Abstract 14454: Remote Atherosclerotic Inflammation following Acute Myocardial Infarction
Introduction: Myocardial infarction is associated with coronary artery and systemic inflammation, but it is unclear whether this drives inflammation within atherosclerosis elsewhere. Using positron emission tomography (PET) combined with computed tomography (CT), we compared thoracic aortic 18F-fluorodeoxyglucose (18F-FDG) and 18F-fluoride (18F-NaF) uptake in patients with either a recent myocardial infarction or stable coronary artery disease.
Methods: In this prospective clinical trial, patients with a myocardial infarction (n=40) and stable angina (n=40) underwent thoracic 18F-FDG PET-CT, 18F-NaF PET-CT, aortic calcium score and CT angiography. Tracer activity was measured in non-vascular tissue (para-spinal muscle) as a control region.
Results: Despite less coronary atherosclerotic burden (coronary Agatston score 159 [42-456]) versus 599 [60-1302], p=0.006), patients with recent myocardial infarction had higher aortic 18F-FDG uptake (mean TBR max 2.15±0.30 versus 1.84±0.18, P<0.0001) compared to those with stable angina but similar para-spinal muscular uptake (0.72±0.18 versus 0.75±0.17, P=0.41). The uptake was greater in patients with ST-elevation myocardial infarction than non-ST elevation myocardial infarction (2.24±0.32 versus 2.02±0.21, p=0.03). Modest correlations were observed between 18F-FDG uptake and the peak plasma troponin concentrations (r=0.42, P=0.01). In contrast, aortic 18F-NaF uptake was similar across both patient cohorts (2.03±0.29 versus 1.97±0.33; P=0.40).
Conclusions: In comparison to those with stable disease, patients with unstable coronary disease have increased aortic atherosclerotic metabolic activity. This suggests either that myocardial infarction is precipitated by a generalized increase in atherosclerotic inflammation or that myocardial infarction itself causes increased systemic atherosclerotic inflammation.
- © 2013 by American Heart Association, Inc.