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

Nikhil V Joshi; Iqbal Toor; Anoop S V Shah; Kathryn Carruthers; Alex T Vesey; Shirjel R Alam; Andrew Sills; Teng Y Hoo; Adam J Melville; Sarah P Langlands; William S A Jenkins; Neal G Uren; Nicholas L Mills; Alison M Fletcher; Edwin J R van Beek; James H F Rudd; Keith A A Fox; Marc R Dweck; David E Newby

doi:10.1161/JAHA.115.001956

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

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

Research output: Contribution to journal › Article › peer-review

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.

Original language	English
Pages (from-to)	e001956
Journal	Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease
Volume	4
Issue number	9
DOIs	https://doi.org/10.1161/JAHA.115.001956
Publication status	Published - 27 Aug 2015

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10.1161/JAHA.115.001956

Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction
© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Final published version, 946 KBLicence: Creative Commons: Attribution Non-Commercial (CC-BY-NC)

NOVEL IMAGING APPROACHES TO IDENTIFY UNSTABLE ATHEROSCLEROTIC CORONARY PLAQUES
Newby, D. (Principal Investigator)
UK central government bodies/local authorities, health and hospital authorities
1/11/11 → 30/04/13
Project: Research
Derivation and characterisation of endothelial cells from induced pluripotent stem cells in patients with atherosclerosis
Mills, N. (Principal Investigator)
UK-based charities
2/02/11 → 1/02/16
Project: Research
CLINICAL RESEARCH TRAINING F/SHIP: M DWECH - ROLE OF INFLAMMATION AND CALCIFICATION IN THE PROGRESSION OF AORTIC STENOSIS : THE RING OF FIRE
Newby, D. (Principal Investigator)
UK-based charities
1/03/10 → 31/08/14
Project: Research

Cite this

Joshi, N. V., Toor, I., Shah, A. S. V., Carruthers, K., Vesey, A. T., Alam, S. R., Sills, A., Hoo, T. Y., Melville, A. J., Langlands, S. P., Jenkins, W. S. A., Uren, N. G., Mills, N. L., Fletcher, A. M., van Beek, E. J. R., Rudd, J. H. F., Fox, K. A. A., Dweck, M. R., & Newby, D. E. (2015). Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction. Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease, 4(9), e001956. https://doi.org/10.1161/JAHA.115.001956

@article{e74f61eeab374ac2b3dbca4d2ef76358,

title = "Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction",

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.",

author = "Joshi, {Nikhil V} and Iqbal Toor and Shah, {Anoop S V} and Kathryn Carruthers and Vesey, {Alex T} and Alam, {Shirjel R} and Andrew Sills and Hoo, {Teng Y} and Melville, {Adam J} and Langlands, {Sarah P} and Jenkins, {William S A} and Uren, {Neal G} and Mills, {Nicholas L} and Fletcher, {Alison M} and {van Beek}, {Edwin J R} and Rudd, {James H F} and Fox, {Keith A A} and Dweck, {Marc R} and Newby, {David E}",

note = "Date of Acceptance: 20/05/2015",

year = "2015",

month = aug,

day = "27",

doi = "10.1161/JAHA.115.001956",

language = "English",

volume = "4",

pages = "e001956",

journal = "Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease",

issn = "2047-9980",

publisher = "Wiley Open Access",

number = "9",

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Joshi, NV, Toor, I, Shah, ASV, Carruthers, K, Vesey, AT, Alam, SR, Sills, A, Hoo, TY, Melville, AJ, Langlands, SP, Jenkins, WSA, Uren, NG, Mills, NL, Fletcher, AM, van Beek, EJR, Rudd, JHF, Fox, KAA , Dweck, MR & Newby, DE 2015, 'Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction', Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease, vol. 4, no. 9, pp. e001956. https://doi.org/10.1161/JAHA.115.001956

Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction: Myocardial Infarction Begets Myocardial Infarction. / Joshi, Nikhil V; Toor, Iqbal; Shah, Anoop S V et al.
In: Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease, Vol. 4, No. 9, 27.08.2015, p. e001956.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - Systemic Atherosclerotic Inflammation Following Acute Myocardial Infarction

T2 - Myocardial Infarction Begets Myocardial Infarction

AU - Joshi, Nikhil V

AU - Toor, Iqbal

AU - Shah, Anoop S V

AU - Carruthers, Kathryn

AU - Vesey, Alex T

AU - Alam, Shirjel R

AU - Sills, Andrew

AU - Hoo, Teng Y

AU - Melville, Adam J

AU - Langlands, Sarah P

AU - Jenkins, William S A

AU - Uren, Neal G

AU - Mills, Nicholas L

AU - Fletcher, Alison M

AU - van Beek, Edwin J R

AU - Rudd, James H F

AU - Fox, Keith A A

AU - Dweck, Marc R

AU - Newby, David E

N1 - Date of Acceptance: 20/05/2015

PY - 2015/8/27

Y1 - 2015/8/27

N2 - 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.

AB - 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.

U2 - 10.1161/JAHA.115.001956

DO - 10.1161/JAHA.115.001956

M3 - Article

C2 - 26316523

SN - 2047-9980

VL - 4

SP - e001956

JO - Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease

JF - Journal of the American Heart Association Cardiovascular and Cerebrovascular Disease

IS - 9

ER -

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

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NOVEL IMAGING APPROACHES TO IDENTIFY UNSTABLE ATHEROSCLEROTIC CORONARY PLAQUES

Derivation and characterisation of endothelial cells from induced pluripotent stem cells in patients with atherosclerosis

CLINICAL RESEARCH TRAINING F/SHIP: M DWECH - ROLE OF INFLAMMATION AND CALCIFICATION IN THE PROGRESSION OF AORTIC STENOSIS : THE RING OF FIRE

Cite this