User login
LIVERPOOL, ENGLAND – Serum levels of the cardiac biomarker troponin might prove useful for assessing the risk of death from cardiovascular causes in patients with inflammatory arthritis, according to study findings presented at the British Society for Rheumatology annual conference.
“In this analysis we have shown that baseline troponin levels predict cardiovascular death in inflammatory arthritis, and this association is independent of the traditional risk factors, inflammation, and disease characteristics at baseline,” said study author Sarah Skeoch, MBChB, who works at the Arthritis Research UK Centre for Epidemiology in the division of musculoskeletal and dermatological sciences at the University of Manchester (England).
Furthermore, the association remained in patients who had rheumatoid arthritis classified according to the 2010 American College of Rheumatology and European League Against Rheumatism criteria (overall adjusted HR, 2.25) and in those without prior cardiovascular disease at baseline (HR, 1.63).
Individuals with inflammatory arthritis are known to have an increased risk of developing cardiovascular problems versus the general population, but current prediction models using traditional risk factors do not fully account for the increased risk seen in patients with inflammatory arthritis, Dr. Skeoch explained.
“There has been some work looking at troponin in inflammatory arthritis already,” she said, with “higher levels observed versus age- and sex-matched controls, and associations have been shown with traditional risk factors.” There has also been a link to C-reactive protein levels and disease activity, and there has also been an association with coronary stenosis on CT scans. The aim of the current study was to see if there was any link to cardiovascular events and death.
A total of 1,023 patients who had been recruited into NOAR between 2000 and 2009 were studied. NOAR is an inception cohort study that includes patients with a history of two or more swollen joints for 4 weeks or more and has been running for almost 30 years. At baseline serum samples are taken and a variety of assessments made, including cardiovascular risk factors.
The study population was mostly female (66%), aged a median of 56 years, and had symptoms for a median of 10.6 months. Around half were seropositive for rheumatoid factor, anti–citrullinated protein antibodies, or both. The median baseline disease activity score in 28 joints (DAS28) was 3.73, and 61% met ACR/EULAR 2010 criteria for RA.
Baseline serum samples were analyzed using a chemiluminescent assay to determine hs-TnI levels, with the median being 6.3 pg/mL. All patients had detectable hs-TnI levels, and 2.6% had levels exceeding 26.1 pg/mL, which is the level associated with having had an acute myocardial infarction. Almost 4% had a previous cardiovascular event, and 7% had diabetes. One in five were current smokers, and roughly 18% had hypertension. The investigators adjusted for all of these factors in the multivariate analyses.
The median follow up was 11.2 years, totaling 11,237 person-years, and during that time 158 deaths occurred, of which 27 were due to ischemic events. The median time from inclusion in NOAR to death was 7.4 years.
When levels of hs-TnI were separated into tertiles, a 12.5-fold increased risk was observed when comparing patients in the highest (more than 7.7 pg/mL) to lowest tertiles (less than 5.2 pg/mL).
“The magnitude of risk between the highest and the lowest tertile was much greater than observed in the general population,” Dr. Skeoch said, and although not directly comparable, she said the hazard ratios were 12.5 and 1.67, “which again suggests that troponin may be an effective tool or addition to the risk prediction models in inflammatory arthritis.”
Unlike some biomarkers, assays to assess troponin are already available in the clinic, Dr. Skeoch commented, “so if further work by us and other groups do suggest a role for troponin, this could be translated fairly rapidly into clinical practice.”
Further research needs to look at why troponin is raised and what is its relationship to other risk factors. “There is a strong association with traditional risk factors such as lipids, so it would stand to reason that managing those risk factors, as well as lifestyle factors, would have a positive impact,” Dr. Skeoch suggested.
The NOAR register is funded by Arthritis Research UK and the U.K. National Institute for Health Research. Dr. Skeoch and her coauthors had no relevant financial conflicts of interest.
SOURCE: Skeoch S et al. BSR 2018. Rheumatology. 2018;57[Suppl. 3]:key075.192.
LIVERPOOL, ENGLAND – Serum levels of the cardiac biomarker troponin might prove useful for assessing the risk of death from cardiovascular causes in patients with inflammatory arthritis, according to study findings presented at the British Society for Rheumatology annual conference.
