Shigeru Masuda

The effects of a myocardial bridge on coronary atherosclerosis and ischaemia

The term myocardial bridge (MB) describes the surprisingly common situation in which part of the left anterior descending coronary artery (LAD), running in epicardial adipose tissue, is covered by a bridge of myocardial tissue. The presence of an MB may influence arterial tissue through the alteration of haemodynamic forces by the myocardial contraction of the bridge itself. Histopathologically and ultrastructurally, any manifestations of atherosclerosis elsewhere in the LAD are suppressed in the intima beneath the MB. By scanning electron microscopy, abrupt changes in endothelial cell morphology indicate that the intima beneath the bridge is protected by haemodynamic factors. Furthermore, the closer the bridge to the left coronary ostium, the greater the extent of proximal intimal thickening. In parallel with this, considering the occurrence of myocardial infarction in cases of proximal MB together with previous reports on relationships between MB and coronary ischaemia, it appears that anatomical characteristics such as the location, length, and thickness of the MB have a bearing on the effects of this abnormality. When the pathologist examines the heart at autopsy, this quite common condition should be borne in mind, in view of its potential but complex relationship to atherosclerosis and ischaemic heart disease.

Absence of atherosclerosis evolution in the coronary arterial segment covered by myocardial tissue in cholesterol-fed rabbits.

The evolution of atherosclerotic lesions is suppressed in the intima of the human coronary artery, beneath myocardial bridges. To elucidate the mechanism of the protective effect, we investigated morphological changes using the rabbit coronary artery as a model. Rabbits fed a 1%-cholesterol diet were killed at intervals up to 20 weeks. Two short segments of the left coronary arteries running in the epicardial adipose tissue (EpiLAD) and subsequently running in the myocardium (MyoLAD) were compared morphologically. The intima of the EpiLAD had flat endothelial cells with a polygonal shape, and demonstrated raised atherosclerotic lesions with increase in serum cholesterol level. In contrast, the intima of the MyoLAD was free of atherosclerotic lesions throughout the study, and the endothelial cells were spindle-shaped and engorged. While ferritin particles reached only the surroundings of the internal elastic lamina in the MyoLAD, they permeated into the media of the EpiLAD. We suggest that myocardial bridges suppress coronary atherosclerosis by an alteration of endothelial permeability, which may be due to changes in haemodynamic force tending towards a higher shear stress. The data provide an insight into the relationship between haemodynamics and the development of coronary atherosclerosis.

Distribution and Synthesis of Apolipoprotein J in the Atherosclerotic Aorta

The distribution of apolipoprotein (apo) J during the development of atherosclerosis in the human aorta was evaluated by immununohistochemical observation, together with the other apolipoprotein A-I, A-II, B, C-III, and E. Although apoJ was never observed in the normal aorta (ie, without any intimal lesions or intimal thickening), it was distributed not only in the intima but also in the media of aortas with diffuse, intimal thickening or atherosclerotic lesions. Double immunostaining with antibodies for apoJ and alpha-smooth muscle actin revealed apoJ deposition in smooth muscle cells (SMCs) or the aortic stroma in the vicinity of SMCs. The extent of apoJ distribution in the aortic wall increased with the degree of atherosclerosis development. In addition, the distribution pattern of apoJ was very similar to that of apoA-I and E. In situ hybridization with human apoJ cDNA demonstrated intense signals in cells scattered within the subendothelial space and medial SMCs of the aorta with advanced atherosclerosis but not in those of the normal aorta without intimal thickening. Furthermore, reverse transcriptase-polymerase chain reaction of the cultured human aortic SMCs revealed apoJ mRNA expression in these cells. The results indicate that apoJ in the aortic wall originates from not only apoJ circulated in the plasma but also apoJ produced by SMCs in the aortic wall. Considering the similarities of the distribution between apoJ and apo-A-I or E, we hypothesize that apoJ possibly has a protective role against human atherosclerosis by its involvement with cholesterol transport from the aortic wall to the liver.

A case of basaloid‐squamous carcinoma of the esophagus: Immunohistochemical and ultrastructural studies

A case of basaloid‐squamous carcinoma of the esophagus in an 83 year old man is reported. The esophageal tumor showed a fungating growth at the junction of the middle and lower esophagus and was composed microscopically of submucosal multiple nests with solid and cribriform‐like patterns accompanied with a small focus of squamous cell carcinoma adjacent to the overlying esophageal epithelium. The structural features closely resembled those of basaloid‐squamous carcinoma. The submucosal tumor cells were immunohistochemicaliy positive for epithelial membrane antigen, wide spectral keratin, alpha actin and S‐100 protein. By electron microscopy, the tumor cells had microvilli, des‐mosomes and bundles of myofilaments, and replicated basement membranes were frequently observed adjacent to the nests. The positive immunoreaction of S‐100 protein and alpha actin and the existence of bundles of myofilaments indicated that the present tumor did not correspond well with basaloid‐squamous carcinoma. In addition, there was no evidence of true glandular lumina in the tumor nests, a finding which was inconsistent with that of adenoid cystic carcinoma. From the immunoreactivity of S‐100 protein and ultrastructural features, it was considered that the present submucosal tumor had originated from undifferentiated pluripotential primitive cells, which differentiated to myoepithelial cells.

