systemic inflammatory process, disease&#xD;
      duration and therapeutic strategies .&#xD;
&#xD;
      Chronic inflammation and high disease activity are reportedly associated with atherosclerotic&#xD;
      burden, higher incidence of cerebrovascular disease (CVD), chronic heart failure (CHF), and&#xD;
      mortality of patients with RA . Residual disease activity may further associate with more&#xD;
      advanced, complex and prone-to-rupture coronary plaques .&#xD;
&#xD;
      Pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), reflect clinical&#xD;
      activity and structural damage in RA and are elevated in the blood of RA patients compared&#xD;
      with controls , the same cytokine have been identified in atherosclerotic plaque and&#xD;
      correlated with subclinical atherosclerosis independent of cardiac risk factors coronary&#xD;
      plaque complexity , plaque destabilization and CVEs in subjects without autoimmune disease .&#xD;
&#xD;
      Cardiac troponins (cTn) are components of the cardiomyocyte contractile apparatus, and&#xD;
      circulating concentrations are elevated in the setting of myocardial injury, such as acute&#xD;
      coronary syndromes (ACS) .&#xD;
&#xD;
      High-sensitivity (hs) cTn assays allow measurement of troponin concentrations below&#xD;
      conventional levels of detection and have revealed a spectrum of circulating cTn&#xD;
      concentrations spanning low and high levels in both healthy subjects and in patients with&#xD;
      overt cardiovascular disease&#xD;
&#xD;
      Additionally, both high-sensitivity cardiac troponin T (hs-cTnT) and high-sensitivity cardiac&#xD;
      troponin I (hs-cTnI) predicted a greater risk of fatal and non-fatal coronary heart disease,&#xD;
      heart failure hospitalization and overall mortality in the general population .&#xD;
&#xD;
      Aim of the study&#xD;
&#xD;
        1. Detection of subclinical atherosclerosis in RA patients by means of carotid Doppler&#xD;
&#xD;
        2. Detection of levels of high sensitive cardiac troponin I and TNF-α in RA patients&#xD;
&#xD;
        3. Correlation between high sensitive cardiac troponin I and TNF- α to disease activity and&#xD;
           to the presence of subclinical atherosclerosis in RA patients&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Completed</overall_status>
  <start_date type="Actual">April 15, 2019</start_date>
  <completion_date type="Actual">July 1, 2021</completion_date>
  <primary_completion_date type="Actual">March 1, 2021</primary_completion_date>
  <study_type>Observational</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <observational_model>Case-Control</observational_model>
    <time_perspective>Other</time_perspective>
  </study_design_info>
  <primary_outcome>
    <measure>detection of subclinical atherosclerosis in RA patients who have no cardiovascular risk factors</measure>
    <time_frame>baseline</time_frame>
    <description>Correlation between high sensitive cardiac troponin I and TNF- α to disease activity and presence of subclinical atherosclerosis in RA patients</description>
  </primary_outcome>
  <number_of_groups>2</number_of_groups>
  <enrollment type="Actual">160</enrollment>
  <condition>Rheumatoid Arthritis</condition>
  <arm_group>
    <arm_group_label>cases</arm_group_label>
    <description>Eighty rheumatoid arthritis patients fulfilling American College of Rheumatology (ACR) 2010 classification criteria, all of them will be subjected to&#xD;
History including disease duration , course and associated diseases&#xD;
Clinical examination with specific joint examination&#xD;
RA disease activity will be evaluated by a 28- joint DAS (DAS28). 4-12-lead ECG&#xD;
5-Echocardiography 6-Carotid intima media thickness using carotid doppler 7-Venous blood will be withdrawn to do the following laboratory tests&#xD;
Complete Blood Count(CBC)&#xD;
Erythrocyte Sedimentation Rate (ESR) &amp;C Reactive Protein(CRP)&#xD;