“In this analysis we have shown that baseline troponin levels predict cardiovascular death in inflammatory arthritis, and this association is independent of the traditional risk factors, inflammation, and disease characteristics at baseline,” said study author Sarah Skeoch, MBChB, who works at the Arthritis Research UK Centre for Epidemiology in the division of musculoskeletal and dermatological sciences at the University of Manchester (England).
Furthermore, the association remained in patients who had rheumatoid arthritis classified according to the 2010 American College of Rheumatology and European League Against Rheumatism criteria (overall adjusted HR, 2.25) and in those without prior cardiovascular disease at baseline (HR, 1.63).
Individuals with inflammatory arthritis are known to have an increased risk of developing cardiovascular problems versus the general population, but current prediction models using traditional risk factors do not fully account for the increased risk seen in patients with inflammatory arthritis, Dr. Skeoch explained.
“There has been some work looking at troponin in inflammatory arthritis already,” she said, with “higher levels observed versus age- and sex-matched controls, and associations have been shown with traditional risk factors.” There has also been a link to C-reactive protein levels and disease activity, and there has also been an association with coronary stenosis on CT scans. The aim of the current study was to see if there was any link to cardiovascular events and death.
A total of 1,023 patients who had been recruited into NOAR between 2000 and 2009 were studied. NOAR is an inception cohort study that includes patients with a history of two or more swollen joints for 4 weeks or more and has been running for almost 30 years. At baseline serum samples are taken and a variety of assessments made, including cardiovascular risk factors.
The study population was mostly female (66%), aged a median of 56 years, and had symptoms for a median of 10.6 months. Around half were seropositive for rheumatoid factor, anti–citrullinated protein antibodies, or both. The median baseline disease activity score in 28 joints (DAS28) was 3.73, and 61% met ACR/EULAR 2010 criteria for RA.
Baseline serum samples were analyzed using a chemiluminescent assay to determine hs-TnI levels, with the median being 6.3 pg/mL. All patients had detectable hs-TnI levels, and 2.6% had levels exceeding 26.1 pg/mL, which is the level associated with having had an acute myocardial infarction. Almost 4% had a previous cardiovascular event, and 7% had diabetes. One in five were current smokers, and roughly 18% had hypertension. The investigators adjusted for all of these factors in the multivariate analyses.
The median follow up was 11.2 years, totaling 11,237 person-years, and during that time 158 deaths occurred, of which 27 were due to ischemic events. The median time from inclusion in NOAR to death was 7.4 years.
When levels of hs-TnI were separated into tertiles, a 12.5-fold increased risk was observed when comparing patients in the highest (more than 7.7 pg/mL) to lowest tertiles (less than 5.2 pg/mL).
“The magnitude of risk between the highest and the lowest tertile was much greater than observed in the general population,” Dr. Skeoch said, and although not directly comparable, she said the hazard ratios were 12.5 and 1.67, “which again suggests that troponin may be an effective tool or addition to the risk prediction models in inflammatory arthritis.”
Unlike some biomarkers, assays to assess troponin are already available in the clinic, Dr. Skeoch commented, “so if further work by us and other groups do suggest a role for troponin, this could be translated fairly rapidly into clinical practice.”
Further research needs to look at why troponin is raised and what is its relationship to other risk factors. “There is a strong association with traditional risk factors such as lipids, so it would stand to reason that managing those risk factors, as well as lifestyle factors, would have a positive impact,” Dr. Skeoch suggested.
The NOAR register is funded by Arthritis Research UK and the U.K. National Institute for Health Research. Dr. Skeoch and her coauthors had no relevant financial conflicts of interest.
SOURCE: Skeoch S et al. BSR 2018. Rheumatology. 2018;57[Suppl. 3]:key075.192.
LIVERPOOL, ENGLAND – Serum levels of the cardiac biomarker troponin might prove useful for assessing the risk of death from cardiovascular causes in patients with inflammatory arthritis, according to study findings presented at the British Society for Rheumatology annual conference.
