Linda C Battes1, Jin M Cheng2, Rohit M Oemrawsingh3, Eric Boersma4, Hector M Garcia-Garcia5, Sanneke P M de Boer6, Nermina Buljubasic7, Nicolas A van Mieghem8, Evelyn Regar9, Robert-Jan van Geuns10, Patrick W Serruys11, K Martijn Akkerhuis12, Isabella Kardys13. 1. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: battes@erasmusmc.nl. 2. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: j.cheng@erasmusmc.nl. 3. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: r.oemrawsingh@erasmusmc.nl. 4. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. 5. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: h.garciagarcia@erasmusmc.nl. 6. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: s.p.m.deboer@erasmusmc.nl. 7. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: n.buljubasic@erasmusmc.nl. 8. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: n.vanmieghem@erasmusmc.nl. 9. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: e.regar@erasmusmc.nl. 10. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: r.vangeuns@erasmusmc.nl. 11. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: p.w.j.c.serruys@erasmusmc.nl. 12. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: k.m.akkerhuis@erasmusmc.nl. 13. Clinical Epidemiology Unit, Department of Cardiology, Erasmus MC, Thoraxcenter, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. Electronic address: i.kardys@erasmusmc.nl.
Abstract
OBJECTIVE: We investigated whether concentrations of TNF-α, TNF-β, TNF-receptor 2, interferon-γ, IL-6, IL-8, IL-10 and IL-18 are associated with extent and composition of coronary atherosclerosis determined by grayscale and virtual histology (VH)- intravascular ultrasound (IVUS). METHODS: Between 2008 and 2011, IVUS(-VH) imaging of a non-culprit coronary artery was performed in 581 patients (stable angina pectoris (SAP), n = 261; acute coronary syndrome (ACS), n = 309) undergoing coronary angiography from the ATHEROREMO-IVUS study. Plaque burden, presence of VH-IVUS-derived thin-cap fibroatheroma (TCFA) lesions, and presence of VH-TCFA lesions with plaque burden ≥70% were assessed. Blood samples for cytokine measurement were drawn from the arterial sheath prior to the angiography procedure. We applied linear and logistic regression. RESULTS: TNF-α levels were positively associated with plaque burden (beta (β) [95%CI]: 4.45 [0.99-7.91], for highest vs lowest TNF-α tertile) and presence of VH-TCFA lesions (odds ratio (OR) [95%CI] 2.30 (1.17-4.52), highest vs lowest TNF-α tertile) in SAP patients. Overall, an inverse association was found between IL-10 concentration and plaque burden (β [95%CI]: -1.52 [-2.49 to -0.55], per Ln (pg/mL) IL-10) as well as IL-10 and VH-TCFA lesions with plaque burden ≥70% (OR: 0.31 [0.12-0.80],highest vs lowest IL-10 tertile). These effects did not reach statistical significance in the separate SAP and ACS groups. CONCLUSION: Higher circulating TNF-α was associated with higher plaque burden and VH-TCFA lesions in SAP patients. Lower circulating IL-10 was associated with higher plaque burden and large VH-TCFA lesions. These in-vivo findings suggest a role for these cytokines in extent and vulnerability of atherosclerosis.
OBJECTIVE: We investigated whether concentrations of TNF-α, TNF-β, TNF-receptor 2, interferon-γ, IL-6, IL-8, IL-10 and IL-18 are associated with extent and composition of coronary atherosclerosis determined by grayscale and virtual histology (VH)- intravascular ultrasound (IVUS). METHODS: Between 2008 and 2011, IVUS(-VH) imaging of a non-culprit coronary artery was performed in 581 patients (stable angina pectoris (SAP), n = 261; acute coronary syndrome (ACS), n = 309) undergoing coronary angiography from the ATHEROREMO-IVUS study. Plaque burden, presence of VH-IVUS-derived thin-cap fibroatheroma (TCFA) lesions, and presence of VH-TCFA lesions with plaque burden ≥70% were assessed. Blood samples for cytokine measurement were drawn from the arterial sheath prior to the angiography procedure. We applied linear and logistic regression. RESULTS: TNF-α levels were positively associated with plaque burden (beta (β) [95%CI]: 4.45 [0.99-7.91], for highest vs lowest TNF-α tertile) and presence of VH-TCFA lesions (odds ratio (OR) [95%CI] 2.30 (1.17-4.52), highest vs lowest TNF-α tertile) in SAPpatients. Overall, an inverse association was found between IL-10 concentration and plaque burden (β [95%CI]: -1.52 [-2.49 to -0.55], per Ln (pg/mL) IL-10) as well as IL-10 and VH-TCFA lesions with plaque burden ≥70% (OR: 0.31 [0.12-0.80],highest vs lowest IL-10 tertile). These effects did not reach statistical significance in the separate SAP and ACS groups. CONCLUSION: Higher circulating TNF-α was associated with higher plaque burden and VH-TCFA lesions in SAPpatients. Lower circulating IL-10 was associated with higher plaque burden and large VH-TCFA lesions. These in-vivo findings suggest a role for these cytokines in extent and vulnerability of atherosclerosis.
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