Rheumatoid Factor (RF)&amp; anti cyclic citrullinated peptide (Anti-CCP)&#xD;
Urine analysis , Urea and creatinine ,&#xD;
Uric acid level&#xD;
Lipogram&#xD;
HA1C&#xD;
TNF α&#xD;
hs-cTnI</description>
  </arm_group>
  <arm_group>
    <arm_group_label>control</arm_group_label>
    <description>Eighty healthy subjects age and sex matched will be included , all of them will be subjected to&#xD;
History&#xD;
Clinical examination . 3-12-lead ECG&#xD;
4-Echocardiography 5-Carotid intima media thickness using carotid doppler 6-Venous blood will be withdrawn to do the following laboratory tests&#xD;
Complete Blood Count (CBC)&#xD;
ESR &amp; CRP&#xD;
RF&amp; Anti-CCP&#xD;
Urine analysis , Urea and creatinine&#xD;
Uric acid level&#xD;
Lipogram&#xD;
HA1C&#xD;
TNF α&#xD;
hs-cTnI</description>
  </arm_group>
  <eligibility>
    <study_pop>
      <textblock>
        Eighty rheumatoid arthritis patients fulfilling ACR 2010 classification criteria will be in&#xD;
        rolled in the study also eighty healthy subjects age and sex matched will be included .&#xD;
      </textblock>
    </study_pop>
    <sampling_method>Non-Probability Sample</sampling_method>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  RA patients fulfilling ACR 2010 classification criteria over the age of 18 who have&#xD;
             active RA (either early with symptoms lasting &lt; 6 months or established disease&#xD;
             lasting &gt; 6 months) .&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
        Patients who have previously experienced cardiovascular illness, e.g., heart failure, acute&#xD;
        coronary syndrome, revascularization, transient ischemic attacks, and cerebrovascular&#xD;
        stroke. Patients who have concomitant hepatic or renal diseases, active infections,&#xD;
        malignancy, smoking, hypertension, dyslipidemia, obesity, diabetes mellitus, and&#xD;
        hyperuricemia. Patients who are receiving anti-TNF-α therapy.&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>Accepts Healthy Volunteers</healthy_volunteers>
  </eligibility>
  <location>
    <facility>
      <name>Assiut university hospital</name>
      <address>
        <city>Assiut</city>
        <zip>088</zip>
        <country>Egypt</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>Egypt</country>
  </location_countries>
  <reference>
    <citation>Ambrosino P, Lupoli R, Di Minno A, Tasso M, Peluso R, Di Minno MN. Subclinical atherosclerosis in patients with rheumatoid arthritis. A meta-analysis of literature studies. Thromb Haemost. 2015 May;113(5):916-30. doi: 10.1160/TH14-11-0921. Epub 2015 Feb 26.</citation>
    <PMID>25716931</PMID>
  </reference>
  <reference>
    <citation>Baghdadi LR, Woodman RJ, Shanahan EM, Mangoni AA. The impact of traditional cardiovascular risk factors on cardiovascular outcomes in patients with rheumatoid arthritis: a systematic review and meta-analysis. PLoS One. 2015 Feb 17;10(2):e0117952. doi: 10.1371/journal.pone.0117952. eCollection 2015.</citation>
    <PMID>25689371</PMID>
  </reference>
  <reference>
    <citation>Amar J, Fauvel J, Drouet L, Ruidavets JB, Perret B, Chamontin B, Boccalon H, Ferrieres J. Interleukin 6 is associated with subclinical atherosclerosis: a link with soluble intercellular adhesion molecule 1. J Hypertens. 2006 Jun;24(6):1083-8. doi: 10.1097/01.hjh.0000226198.44181.0c.</citation>
    <PMID>16685208</PMID>
  </reference>
  <reference>
    <citation>Bradham WS, Bian A, Oeser A, Gebretsadik T, Shintani A, Solus J, Estis J, Lu QA, Todd J, Raggi P, Stein CM. High-sensitivity cardiac troponin-I is elevated in patients with rheumatoid arthritis, independent of cardiovascular risk factors and inflammation. PLoS One. 2012;7(6):e38930. doi: 10.1371/journal.pone.0038930. Epub 2012 Jun 28.</citation>
    <PMID>22761714</PMID>
  </reference>
  <reference>
