Acute anterior myocardial infarction seen on conventional iodine-contrast CT.
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ABSTRACT:
SUBMITTER: Hagdrup C
PROVIDER: S-EPMC5552012 | biostudies-other | 2017 Sep
REPOSITORIES: biostudies-other
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Project description: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.
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Project description:BackgroundBoth stress cardiomyopathy (SCMP) and acute myocardial infarction (AMI) present with similar clinical symptoms and signs, and apical akinesis.HypothesisQuantitative segmental analysis of myocardial contrast echocardiography (MCE) helps to differentiate AMI from SCMP.MethodsReal-time MCE was performed in 33 consecutive patients who presented with an acute symptom/sign and a new apical akinesis on echocardiography. In 18 left ventricular (LV) myocardial segments, a replenishment curve was obtained in each segment to measure peak plateau myocardial contrast intensity (MCI) (A) and the replenishment curve slope (β). The calibrated MCI was also measured in each segment.ResultsAmong 33 patients, 22 were diagnosed with SCMP and 11 were diagnosed with AMI according to comprehensive diagnostic criteria. A, β, Aβ, and the calibrated MCI were lower in akinetic than in normokinetic segments in both the SCMP and AMI groups. In the akinetic segments, A, β, Aβ, and the calibrated MCI in SCMP patients were each higher than those in AMI patients. In patient-based analyses, areas under the ROC curves of A, β, Aβ, and the calibrated MCI for diagnosing AMI were 0.769, 0.607, 0.822, and 0.934, respectively. The optimal cutoff values to diagnose AMI were Aβ < 3.7 dB/sec (sensitivity 82%, specificity 82%) and a calibrated MCI < -23 dB (sensitivity 91%, specificity 95%).ConclusionsAlthough myocardial perfusion is relatively reduced in the akinetic segments of SCMP, a quantitative segmental analysis of myocardial perfusion using MCE helps to discriminate AMI from SCMP.
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