Joshi Nikhil V, Toor Iqbal, Shah Anoop S V, Carruthers Kathryn, Vesey Alex T, Alam Shirjel R, Sills Andrew, Hoo Teng Y, Melville Adam J, Langlands Sarah P, Jenkins William S A, Uren Neal G, Mills Nicholas L, Fletcher Alison M, van Beek Edwin J R, Rudd James H F, Fox Keith A A, Dweck Marc R, Newby David E
Centre for Cardiovascular Science, University of Edinburgh, United Kingdom (N.V.J., I.T., A.V.S., K.C., A.T.V., S.R.A., A.S., T.Y.H., A.J.M., S.P.L., W.A.J., N.G.U., N.L.M., K.A.F., M.R.D., D.E.N.) Clinical Research Imaging Centre, University of Edinburgh, United Kingdom (N.V.J., I.T., A.V.S., K.C., A.T.V., S.R.A., W.A.J., N.G.U., N.L.M., A.M.F., E.R.B., K.A.F., M.R.D., D.E.N.) Edinburgh Heart Centre, Royal Infirmary of Edinburgh, United Kingdom (N.V.J., I.T., A.V.S., K.C., A.T.V., S.R.A., W.A.J., N.G.U., N.L.M., K.A.F., M.R.D., D.E.N.).
Centre for Cardiovascular Science, University of Edinburgh, United Kingdom (N.V.J., I.T., A.V.S., K.C., A.T.V., S.R.A., A.S., T.Y.H., A.J.M., S.P.L., W.A.J., N.G.U., N.L.M., K.A.F., M.R.D., D.E.N.).
J Am Heart Assoc. 2015 Aug 27;4(9):e001956. doi: 10.1161/JAHA.115.001956.
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.
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.
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.
URL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254.
临床前数据表明，心肌梗死（MI）后的急性炎症反应会加速全身性动脉粥样硬化。我们使用正电子发射断层扫描与计算机断层扫描相结合的方法，研究了这种现象是否在人类中发生。
总共40例心肌梗死患者和40例稳定型心绞痛患者接受了胸部18F-氟脱氧葡萄糖正电子发射断层扫描与计算机断层扫描联合检查。测量了主动脉粥样硬化斑块和非血管组织（椎旁肌）中的放射性示踪剂摄取情况。在纳入全球急性冠状动脉事件注册研究的1003例患者中，我们评估了梗死面积是否可预测早期（≤30天）和晚期（>30天）复发性冠状动脉事件。与稳定型心绞痛患者相比，心肌梗死患者的主动脉18F-氟脱氧葡萄糖摄取更高（组织与本底比值为2.15±0.30比1.84±0.18，P<0.0001），血浆C反应蛋白浓度更高（6.50[2.00至12.75]比2.00[0.50至4.00]mg/dL，P=0.0005），尽管他们的主动脉粥样硬化负担相似（P=0.12），冠状动脉粥样硬化负担较轻（P=0.006），且椎旁肌18F-氟脱氧葡萄糖摄取相似（P=0.52）。ST段抬高型心肌梗死患者的梗死面积更大（血浆肌钙蛋白峰值为32300[10200至>50000]比3800[1000至9200]ng/L，P<0.0001），主动脉18F-氟脱氧葡萄糖摄取更高（2.24±0.32比2.02±0.21，P=0.03），高于非ST段抬高型心肌梗死患者。血浆肌钙蛋白峰值浓度与主动脉18F-氟脱氧葡萄糖摄取相关（r=0.43，P=0.01），多变量分析显示，其可独立预测早期（三分位数3与三分位数1相比：相对风险4.40[95%CI1.90至10.19]，P=0.001）而非晚期复发性心肌梗死。
心肌梗死的存在和范围与主动脉粥样硬化炎症增加和早期复发性心肌梗死相关。这一发现支持了急性心肌梗死会加剧全身性动脉粥样硬化炎症和远处斑块不稳定的假说：心肌梗死引发心肌梗死。
