Rohit M Oemrawsingh1, Jin M Cheng2, Héctor M García-García3, Isabella Kardys2, Ron H N van Schaik4, Evelyn Regar2, Robert-Jan van Geuns2, Patrick W Serruys2, Eric Boersma5, K Martijn Akkerhuis2. 1. Thoraxcenter, Department of Cardiology, ErasmusMC and Cardiovascular Research Institute COEUR, Rotterdam, The Netherlands; Netherlands Heart Institute/Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands. 2. Thoraxcenter, Department of Cardiology, ErasmusMC and Cardiovascular Research Institute COEUR, Rotterdam, The Netherlands. 3. Cardialysis BV, Rotterdam, The Netherlands; Washington Hospital Center, Department of Cardiology, Washington DC, United States. 4. Department of Clinical Chemistry, ErasmusMC, Rotterdam, The Netherlands. 5. Thoraxcenter, Department of Cardiology, ErasmusMC and Cardiovascular Research Institute COEUR, Rotterdam, The Netherlands. Electronic address: h.boersma@erasmusmc.nl.
Abstract
BACKGROUND AND AIMS: To assess the relationship between the extent and phenotype of coronary atherosclerosis, as assessed by in-vivo grayscale and radiofrequency intravascular ultrasound (IVUS), and circulating Troponin levels in patients with established stable coronary artery disease (CAD). METHODS: In this single-center, cross-sectional analysis, high-sensitivity Troponin T (hsTnT) was measured and IVUS was performed in a predefined non-stenotic segment of a non-culprit coronary artery in 231 patients with stable CAD undergoing elective angiography. RESULTS: HsTnT was detectable (>3 pg/mL) in 212 patients (92%) and a concentration above 14 pg/mL was observed in 19.5%. Normalised segmental plaque volumes were positively associated with hsTnT levels (25.0 mm(3) increase in segmental plaque volume per SD increase in ln-transformed hsTnT, 95% CI: 6.0-44.0, p = 0.010). Higher hsTnT levels were measured in patients with a virtual histology derived thin-cap fibroatheroma (VH-TCFA, adj. odds ratio for presence of VH-TCFA = 1.52 per SD increase in ln-transformed hsTnT, 95% CI: 1.10-2.11, p = 0.011). Patients with a VH-TCFA had a 2-fold increased prevalence of hsTnT concentration ≥14 pg/mL (adj. OR 2.35, 95% CI: 1.12-4.91, p = 0.024). In addition, a 3-fold increased prevalence of hsTnT concentration ≥14 pg/mL was observed in patients with a VH-TCFA with a lesional plaque volume higher than the median (adj. OR 3.36, 95% CI: 1.44-7.84, p = 0.005). CONCLUSIONS: Segmental plaque volume and presence of VH-TCFA lesions are associated with higher circulating hsTnT concentrations in stable CAD patients. Subclinical plaque rupture or erosion and distal embolisation may be hypothesized as a potential pathophysiological mechanism with respect to Troponin elevation and its relation with adverse outcome in this patient population.
BACKGROUND AND AIMS: To assess the relationship between the extent and phenotype of coronary atherosclerosis, as assessed by in-vivo grayscale and radiofrequency intravascular ultrasound (IVUS), and circulating Troponin levels in patients with established stable coronary artery disease (CAD). METHODS: In this single-center, cross-sectional analysis, high-sensitivity Troponin T (hsTnT) was measured and IVUS was performed in a predefined non-stenotic segment of a non-culprit coronary artery in 231 patients with stable CAD undergoing elective angiography. RESULTS: HsTnT was detectable (>3 pg/mL) in 212 patients (92%) and a concentration above 14 pg/mL was observed in 19.5%. Normalised segmental plaque volumes were positively associated with hsTnT levels (25.0 mm(3) increase in segmental plaque volume per SD increase in ln-transformed hsTnT, 95% CI: 6.0-44.0, p = 0.010). Higher hsTnT levels were measured in patients with a virtual histology derived thin-cap fibroatheroma (VH-TCFA, adj. odds ratio for presence of VH-TCFA = 1.52 per SD increase in ln-transformed hsTnT, 95% CI: 1.10-2.11, p = 0.011). Patients with a VH-TCFA had a 2-fold increased prevalence of hsTnT concentration ≥14 pg/mL (adj. OR 2.35, 95% CI: 1.12-4.91, p = 0.024). In addition, a 3-fold increased prevalence of hsTnT concentration ≥14 pg/mL was observed in patients with a VH-TCFA with a lesional plaque volume higher than the median (adj. OR 3.36, 95% CI: 1.44-7.84, p = 0.005). CONCLUSIONS: Segmental plaque volume and presence of VH-TCFA lesions are associated with higher circulating hsTnT concentrations in stable CAD patients. Subclinical plaque rupture or erosion and distal embolisation may be hypothesized as a potential pathophysiological mechanism with respect to Troponin elevation and its relation with adverse outcome in this patient population.
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