    <citation>deFilippi CR, de Lemos JA, Christenson RH, Gottdiener JS, Kop WJ, Zhan M, Seliger SL. Association of serial measures of cardiac troponin T using a sensitive assay with incident heart failure and cardiovascular mortality in older adults. JAMA. 2010 Dec 8;304(22):2494-502. doi: 10.1001/jama.2010.1708. Epub 2010 Nov 15.</citation>
    <PMID>21078811</PMID>
  </reference>
  <reference>
    <citation>Gupta S, de Lemos JA. Use and misuse of cardiac troponins in clinical practice. Prog Cardiovasc Dis. 2007 Sep-Oct;50(2):151-65. doi: 10.1016/j.pcad.2007.01.002.</citation>
    <PMID>17765476</PMID>
  </reference>
  <reference>
    <citation>Karpouzas GA, Malpeso J, Choi TY, Li D, Munoz S, Budoff MJ. Prevalence, extent and composition of coronary plaque in patients with rheumatoid arthritis without symptoms or prior diagnosis of coronary artery disease. Ann Rheum Dis. 2014 Oct;73(10):1797-804. doi: 10.1136/annrheumdis-2013-203617. Epub 2013 Jul 25.</citation>
    <PMID>23887286</PMID>
  </reference>
  <reference>
    <citation>Lazzerini PE, Capecchi PL, Acampa M, Galeazzi M, Laghi-Pasini F. Arrhythmic risk in rheumatoid arthritis: the driving role of systemic inflammation. Autoimmun Rev. 2014 Sep;13(9):936-44. doi: 10.1016/j.autrev.2014.05.007. Epub 2014 May 27.</citation>
    <PMID>24874445</PMID>
  </reference>
  <reference>
    <citation>Fransen J, Kazemi-Bajestani SM, Bredie SJ, Popa CD. Rheumatoid Arthritis Disadvantages Younger Patients for Cardiovascular Diseases: A Meta-Analysis. PLoS One. 2016 Jun 16;11(6):e0157360. doi: 10.1371/journal.pone.0157360. eCollection 2016.</citation>
    <PMID>27310259</PMID>
  </reference>
  <reference>
    <citation>McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011 Dec 8;365(23):2205-19. doi: 10.1056/NEJMra1004965. No abstract available.</citation>
    <PMID>22150039</PMID>
  </reference>
  <reference>
    <citation>Navarro-Millan I, Yang S, DuVall SL, Chen L, Baddley J, Cannon GW, Delzell ES, Zhang J, Safford MM, Patkar NM, Mikuls TR, Singh JA, Curtis JR. Association of hyperlipidaemia, inflammation and serological status and coronary heart disease among patients with rheumatoid arthritis: data from the National Veterans Health Administration. Ann Rheum Dis. 2016 Feb;75(2):341-7. doi: 10.1136/annrheumdis-2013-204987. Epub 2015 Jan 21.</citation>
    <PMID>25609412</PMID>
  </reference>
  <reference>
    <citation>Niemann-Jonsson A, Dimayuga P, Jovinge S, Calara F, Ares MP, Fredrikson GN, Nilsson J. Accumulation of LDL in rat arteries is associated with activation of tumor necrosis factor-alpha expression. Arterioscler Thromb Vasc Biol. 2000 Oct;20(10):2205-11. doi: 10.1161/01.atv.20.10.2205.</citation>
    <PMID>11031205</PMID>
  </reference>
  <verification_date>January 2023</verification_date>
  <study_first_submitted>January 27, 2019</study_first_submitted>
  <study_first_submitted_qc>January 27, 2019</study_first_submitted_qc>
  <study_first_posted type="Actual">January 29, 2019</study_first_posted>
  <last_update_submitted>January 23, 2023</last_update_submitted>
  <last_update_submitted_qc>January 23, 2023</last_update_submitted_qc>
  <last_update_posted type="Actual">January 25, 2023</last_update_posted>
  <responsible_party>
    <responsible_party_type>Principal Investigator</responsible_party_type>
    <investigator_affiliation>Assiut University</investigator_affiliation>
    <investigator_full_name>Sabrin Refaat Mahmoud</investigator_full_name>
    <investigator_title>principle investigator</investigator_title>
  </responsible_party>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Arthritis</mesh_term>
    <mesh_term>Arthritis, Rheumatoid</mesh_term>
    <mesh_term>Atherosclerosis</mesh_term>
  </condition_browse>
  <patient_data>
    <sharing_ipd>No</sharing_ipd>
  </patient_data>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT03821090
org study id: cardiac affection in RA
nct id: NCT03821090
lead sponsor: 
is fda regulated drug: No
is fda regulated device: No
RA is associated with traditional cerebrovascular risk factors as subclinical
      atherosclerosis.