“In this analysis we have shown that baseline troponin levels predict cardiovascular death in inflammatory arthritis, and this association is independent of the traditional risk factors, inflammation, and disease characteristics at baseline,” said study author Sarah Skeoch, MBChB, who works at the Arthritis Research UK Centre for Epidemiology in the division of musculoskeletal and dermatological sciences at the University of Manchester (England).
Furthermore, the association remained in patients who had rheumatoid arthritis classified according to the 2010 American College of Rheumatology and European League Against Rheumatism criteria (overall adjusted HR, 2.25) and in those without prior cardiovascular disease at baseline (HR, 1.63).
Individuals with inflammatory arthritis are known to have an increased risk of developing cardiovascular problems versus the general population, but current prediction models using traditional risk factors do not fully account for the increased risk seen in patients with inflammatory arthritis, Dr. Skeoch explained.
“There has been some work looking at troponin in inflammatory arthritis already,” she said, with “higher levels observed versus age- and sex-matched controls, and associations have been shown with traditional risk factors.” There has also been a link to C-reactive protein levels and disease activity, and there has also been an association with coronary stenosis on CT scans. The aim of the current study was to see if there was any link to cardiovascular events and death.
A total of 1,023 patients who had been recruited into NOAR between 2000 and 2009 were studied. NOAR is an inception cohort study that includes patients with a history of two or more swollen joints for 4 weeks or more and has been running for almost 30 years. At baseline serum samples are taken and a variety of assessments made, including cardiovascular risk factors.
The study population was mostly female (66%), aged a median of 56 years, and had symptoms for a median of 10.6 months. Around half were seropositive for rheumatoid factor, anti–citrullinated protein antibodies, or both. The median baseline disease activity score in 28 joints (DAS28) was 3.73, and 61% met ACR/EULAR 2010 criteria for RA.
Baseline serum samples were analyzed using a chemiluminescent assay to determine hs-TnI levels, with the median being 6.3 pg/mL. All patients had detectable hs-TnI levels, and 2.6% had levels exceeding 26.1 pg/mL, which is the level associated with having had an acute myocardial infarction. Almost 4% had a previous cardiovascular event, and 7% had diabetes. One in five were current smokers, and roughly 18% had hypertension. The investigators adjusted for all of these factors in the multivariate analyses.
The median follow up was 11.2 years, totaling 11,237 person-years, and during that time 158 deaths occurred, of which 27 were due to ischemic events. The median time from inclusion in NOAR to death was 7.4 years.
When levels of hs-TnI were separated into tertiles, a 12.5-fold increased risk was observed when comparing patients in the highest (more than 7.7 pg/mL) to lowest tertiles (less than 5.2 pg/mL).
“The magnitude of risk between the highest and the lowest tertile was much greater than observed in the general population,” Dr. Skeoch said, and although not directly comparable, she said the hazard ratios were 12.5 and 1.67, “which again suggests that troponin may be an effective tool or addition to the risk prediction models in inflammatory arthritis.”
Unlike some biomarkers, assays to assess troponin are already available in the clinic, Dr. Skeoch commented, “so if further work by us and other groups do suggest a role for troponin, this could be translated fairly rapidly into clinical practice.”
Further research needs to look at why troponin is raised and what is its relationship to other risk factors. “There is a strong association with traditional risk factors such as lipids, so it would stand to reason that managing those risk factors, as well as lifestyle factors, would have a positive impact,” Dr. Skeoch suggested.
The NOAR register is funded by Arthritis Research UK and the U.K. National Institute for Health Research. Dr. Skeoch and her coauthors had no relevant financial conflicts of interest.
SOURCE: Skeoch S et al. BSR 2018. Rheumatology. 2018;57[Suppl. 3]:key075.192.
REPORTING FROM BSR 2018
Key clinical point: Cardiovascular mortality was predicted by baseline levels of high-sensitivity troponin I.
Major finding: For every log unit increase in hs-TnI at baseline, there was an increase in cardiovascular mortality (HR, 2.16).
Study details: Analysis of data on 1,023 patients with inflammatory arthritis listed in the Norfolk Arthritis Register.
Disclosures: Dr. Skeoch and coauthors had no relevant financial conflicts of interest.
Source: Skeoch S et al. BSR 2018. Rheumatology. 2018;57[Suppl. 3]:key075.192.