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.

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Cytokines are thought to play an important role in cellular loss and apoptosis during the repair of granulation tissue. In order to investigate the role of apoptosis following the administration of basic fibroblast growth factor (bFGF) to a wound, the present study examined the relationship between the degree of granulation tissue formation and the level of apoptosis in rat skin incisional wounds, following treatment with an intradermal injection of bFGF (0.1 microg and 1 microg per cm of wound). Histological assessment of the width of the wound tissue showed that the degree of granulation tissue in the 1 microg-bFGF-treated group had increased by day 7, but then subsequently diminished by days 14 and 28. The TUNEL index increased rapidly from day 1, peaking on day 7, with the index being higher in the 1 microg-bFGF-treated group on days 4, 7, and 14, when compared with a control group. In parallel with a marked increase in the TUNEL index over the first 14 days, the number of cells positive for vimentin and CD3 in the 1 microg-bFGF-treated wounds had decreased by day 14. The number of PCNA-positive cells, an indicator of cell proliferation, peaked on day 4 in the bFGF-treated wounds and then declined rapidly. On the basis of these results, it is suggested that the suppression of granulation tissue formation in bFGF-treated wounds is mainly due to an early and persistent increase in apoptosis in the granulation tissue cells. The expression of both transforming growth factor (TGF)-beta1 and bFGF was also elevated in the bFGF-treated wounds on days 4 and 7, suggesting that fibroblast apoptosis was induced by bFGF treatment. Unexpectedly, on day 28, the wound breaking strength was not reduced in the bFGF-treated wounds. These results indicate that apoptosis regulation following bFGF administration to an incisional wound may lead effectively to granulation tissue formation and promote a scar-less repair process.