      Chronic inflammation and high disease activity are associated with atherosclerotic burden,
      higher incidence of cerebrovascular disease ,chronic heart failure , and mortality of
      patients with RA .

      High-sensitivity cardiac troponin I (hs-cTnI) predicted a greater risk coronary heart
      disease, heart failure hospitalization and overall mortality in the general population .

      So the aim of the study is to correlate between high sensitive cardiac troponin I , TNF-α to
      disease activity and presence of subclinical atherosclerosis in RA patients
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterized by
      progressive joint destruction, associated with extra-articular manifestations, affecting
      different internal organs .

      Interestingly, these patients show an increased risk of mortality when compared to general
      population and recent evidence clearly confirmed that this risk is largely due to
      cerebro-cardiovascular events (CV Es), this may be explained by the greater prevalence,
      severity, burden and different composition of occult coronary lesions in RA compared with
      age- and gender-matched controls.

      RA is associated with traditional CV risk factors ,subclinical atherosclerosis,arrhythmias ,
      and coronary calcifications .

      Increased subclinical atherosclerosis, mainly carotid artery plaques, may be observed in RA
      patients, the increased carotid intima-media thickness (cIMT) and presence of plaques are
      accepted as strong predictors of generalized atherosclerosis and major CVEs in both non-RA
      and RA subjects.

      The evidence of traditional CV risk factors and subclinical atherosclerosis does not fully
      explain the increased incidence of CVEs in these patients; suggesting that the CV risk may be
      independently associated with RA and in fact, this risk has been shown to be associated with
      additional features specific of RA, such as the systemic inflammatory process, disease
      duration and therapeutic strategies .

      Chronic inflammation and high disease activity are reportedly associated with atherosclerotic
      burden, higher incidence of cerebrovascular disease (CVD), chronic heart failure (CHF), and
      mortality of patients with RA . Residual disease activity may further associate with more
      advanced, complex and prone-to-rupture coronary plaques .

      Pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), reflect clinical
      activity and structural damage in RA and are elevated in the blood of RA patients compared
      with controls , the same cytokine have been identified in atherosclerotic plaque and
      correlated with subclinical atherosclerosis independent of cardiac risk factors coronary
      plaque complexity , plaque destabilization and CVEs in subjects without autoimmune disease .

      Cardiac troponins (cTn) are components of the cardiomyocyte contractile apparatus, and
      circulating concentrations are elevated in the setting of myocardial injury, such as acute
      coronary syndromes (ACS) .

      High-sensitivity (hs) cTn assays allow measurement of troponin concentrations below
      conventional levels of detection and have revealed a spectrum of circulating cTn
      concentrations spanning low and high levels in both healthy subjects and in patients with
      overt cardiovascular disease

      Additionally, both high-sensitivity cardiac troponin T (hs-cTnT) and high-sensitivity cardiac
      troponin I (hs-cTnI) predicted a greater risk of fatal and non-fatal coronary heart disease,
      heart failure hospitalization and overall mortality in the general population .

