Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction

J Am Heart Assoc. 2015 Aug 27;4(9):e001956. doi: 10.1161/JAHA.115.001956.

Abstract

Background: Preclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans.

Methods and results: Overall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non-ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI.

Conclusions: The presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI.

Clinical trial registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254.

Keywords: 18F‐fluorodeoxyglucose positron emission and computed tomography; atherosclerosis; inflammation; vulnerable plaque.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aortitis / blood
  • Aortitis / diagnosis*
  • Aortitis / diagnostic imaging
  • Atherosclerosis / blood
  • Atherosclerosis / diagnosis*
  • Atherosclerosis / diagnostic imaging
  • Biomarkers / blood
  • C-Reactive Protein / metabolism
  • Coronary Artery Disease / blood
  • Coronary Artery Disease / diagnosis*
  • Coronary Artery Disease / diagnostic imaging
  • Female
  • Fluorodeoxyglucose F18
  • Humans
  • Kaplan-Meier Estimate
  • Logistic Models
  • Male
  • Middle Aged
  • Multimodal Imaging / methods
  • Multivariate Analysis
  • Myocardial Infarction / blood
  • Myocardial Infarction / diagnosis*
  • Myocardial Infarction / diagnostic imaging
  • Plaque, Atherosclerotic
  • Positron-Emission Tomography
  • Predictive Value of Tests
  • Prospective Studies
  • Radiopharmaceuticals
  • Recurrence
  • Registries
  • Risk Factors
  • Scotland
  • Time Factors
  • Tomography, X-Ray Computed
  • Troponin / blood

Substances

  • Biomarkers
  • Radiopharmaceuticals
  • Troponin
  • Fluorodeoxyglucose F18
  • C-Reactive Protein

Associated data

  • ClinicalTrials.gov/NCT01749254