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

Author:

Joshi Nikhil V.123,Toor Iqbal123,Shah Anoop S. V.123,Carruthers Kathryn123,Vesey Alex T.123,Alam Shirjel R.123,Sills Andrew1,Hoo Teng Y.1,Melville Adam J.1,Langlands Sarah P.1,Jenkins William S. A.123,Uren Neal G.123,Mills Nicholas L.123,Fletcher Alison M.2,van Beek Edwin J. R.2,Rudd James H. F.4,Fox Keith A. A.123,Dweck Marc R.123,Newby David E.123

Affiliation:

1. Centre for Cardiovascular Science, University of Edinburgh, United Kingdom

2. Clinical Research Imaging Centre, University of Edinburgh, United Kingdom

3. Edinburgh Heart Centre, Royal Infirmary of Edinburgh, United Kingdom

4. Division of Cardiovascular Medicine, University of Cambridge, United Kingdom

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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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