Background-A myocardial bridge (MB) that partially covers the course of the left anterior descending coronary artery (LAD) sometimes causes myocardial ischemia, primarily because of hemodynamic deterioration, but without atherosclerosis. However, the mechanism of occurrence of myocardial infarction (MI) as a result of an MB in patients with spontaneously developing atherosclerosis is unclear. Methods and Results-One hundred consecutive autopsied MI hearts either with MBs [MI(ϩ)MB(ϩ) group; nϭ46] orwithout MBs (nϭ54) were obtained, as were 200 normal hearts, 100 with MBs [MI(Ϫ)MB(ϩ) group] and 100 without MBs. By microscopy on LADs that were consecutively cross-sectioned at 5-mm intervals, the extent and distribution of LAD atherosclerosis were investigated histomorphometrically in conjunction with the anatomic properties of the MB, such as its thickness, length, and location and the MB muscle index (MB thickness multiplied by MB length), according to MI and MB status. In the MI(ϩ)MB(ϩ) group, the MB showed a significantly greater thickness and greater MB muscle index (PϽ0.05) than in the MI(Ϫ)MB(ϩ) group. The intima-media ratio (intimal area/medial area) within 1.0 cm of the left coronary ostium was also greater (PϽ0.05) in the MI(ϩ)MB(ϩ) group than in the other groups. In addition, in the MI(ϩ)MB(ϩ) group, the location of the segment that exhibited the greatest intima-media ratio in the LAD proximal to the MB correlated significantly (PϽ0.001) with the location of the MB entrance, and furthermore, atherosclerosis progression in the LAD proximal to the MB was largest at 2.0 cm from the MB entrance. Conclusions-In the proximal LAD with an MB, MB muscle index is associated with a shift of coronary disease more proximally, an effect that may increase the risk of MI. (Circulation. 2009;120:376-383.)Key Words: myocardium Ⅲ myocardial infarction Ⅲ anatomy Ⅲ atherosclerosis T he coronary artery that runs through epicardial adipose tissue is often covered in part with myocardial tissue. This structure is known as a myocardial bridge (MB) 1 ; it exists almost exclusively in the left anterior descending coronary artery (LAD), 2 and it is regarded as a common anatomic variant rather than a congenital anomaly. 3 The frequency of an MB in the LAD is high, sometimes Ͼ50% by autopsy, 2 but it is Ͻ5% by angiography. 4 Because MBs have been identified angiographically indirectly through a "milking effect" phenomenon induced by systolic compression of the MB, a thin or short MB is often missed. 4 The use of other invasive imaging, such as intracoronary ultrasound and Doppler, has improved MB detection. 5,6 More recently, multidetector computed tomography (CT) has been used noninvasively to detect the MB itself directly, 7 and surprisingly, the use of multidetector CT for myocardial ischemia increases Editorial see p 357 Clinical Perspective on p 383The clinical outcome of patients with MBs has been considered benign 4 ; however, the significance of an MB to myocardial ischemia remains controversial. By multidetector CT imaging,...

Aims:The lymphatic system is involved in fluid homeostasis of the cardiac interstitium, but lymphangiogenesis in myocardial remodelling has not previously been examined histopathologically. The aim was to investigate by D2-40 immunohistochemistry the sequential changes in lymphatic distribution in the process of myocardial remodelling after myocardial infarction (MI). Methods and results: Myocardial tissues in various phases of healing after MI were obtained from 40 autopsied hearts. D2-40+ lymphatic vessel density (LD) and CD34+ blood vessel density (BD) in the lesion were determined. BD decreased with advance of myocardial necrosis, subsequently increased at the early stage of granulation and thereafter decreased with the progression of scar formation. In contrast, lymphatic vessels were not detected in lesions with coagulation necrosis, and newly formed lymphatics first appeared in the early stages of granulation. A subsequent increase in LD was demonstrated in the late stages of granulation, and lymphatics remained up to the scar phase. Vascular endothelial growth factor-C was consistently expressed in viable cardiomyocytes around the lesion in all of these stages. Conclusion: In myocardial remodelling after MI, lymphangiogenesis lags behind blood vessel angiogenesis; newly formed lymphatics may be involved mainly in the maturation of fibrosis and scar formation through the drainage of excessive proteins and fluid.

Dentin matrix protein 1 (DMP1) is an Arg-Gly-Asp-containing acidic phosphoprotein that was originally identified from a rat incisor cDNA library and was thought to be a dentin-specific protein. DMP1 was later shown to express in a number of hard tissue-forming cells, including osteoblasts, osteocytes, ameloblasts, and cementoblasts, and was considered to play important roles in mineralization. Further, DMP1 gene expression was also detected in fetal bovine brain and in newborn mouse brain. These findings indicate the possibility of DMP1 expression in other soft tissues. In the present study, to clarify the significance of DMP1 expression in nonmineralized tissues, we made a specific antibody to mouse DMP1 peptides and demonstrated that DMP1 protein was localized in mouse brain, pancreas, and kidney by immunohistochemistry. Further DMP1 mRNA was detected in nonmineralized mouse tissues including liver, muscle, brain, pancreas, and kidney by RT-PCR. Based on the evidence that the localization and the expression of DMP1 are not restricted to mineralized tissues, we assume that DMP1 may have functions other than the regulation of mineralization.

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The levels of HBV DNA in tear specimens from young children were high. Tears were confirmed to be infectious, using chimeric mice. Strict precautions should be taken against direct contact with body fluids from HBV carriers with high-level viremia.

LN metastasis is regulated not only by the characteristics of cancer cells but also by microenvironmental factors of lymphatics and neutrophils, especially at the invasive front.

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(J Neurol Neurosurg Psychiatry 2001;70:696-699)