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The reliable noninvasive assessment of occluded disrupted plaques and thromboses in culprit vessels could constitute an important step forward in risk stratification of patients early after acute myocardial infarction (AMI).
However, the selection of a target biomarker in culprit atherosclerotic lesions remains challenging [10].
The mean CTFC in culprit arteries 90 minutes after thrombolytic administration followed a continuous unimodal distribution (there were not subpopulations of slow and fast flow) with a mean value of 39.2 +/- 20.0 frames, which improved to 31.7 +/- 12.9 frames by 18 to 36 hours (P <.001).
Hoffmann et al. [24] demonstrated that in contrast to calcified plaques, non-calcified plaques as determined by MSCT were consistently present in culprit lesions of patients with acute coronary syndrome.
In addition, localisation of the culprit lesion in culprit was examined in the anterior or posterior circulation.
Moreover, the expression of IFN- γ was assessed in culprit lesions by immunofluorescence staining (coronary artery from AMI group) with confocal microscopy.
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Elevated hs-CRP has been previously related to the amount of necrotic core in the culprit lesion in SA patients.
This structure can take other forms, too, as in "The culprit is he," in which "the culprit" and "he" refer to the same person.
"Compelling evidence," says Shannon, that the NF1 gene is in fact the culprit in the cancers.
In the human coronary artery, the plaques in ACS culprit lesions have been angioscopically identified as yellow (6– 8).
All patients had TIMI 3 flow in the culprit vessel after pPCI.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com