Whether human coronary arteries undergo compensatory enlargement in the presence of coronary disease has not been clarified. We studied histologic sections of the left main coronary artery in 136 hearts obtained at autopsy to determine whether atherosclerotic human coronary arteries enlarge in relation to plaque (lesion) area and to assess whether such enlargement preserves the cross-sectional area of the lumen. The area circumscribed by the internal elastic lamina (internal elastic lamina area) was taken as a measure of the area of the arterial lumen if no plaque had been present. The internal elastic lamina area correlated directly with the area of the lesion (r = 0.44, P less than 0.001), suggesting that coronary arteries enlarge as lesion area increases. Regression analysis yielded the following equation: Internal elastic lamina area = 9.26 + 0.88 (lesion area) + 0.026 (age) + 0.005 (heart weight). The correlation coefficient for the lesion area was significant (P less than 0.001), whereas the correlation coefficients for age and heart weight were not. The lumen area did not decrease in relation to the percentage of stenosis (lesion area/internal elastic lamina area X 100) for values between zero and 40 percent but did diminish markedly and in close relation to the percentage of stenosis for values above 40 percent (r = -0.73, P less than 0.001). We conclude that human coronary arteries enlarge in relation to plaque area and that functionally important lumen stenosis may be delayed until the lesion occupies 40 percent of the internal elastic lamina area. The preservation of a nearly normal lumen cross-sectional area despite the presence of a large plaque should be taken into account in evaluating atherosclerotic disease with use of coronary angiography.

We studied the relationships among intimal plaque area, lumen area, and artery size in 481 sections of the left anterior descending (LAD) coronary artery taken at four standard sampling sites in 125 pressure-perfusion-fixed postmortem adult human hearts. The internal elastic lamina area was considered to be a measure of artery size or potential lumen area. Artery size correlated strongly with intimal plaque area at each LAD level (p less than 0.0001). Stepwise regression analysis revealed that plaque area was the principal determinant of artery size at each LAD level (r2 = 0.20 to 0.33). Sections of arteries with the most intimal plaque (highest quartile) were compared with those with the least plaque (lowest quartile) at each sample site. In the proximal LAD artery, the most severely diseased arteries increased in size 62% but lumen area decreased 25%. In the midportion of the LAD artery, plaque area was 10 times greater in the most diseased arteries, but lumen area remained normal because of an 80% increase in artery size. In the most severely diseased distal LAD artery sections, despite a fourteenfold increase in plaque area, lumen area almost doubled because of a marked increase in artery size. If no enlargement had occurred, the most severely diseased arteries in the proximal LAD segment would have developed a 92% lumen stenosis rather than the observed 25% lumen stenosis. In the distal LAD artery, without enlargement there would have been a 65% lumen stenosis rather than the 85% increase in lumen area that was found.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

This book is a comprehensive, well-written, beautifully and generously illustrated textbook. It strikes an excellent balance between basic science and diagnostic pathology. Like previous editions of the book it performs admirable service as a PRN reference text for the lesion that is on your microscope's stage. It also provides a course in liver anatomy, physiology, and pathology.It truly is an international effort. Its seven editors and 26 other contributors represent eight countries. The book is divided into 18 chapters; one is devoted to diseases of the bile ducts and one to diseases of the gallbladder. In the first two chapters, the review of anatomy and pathophysiology are a reminder as to why some of the sharpest clinicians and pathologists have a special interest in liver disease. The discussion on the evolving and overlapping concepts of the acinus are of particular interest. The chapters on developmental abnormalities, liver disease in children, and metabolic errors were comprehensive yet readable. The chapter on injury due to drugs and toxins left me wondering whether there were any chemicals or drugs that do not have the potential to damage the liver. The chapter on tumors of the liver was divided into two separate parts, one more clinically oriented, discussing etiology, epidemiology, and pathology, with the other directed towards pathogenesis encompassing a daunting array of metabolic, inherited, genetic, and infectious factors that are involved in hepatic neoplasia. There are also chapters devoted to iron storage diseases, alcoholic liver disease, viral hepatitis, autoimmune hepatitis, vascular disorders, cirrhosis, liver pathology associated with other exogenous or systemic diseases, and transplantation pathology. The last chapter covers diagnostic procedures and includes discussion of the roles of both core biopsy and fine-needle aspiration biopsy. A brief discussion of the differential diagnosis of primary hepatic versus metastatic carcinoma and hepatocellular carcinoma versus reactive and benign disorders is included. There are also encounters with cytopathology in various discussions of infectious diseases and tumors. While useful information on cytopathology is presented, this text is not a substitute for textbooks and monographs that specifically discuss the cytopathology of the liver.This edition encompasses many advances that have occurred since the third edition was published in 1994. These include molecular biology, classification of rejection, grading and staging of various types of hepatitis, stem cells, necrosis, and apoptosis. Negative criticisms are only detectable on an ultrastructural level. Inevitably in a textbook of such breadth, some sections are less up to date-at least once the text directs the reader to the wrong page for a discussion and the index contains a ghost or two from the previous edition. That being said, this is an excellent book that will help any pathologist whose work encompasses hepatopathology.

Though immune responses correlate with prognosis in primary colorectal cancer, the role of tumor immunity in metastatic disease is less clear. We hypothesized that patient survival and tumor recurrence correlate with transcriptional evidence of lymphocyte proliferation/activation in resected colorectal cancer liver metastases (CRLM). Microarray gene analysis was performed on liver tumor specimens from 96 patients who underwent resection for CRLM. A Cox proportional hazards model identified genes associated with overall (OS) and recurrence-free survival (RFS). Conventional gene ontology (GO) enrichment analysis ranked biologically relevant processes. Survival probabilities of prioritized processes were assessed. Protein expression was validated with immunohistochemistry in an independent set of patients. GO analysis identified and ranked unique biologic processes that correlated with survival. Genes that specifically functioned in the biologic process of “T-cell proliferation” were significant predictors of OS (p = 0.01) and both “T-cell proliferation” and “activation” were highly associated with RFS (p≤ 0.01). Analysis of genes in these GO categories identified increased TNFSF14/LIGHT expression to be most associated with improved OS and RFS (p ≤ 0.0006). Immunohistochemistry of an independent validation set of CRLM confirmed that both increased tumor-infiltrating lymphocytes (TIL) and higher LIGHT expression on TILs were associated with improved OS and RFS. Differential expression of genes involved in T-cell proliferation/activation was associated with survival outcomes in a large number of surgical patients who underwent resection of CRLM. These biologic functions determined by GO analysis of the tumor microenvironment have identified specific immune-related genes that may be involved in an antitumor immune response.