Sudden coronary death caused by pathologic intimal thickening without atheromatous plaque formation.
ABSTRACT 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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ABSTRACT: Background Atherosclerosis is considered a chronic inflammatory disease of the entire arterial wall, including the adventitia. Advanced coronary lesions with lipid cores are associated with adventitial inflammation, but the early inflammatory process in human coronary adventitia is largely unknown. We hypothesized that adventitial inflammatory cell infiltration accompanies the early stages of atherogenesis in human coronary arteries, and it is synchronous with the inflammatory process in the intima. Methods Coronary artery samples were obtained from 111 forensic autopsy cases aged from 7 to 25 years. Adventitial and intimal macrophages, T lymphocytes and B lymphocytes, and intimal microvessels were detected by immunohistochemical methods, and quantified by computerized image analysis. Body height, weight, waist circumference, and the size of mesenteric and omental fat depots were measured. Results Adventitial densities of macrophages and T lymphocytes were significantly higher in arteries showing intimal xanthomas than in cases with only scattered intimal macrophages. The xanthoma group also had significantly higher BMI and larger visceral fat depots. Highest densities of all adventitial cell types were seen in intermediate lesions and fibroatheromas. There were significant positive correlations between intimal and adventitial densities of T cells and B cells in the groups with or without intimal xanthomas, but the positive correlation between intimal and adventitial macrophages was significant only in the group without xanthomas. Conclusions Adventitial immune-inflammatory cell accumulation accompanies the early stages of coronary atherogenesis in young individuals, and lymphocyte accumulation seems to be synchronous in the intima and adventitia. Macrophage accumulation is also synchronous before xanthomas are seen.Cardiovascular pathology: the official journal of the Society for Cardiovascular Pathology 07/2014; · 1.63 Impact Factor
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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: We used virtual histology-intravascular ultrasound (VH-IVUS) to investigate the characteristics of culprit lesions in acute coronary syndromes (ACS). Autopsy studies of patients who died of ACS have shown that culprit atheromatous plaques almost always contain a large lipid-necrotic core covered by a ruptured thin fibrous cap. There are no studies of sufficient size that have assessed the in vivo characterization of plaques responsible for ACS. Patients undergoing angiography for stable ischemic heart disease and ACS (with and without ST-segment elevation) were enrolled in a prospective study. Lesions in patients with stable angina were classified as stable and those in patients with ACS as culprit or nonculprit. The study included 189 patients: VH-IVUS was used to assess 253 lesions (73 stable, 82 nonculprit, and 98 culprit lesions). The thin-cap fibroatheroma phenotype (VH-TCFA) was more frequent among lesions in patients with ACS (55.1% in culprit lesions, 36.6% in nonculprit lesions and 14.4% in stable lesions; P = .007). The arc of the VH-TCFA exposed to the vessel lumen was significantly greater in culprit lesions than in nonculprit lesions (122.28° ± 58 vs 89.46° ± 52; respectively; P = .007). Multivariate analysis showed that VH-TCFA (OR 2.1; P = .033), calcified nodules (OR 2.1; P = .046), positive remodeling (OR 3.5; P < .001) and necrotic core volume (OR 1.02;P = .009) were independently associated with a clinically identified culprit lesion. Plaque phenotype, rather than the proportion of each tissue, appears to be associated with plaque instability. VH-TCFA, particularly subtype IV, is associated with lesions responsible for ACS.American heart journal 03/2013; 165(3):400-7. · 4.65 Impact Factor