Sudden coronary death caused by pathologic intimal thickening without atheromatous plaque formation
Atherosclerotic plaques progress from early lesions with little free cholesterol and lipid to late fibroatheromas with necrotic cores that may rupture. The frequency of severe coronary atherosclerosis without core formation in any artery in sudden coronary death is not known.
We studied 314 hearts from 253 men and 61 women who died suddenly from severe coronary stenosis (≥ 1 epicardial artery with ≥ 75% luminal area narrowing) and with no other cause of death. If no section demonstrated any necrotic core, the designation was nonatheromatous atherosclerosis; if there was ≥ 1 necrotic core, the designation was atheromatous atherosclerosis. Plaques were scored for the presence of calcification, intimal inflammation, and neovasculature on a 5-point scale. Plaque burden was estimated semiquantitatively.
In 22 men (9%) and 14 women (23%), there were no necrotic cores in any plaque (nonatheromatous atherosclerosis). Fourteen of these 36 nonatheromatous atherosclerosis cases had focal acute thrombus due to erosion (39%). Of the remaining 278 cases (atheromatous atherosclerosis), acute erosions were present in 25 (9%; P<.0001). Sudden death due to nonatheromatous atherosclerosis occurred more frequently in women (P<.001), in Blacks (20%; P=.003), and at a younger age (44± 12 years) than atheromatous atherosclerosis (52 ± 12 years; P=.0003). On multivariate analysis, nonatheromatous atherosclerosis was associated with younger age (P=.001), female gender (P=.004), and Black race (P=.006).
Nonatheromatous atherosclerosis constitutes slightly >10% of sudden coronary deaths and is more frequent in young Black women. Nonatheromatous atherosclerosis is a relatively infrequent pathway for coronary plaque progression, leading to severe disease and sudden death that may involve plaque erosion.
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- "Plaque erosion is observed in around 25% of patients with ACS, and sudden death not infrequently occurs in this group of patients  . Although erosion can be detected by angioscopy and OCT, what kind of images represents the prestage of erosion by these and other imaging tools had been unclear. "
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ABSTRACT: Angioscopy enables macroscopic pathological diagnosis of cardiovascular diseases from the inside. This imaging modality has been intensively directed to characterizing vulnerable coronary plaques. Scoring of plaque color was developed, and based on prospective studies; dark yellow or glistening yellow plaques were proposed as vulnerable ones. Colorimetry apparatus was developed to assess the yellow color of the plaques quantitatively. The effects of lipid-lowering therapies on coronary plaques were confirmed by angioscopy. However, since observation is limited to surface color and morphology, pitfalls of this imaging technology became evident. Dye-staining angioscopy and near-infrared fluorescence angioscopy were developed for molecular imaging, and the latter method was successfully applied to patients. Color fluorescence angioscopy was also established for molecular and chemical basis characterization of vulnerable coronary plaques in both in vitro and in vivo. Drug-eluting stents (DES) reduce coronary restenosis significantly, however, late stent thrombosis (LST) occurs, which requires long-term antiplatelet therapy. Angioscopic grading of neointimal coverage of coronary stent struts was established, and it was revealed that neointimal formation is incomplete and prevalence of LST is higher in DES when compared to bare-metal stent. Many new stents were devised and they are now under experimental or clinical investigations to overcome the shortcomings of the stents that have been employed clinically. Endothelial cells are highly anti-thrombotic. Neoendothelial cell damage is considered to be caused by friction between the cells and stent struts due to the thin neointima between them that might act as a cushion. Therefore, development of a DES that causes an appropriate thickness (around 100 μm) of the neointima is a potential option with which to prevent neoendothelial cell damage and consequent LST while preventing restenosis.
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ABSTRACT: Scientists here recently received training and developed assays clearing the way for the Armed Forces Institute of Pathology to become an H1N1 testing site. "Today our institute is a Centers for Disease Control and Prevention approved DOD testing site for human swine influenza," said Dr. Mina Izadjoo, chief of the Division of Wound Biology and Translational Research. "This will provide an additional site for DOD that can analyze service members' samples. This is all about our Institute supporting readiness for swine flu outbreaks." Initially, AFIP became involved in H1N1 flu research after receiving a number of requests for testing from the Walter Reed Army Medical Center, said Izadjoo. "They had a dramatic increase in the number of tests that they had to do and asked us to help and started sending us suspected cases to see if we could detect swine influenza. We have obtained all the necessary instrumentation to officially report our diagnostic results. We also have the capability in our division for developing and testing vaccines and performing drug screening."
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ABSTRACT: A multilayer neural network, trained with the back-propagation
algorithm, is used to classify impulse radar waveforms from
asphalt-covered bridge decks. A strategy for determining the structure
of a bridge deck by using principal components analysis to reduce the
dimensionality of the input data is demonstrated, showing classification
accuracies ranging between 95.6% and 100%. The results show that neural
networks can be used to extract information about a bridge deck's
structure when waveforms from the deck are presented to it. Once the
network has been trained to recognize several different structures, it
should be possible to obtain very accurate estimates about the specific
deck structure. The neural network will eliminate the need for taking
core samples from the bridge deck, and a truly nondestructive
bridge-deck evaluation system will be realized
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