      Aim of the study

        1. Detection of subclinical atherosclerosis in RA patients by means of carotid Doppler

        2. Detection of levels of high sensitive cardiac troponin I and TNF-α in RA patients

        3. Correlation between high sensitive cardiac troponin I and TNF- α to disease activity and
           to the presence of subclinical atherosclerosis in RA patients
observational model: Case-Control
time perspective: Other
measure: detection of subclinical atherosclerosis in RA patients who have no cardiovascular risk factors
time frame: baseline
description: Correlation between high sensitive cardiac troponin I and TNF- α to disease activity and presence of subclinical atherosclerosis in RA patients
arm group label: cases
description: Eighty rheumatoid arthritis patients fulfilling American College of Rheumatology (ACR) 2010 classification criteria, all of them will be subjected to
History including disease duration , course and associated diseases
Clinical examination with specific joint examination
RA disease activity will be evaluated by a 28- joint DAS (DAS28). 4-12-lead ECG
5-Echocardiography 6-Carotid intima media thickness using carotid doppler 7-Venous blood will be withdrawn to do the following laboratory tests
Complete Blood Count(CBC)
Erythrocyte Sedimentation Rate (ESR) &C Reactive Protein(CRP)
Rheumatoid Factor (RF)& anti cyclic citrullinated peptide (Anti-CCP)
Urine analysis , Urea and creatinine ,
Uric acid level
Lipogram
HA1C
TNF α
hs-cTnI
arm group label: control
description: Eighty healthy subjects age and sex matched will be included , all of them will be subjected to
History
Clinical examination . 3-12-lead ECG
4-Echocardiography 5-Carotid intima media thickness using carotid doppler 6-Venous blood will be withdrawn to do the following laboratory tests
Complete Blood Count (CBC)
ESR & CRP
RF& Anti-CCP
Urine analysis , Urea and creatinine
Uric acid level
Lipogram
HA1C
TNF α
hs-cTnI
study pop: 
sampling method: Non-Probability Sample
criteria: 
gender: All
minimum age: 18 Years
maximum age: N/A
healthy volunteers: Accepts Healthy Volunteers
facility: 
country: Egypt
citation: Ambrosino P, Lupoli R, Di Minno A, Tasso M, Peluso R, Di Minno MN. Subclinical atherosclerosis in patients with rheumatoid arthritis. A meta-analysis of literature studies. Thromb Haemost. 2015 May;113(5):916-30. doi: 10.1160/TH14-11-0921. Epub 2015 Feb 26.
PMID: 25716931
citation: Baghdadi LR, Woodman RJ, Shanahan EM, Mangoni AA. The impact of traditional cardiovascular risk factors on cardiovascular outcomes in patients with rheumatoid arthritis: a systematic review and meta-analysis. PLoS One. 2015 Feb 17;10(2):e0117952. doi: 10.1371/journal.pone.0117952. eCollection 2015.
PMID: 25689371
citation: Amar J, Fauvel J, Drouet L, Ruidavets JB, Perret B, Chamontin B, Boccalon H, Ferrieres J. Interleukin 6 is associated with subclinical atherosclerosis: a link with soluble intercellular adhesion molecule 1. J Hypertens. 2006 Jun;24(6):1083-8. doi: 10.1097/01.hjh.0000226198.44181.0c.
PMID: 16685208
citation: Bradham WS, Bian A, Oeser A, Gebretsadik T, Shintani A, Solus J, Estis J, Lu QA, Todd J, Raggi P, Stein CM. High-sensitivity cardiac troponin-I is elevated in patients with rheumatoid arthritis, independent of cardiovascular risk factors and inflammation. PLoS One. 2012;7(6):e38930. doi: 10.1371/journal.pone.0038930. Epub 2012 Jun 28.
PMID: 22761714
citation: deFilippi CR, de Lemos JA, Christenson RH, Gottdiener JS, Kop WJ, Zhan M, Seliger SL. Association of serial measures of cardiac troponin T using a sensitive assay with incident heart failure and cardiovascular mortality in older adults. JAMA. 2010 Dec 8;304(22):2494-502. doi: 10.1001/jama.2010.1708. Epub 2010 Nov 15.
PMID: 21078811
citation: Gupta S, de Lemos JA. Use and misuse of cardiac troponins in clinical practice. Prog Cardiovasc Dis. 2007 Sep-Oct;50(2):151-65. doi: 10.1016/j.pcad.2007.01.002.
PMID: 17765476
citation: Karpouzas GA, Malpeso J, Choi TY, Li D, Munoz S, Budoff MJ. Prevalence, extent and composition of coronary plaque in patients with rheumatoid arthritis without symptoms or prior diagnosis of coronary artery disease. Ann Rheum Dis. 2014 Oct;73(10):1797-804. doi: 10.1136/annrheumdis-2013-203617. Epub 2013 Jul 25.
PMID: 23887286
citation: Lazzerini PE, Capecchi PL, Acampa M, Galeazzi M, Laghi-Pasini F. Arrhythmic risk in rheumatoid arthritis: the driving role of systemic inflammation. Autoimmun Rev. 2014 Sep;13(9):936-44. doi: 10.1016/j.autrev.2014.05.007. Epub 2014 May 27.
PMID: 24874445
citation: Fransen J, Kazemi-Bajestani SM, Bredie SJ, Popa CD. Rheumatoid Arthritis Disadvantages Younger Patients for Cardiovascular Diseases: A Meta-Analysis. PLoS One. 2016 Jun 16;11(6):e0157360. doi: 10.1371/journal.pone.0157360. eCollection 2016.
PMID: 27310259
citation: McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011 Dec 8;365(23):2205-19. doi: 10.1056/NEJMra1004965. No abstract available.
PMID: 22150039
citation: Navarro-Millan I, Yang S, DuVall SL, Chen L, Baddley J, Cannon GW, Delzell ES, Zhang J, Safford MM, Patkar NM, Mikuls TR, Singh JA, Curtis JR. Association of hyperlipidaemia, inflammation and serological status and coronary heart disease among patients with rheumatoid arthritis: data from the National Veterans Health Administration. Ann Rheum Dis. 2016 Feb;75(2):341-7. doi: 10.1136/annrheumdis-2013-204987. Epub 2015 Jan 21.
PMID: 25609412
citation: Niemann-Jonsson A, Dimayuga P, Jovinge S, Calara F, Ares MP, Fredrikson GN, Nilsson J. Accumulation of LDL in rat arteries is associated with activation of tumor necrosis factor-alpha expression. Arterioscler Thromb Vasc Biol. 2000 Oct;20(10):2205-11. doi: 10.1161/01.atv.20.10.2205.
PMID: 11031205
responsible party type: Principal Investigator
investigator affiliation: Assiut University
investigator full name: Sabrin Refaat Mahmoud
investigator title: principle investigator
mesh term: Arthritis
mesh term: Arthritis, Rheumatoid
mesh term: Atherosclerosis
sharing ipd: No