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Monocyte chemoattractant protein-1 is not predictive of cardiac events in patients with non-low-risk chest pain
  1. Nicklaus P Ashburn1,2,
  2. Anna C Snavely1,3,
  3. Brandon R Allen4,
  4. Robert H Christenson5,
  5. David M Herrington2,
  6. Brian C Hiestand1,
  7. Chadwick D Miller1,
  8. Jason P Stopyra1,
  9. Simon A Mahler1,6
  1. 1Department of Emergency Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA
  2. 2Department of Cardiology, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA
  3. 3Department of Biostatistics and Data Science, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA
  4. 4Department of Emergency Medicine, University of Florida College of Medicine, Gainesville, Florida, USA
  5. 5Department of Pathology, University of Maryland School of Medicine, Baltimore, Maryland, USA
  6. 6Departments of Epidemiology and Prevention and Implementation Science, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA
  1. Correspondence to Dr Nicklaus P Ashburn, Department of Emergency Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA; N.Ashburn{at}wakehealth.edu

Abstract

Background Prior studies suggest monocyte chemoattractant protein-1 (MCP-1) may be useful for risk stratifying ED patients with chest pain. We hypothesise that MCP-1 will be predictive of 90-day major adverse cardiovascular events (MACEs) in non-low-risk patients.

Methods A case–control study was nested within a prospective multicentre cohort (STOP-CP), which enrolled adult patients being evaluated for acute coronary syndrome at eight US EDs from 25 January 2017 to 06 September 2018. Patients with a History, ECG, Age, and Risk factor score (HEAR score) ≥4 or coronary artery disease (CAD), a non-ischaemic ECG, and non-elevated contemporary troponins at 0 and 3 hours were included. Cases were patients with 90-day MACE (all-cause death, myocardial infarction or revascularisation). Controls were patients without MACE selected with frequency matching using age, sex, race, and HEAR score or the presence of CAD. Serum MCP-1 was measured. Sensitivity and specificity were determined for cut-off points of 194 pg/mL, 200 pg/mL, 238 pg/mL and 281 pg/mL. Logistic regression adjusting for age, sex, race, and HEAR score/presence of CAD was used to determine the association between MCP-1 and 90-day MACE. A separate logistic model also included high-sensitivity troponin (hs-cTnT).

Results Among 40 cases and 179 controls, there was no difference in age (p=0.90), sex (p=1.00), race (p=0.85), or HEAR score/presence of CAD (p=0.89). MCP-1 was similar in cases (median 191.9 pg/mL, IQR: 161.8–260.1) and controls (median 196.6 pg/mL, IQR: 163.0–261.1) (p=0.48). At a cut-off point of 194 pg/mL, MCP-1 was 50.0% (95% CI 33.8% to 66.2%) sensitive and 46.9% (95% CI 39.4% to 54.5%) specific for 90-day MACE. After adjusting for covariates, MCP-1 was not associated with 90-day MACE at any cut-off point (at 194 pg/mL, OR 0.88 (95% CI 0.43 to 1.79)). When including hs-cTnT in the model, MCP-1 was not associated with 90-day MACE at any cut-off point (at 194 pg/mL, OR 0.85 (95% CI 0.42 to 1.73)).

Conclusion MCP-1 is not predictive of 90-day MACE in patients with non-low-risk chest pain.

  • cardiac care
  • acute coronary syndrome
  • acute myocardial infarct
  • diagnosis
  • chest

Data availability statement

No data are available. The data, analytical methods and study materials will not be made available to other researchers for purposes of reproducing the results or replicating the procedure.

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Data availability statement

No data are available. The data, analytical methods and study materials will not be made available to other researchers for purposes of reproducing the results or replicating the procedure.

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Footnotes

  • Handling editor Richard Body

  • Twitter @nick_ashburn1

  • Presented at Preliminary results were presented at the American College of Physicians’ 2020 Research Forum.

  • Contributors NPA, JPS and SAM conceived the study idea. SAM and BA were co-PIs for the parent study (STOP-CP). RHC performed biomarker analyses. ACS coordinated data management and performed the statistical analyses. DMH, BH, CDM, JPS, and SAM provided biomarker and cardiac risk stratification expertise. NPA drafted the manuscript. All authors contributed to the manuscript and substantially to its revision. NPA takes responsibility for the manuscript as a whole and acts as guarantor.

  • Funding This project was funded by the Emergency Medicine Foundation. STOP-CP was funded by Roche Diagnostics.

  • Competing interests NPA receives research funding from the Emergency Medicine Foundation (EMF18_EMRA_RESR_0012). ACS receives funding from NHLBI (1RO1HL118263-01) and HRSA (1H2ARH399760100). BA receives research funding from Roche Diagnostics and Beckman Coulter. He is a consultant for Roche Diagnostics. RHC is a consultant for and receives funding from Roche Diagnostics, Siemens Healthineers, Beckman Coulter Diagnostics, Becton Dickinson and Company, Quidel Corporation and Sphingotec. DMH receives support from the North Carolina State Legislature, Centers for Disease Control and Prevention, NHLBI/NIH (R01 HL0133932, 2R01HL11136, HHSN268201500003I, UH3AT009149), AstraZeneca, DalCor Pharma, Amgen and Esperion. BH has received research funding from Siemens. CDM receives research funding from Siemens, Abbott Point of Care, Creavo Medical Technologies, Grifols and NHLBI (5U01HL123027, 1 R01 HL118263). He has a US patent on cardiac biomarkers for coronary artery disease not related to MCP-1. JPS receives research funding from NCATS/NIH (KL2TR001421), HRSA (H2ARH39976-01-00), NHLBI (U01HL123027), Roche Diagnostics, and Abbott Point of Care. SAM receives funding/support from Roche Diagnostics, Abbott Laboratories, Ortho Clinical Diagnostics, Siemens, Grifols, Pathfast, Quidel, Genetesis AHRQ, PCORI, NIDA and NHLBI (1RO1HL118263-01), and HRSA (1H2ARH399760100). He is a consultant for Roche and Amgen and the Chief Medical Officer for Impathiq.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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