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,...

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We investigated clinicopathologically the pyramidal signs, including spasticity, hyperreflexia, and Babinski's sign, and the involvement of the pyramidal tract and primary motor cortex, in seven Japanese autopsy cases of multiple system atrophy (MSA). Pyramidal signs were observed in six (86%) of the seven autopsy cases. Hyperreflexia and Babinski's sign were each evident in five patients, but spasticity was observed in only one patient. Loss of Betz cells and presence of glial cytoplasmic inclusions in the primary motor cortex were noticed in all seven cases. Astrocytosis in the fifth layer of the primary motor cortex was noticed in five cases, but its presence was not related to the duration of the disease. Involvement of the pyramidal tract in the spinal cord, particularly of the small myelinated fibers, was observed in all seven cases, but no involvement of the pyramidal tract in the midbrain was evident in any of the six cases in which this structure was examined. In MSA, pyramidal signs were shown to be present more frequently than believed before, and the clinicopathological correlation between pyramidal signs and involvement of the pyramidal tract was obvious. Constant involvement of Betz cells in MSA has not been reported. Our clinicopathological findings may also make a contribution to the understanding of the clinicopathological hallmarks of MSA.

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