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Nathaniel Cresswell

Researcher at Armed Forces Institute of Pathology

Publications -  11
Citations -  341

Nathaniel Cresswell is an academic researcher from Armed Forces Institute of Pathology. The author has contributed to research in topics: Sudden death & Cardiomyopathy. The author has an hindex of 9, co-authored 11 publications receiving 297 citations. Previous affiliations of Nathaniel Cresswell include University of Maryland, College Park & University of Maryland Medical Center.

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Comparison of Necropsy Findings in Patients With Sarcoidosis Dying Suddenly from Cardiac Sarcoidosis Versus Dying Suddenly from Other Causes

TL;DR: In this paper, a retrospective search of sudden cardiac deaths was performed from a reference laboratory and statewide medical examiner system for a 12-year period, and planimetry was performed on gross photographs of transverse shortaxis sections, and the phase of the lesion and the portion of myocardium extent was estimated histologically.
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Immunolocalisation of fibrin in coronary atherosclerosis: implications for necrotic core development

TL;DR: Fibrin in necrotic cores is present proportional to intraplaque vasa vasorum and before red cells, suggesting leakage of vessels before frank intraplaques haemorrhage and fibrin may play a role in the bridge between pre‐atheroma and atheroma.
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Sudden coronary death caused by pathologic intimal thickening without atheromatous plaque formation.

TL;DR: 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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Distribution of biventricular disease in arrhythmogenic cardiomyopathy: an autopsy study.

TL;DR: There is a trend that univentricular involvement occurs at an earlier age and that right ventricular involvement shows more inflammation, suggesting different stages of disease.
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In-stent restenosis is associated with neointimal angiogenesis and macrophage infiltrates.

TL;DR: It is concluded that in-stent restenosis is associated with neointimal angiogenesis which is accompanied by macrophage inflammation, and the relevance of these findings to treatment and prevention of in-Stent Restenosis needs to be further explored.