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

Authors :
Joshi NV
Toor I
Shah AS
Carruthers K
Vesey AT
Alam SR
Sills A
Hoo TY
Melville AJ
Langlands SP
Jenkins WS
Uren NG
Mills NL
Fletcher AM
van Beek EJ
Rudd JH
Fox KA
Dweck MR
Newby DE
Source :
Journal of the American Heart Association [J Am Heart Assoc] 2015 Aug 27; Vol. 4 (9), pp. e001956. Date of Electronic Publication: 2015 Aug 27.
Publication Year :
2015

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.<br />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.<br />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.<br />Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254.<br /> (© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Details

Language :
English
ISSN :
2047-9980
Volume :
4
Issue :
9
Database :
MEDLINE
Journal :
Journal of the American Heart Association
Publication Type :
Academic Journal
Accession number :
26316523
Full Text :
https://doi.org/10.1161/JAHA.115.001956