Harald Seifarth1, Christopher L Schlett2, Sam J Lehman3, Fabian Bamberg3, Patrick Donnelly3, James L Januzzi4, Wolfgang Koenig5, Quynh A Truong6, Udo Hoffmann7. 1. Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, 165 Cambridge Street, Boston, MA 02114, USA; Department of Diagnostic and Interventional Radiology, Esslingen Hospital, Esslingen, Germany. 2. Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, 165 Cambridge Street, Boston, MA 02114, USA; Department of Diagnostic and Interventional Radiology, University Hospital Heidelberg, Germany. 3. Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, 165 Cambridge Street, Boston, MA 02114, USA. 4. Division of Cardiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 5. Department of Internal Medicine II and Cardiology, University of Ulm Medical Center, Ulm, Germany. 6. Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, 165 Cambridge Street, Boston, MA 02114, USA; Division of Cardiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 7. Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, 165 Cambridge Street, Boston, MA 02114, USA. Electronic address: uhoffmann@partners.org.
Abstract
BACKGROUND: Elevated levels of inflammatory biomarkers are associated with increased cardiovascular morbidity and mortality. OBJECTIVE: We sought to determine whether elevated concentrations of high-sensitivity troponin T (hs-TnT) and high-sensitivity C-reactive protein (hs-CRP) predict progression of coronary artery disease (CAD) as determined by coronary CT angiography (coronary CTA). METHODS: Patients presenting to the emergency department with acute chest pain who initially showed no evidence of an acute coronary syndrome underwent baseline and follow-up coronary CTA (median follow-up, 23.9 months) using identical acquisition and reconstruction parameters. Coronary CTA data of each major coronary artery were co-registered. Cross-sections were assessed for the presence of calcified and noncalcified plaques. Progression of atherosclerotic plaque and change of plaque composition from noncalcified to calcified plaque was evaluated and correlated to levels of hs-TnT and hs-CRP at the time of the baseline CT. RESULTS: Fifty-four patients (mean age, 54.1 years; 59% male) were included, and 6775 cross-sections were compared. CAD was detected in 12.2 ± 21.2 cross-sections per patient at baseline. Prevalence of calcified plaque increased by 1.5 ± 2.4 slices per patient (P < .0001) over the follow-up period. On average, 1.6 ± 3.6 slices with new noncalcified plaque were found per patient (P < .0001) and 0.7 ± 1.7 slices with pre-existing noncalcified plaque had progressed to calcified plaque (P < .0001). After multivariate adjustment, change of overall CAD burden was predicted by baseline hs-TnT and hs-CRP (r = 0.29; P = .039 and r = 0.40; P = .004). Change of plaque composition was associated with baseline hs-TnT (r = 0.29; P = .03). CONCLUSION: Concentrations of hs-TnT and hs-CRP are weakly associated with a significant increase in CAD burden and change in plaque composition over 24 months independent of baseline risk factors.
BACKGROUND: Elevated levels of inflammatory biomarkers are associated with increased cardiovascular morbidity and mortality. OBJECTIVE: We sought to determine whether elevated concentrations of high-sensitivity troponin T (hs-TnT) and high-sensitivity C-reactive protein (hs-CRP) predict progression of coronary artery disease (CAD) as determined by coronary CT angiography (coronary CTA). METHODS:Patients presenting to the emergency department with acute chest pain who initially showed no evidence of an acute coronary syndrome underwent baseline and follow-up coronary CTA (median follow-up, 23.9 months) using identical acquisition and reconstruction parameters. Coronary CTA data of each major coronary artery were co-registered. Cross-sections were assessed for the presence of calcified and noncalcified plaques. Progression of atherosclerotic plaque and change of plaque composition from noncalcified to calcified plaque was evaluated and correlated to levels of hs-TnT and hs-CRP at the time of the baseline CT. RESULTS: Fifty-four patients (mean age, 54.1 years; 59% male) were included, and 6775 cross-sections were compared. CAD was detected in 12.2 ± 21.2 cross-sections per patient at baseline. Prevalence of calcified plaque increased by 1.5 ± 2.4 slices per patient (P < .0001) over the follow-up period. On average, 1.6 ± 3.6 slices with new noncalcified plaque were found per patient (P < .0001) and 0.7 ± 1.7 slices with pre-existing noncalcified plaque had progressed to calcified plaque (P < .0001). After multivariate adjustment, change of overall CAD burden was predicted by baseline hs-TnT and hs-CRP (r = 0.29; P = .039 and r = 0.40; P = .004). Change of plaque composition was associated with baseline hs-TnT (r = 0.29; P = .03). CONCLUSION: Concentrations of hs-TnT and hs-CRP are weakly associated with a significant increase in CAD burden and change in plaque composition over 24 months independent of baseline risk factors.
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