Myocardial ischemia due to vascular systemic amyloidosis: A quantitative analysis of autopsy findings on stenosis of the intramural coronary arteries

A case is reported of a 65 year old man who suffered myocardial ischemia resulting from extensive stenosis of the intramural coronary arteries secondary to systemic vascular involvement by primary amyloidosis. In the myocardium, there were multiple fibrotic foci scattered mainly in the sub‐endocardlal region of the ventricle. Intramural coronary arteries were stenotic or occlusive due to amyloid‐induced luminal narrowing, but there was no significant stenosis of the epicardial coronary arteries. Quantitative analysis of amyloid deposits in the intramural coronary arteries demonstrated that occlusive arteries were predominant in the surrounding area of myocardial fibrosis, and the extent of coronary stenosis by amyloid deposition was significantly more severe than in hearts of the five control patients who had coronary amyloidosis without myocardial fibrosis. These results indicate that myocardial fibrosis originates from coronary Ischemia due to vascular amyloid deposition. This is the first time that the relationship between myocardial lesions and coronary amyloid deposition has been elucidated using histopathologic quantitative analysis.

Earlobe crease and atherosclerosis. An autopsy study.

The association between earlobe crease (ELC) and coronary and aortic atherosclerosis in 100 autopsied men ranging in age from 50 to 79 years, who died free of vascular diseases or related conditions, was studied in conjunction with blood pressure and serum total cholesterol (TC) levels. Earlobe crease was graded and defined as groups 1, 2, and 3 according to the depth and length in both ears. The extent of atherosclerosis in the coronary arteries and aortas was visually graded. Coronary atherosclerosis was significantly more severe in group 3 in all the decades examined than in groups 1 or 2. Aortic atherosclerosis in group 3 was significantly greater than in group 1 in all the decades examined, and was greater than in group 2 in the seventh and eighth decades. The TC level was significantly higher in group 3 than in groups 1 or 2 except in the sixth decade. Multivariate regression analyses demonstrated that the degree of ELC was dependent on the extent of coronary and aortic atherosclerosis, but was independent of age. Conversely, the extent of coronary atherosclerosis was dependent on the degree of ELC, but was independent of age. The extent of aortic atherosclerosis was, however, dependent not only on the appearance of ELC and TC, but on age. It is thus concluded that ELC provides a significant external marker for atherosclerosis and may reflect a persistent overload of atherosclerosis risk factors, such as TC.

Castleman's disease of the abdomen and pelvis: Report of three cases and a review of the literature

Three cases of Castlemans disease (CD) of the abdomen and pelvis are reported. Tumoral lesions were located in the lymph nodes of the head of the pancreas, the gastropancreatic fold, and around the left iliac artery. Histologically, all the tumoral leasions demonstrated the hyalinevascular type of CD. This unusual presentation made CD difficult to diagnose preoperatively, since these lesions more closely resembled malignant tumors on computed tomography and angiography. We discuss the problems of diagnosing and classifying CD, together with a review of the literature.

Multiple penetrating colonic ulcers in secondary amyloidosis caused by rheumatoid arthritis

An autopsy case of multiple penetrated colonic ulcers with secondary amyloidosis caused by rheumatoid arthritis in a 61 year old woman is reported. Amyloid deposition was conspicuous in the transverse colon with numerous penetrating ulcers that were circumferentially scattered. Deposition was mainly in the small vessel walls of the submucosal layers. In the quantitative comparison of the histological components between the colonic segments affected by severe and mild ulcer formation, occlusive vascular amyloid deposition was revealed more frequently in the severe involved portion than in the mild involved portion. In addition, submucosal fibrosis that tended to appear around ulcers was more extensive and thicker in the former than in the latter. The complete vascular occlusion caused by amyloid deposition was particularly concentrated in the submucosal layer adjacent to the ulcer. These findings indicate that peripheral circulatory disturbance by amyloid deposition in the small vascular walls leads to ulcer formation in the colon.

Spontaneous Rupture of Aortic Arch through an Atheromatous Plaque Resulting in Pseudoaneurysm

An autopsy case of spontaneous rupture of aortic arch through an atheromatous plaque which resulted in pseudoaneurysm is reported. The aorta was involved by severe atherosclerosis with scattered calcifications over the entire surface, and there was a fusiform aneurysm protruding from a transmural tear in the aortic arch. Histopath‐ologically, no evidence of dissection or inflammatory change was noted in the aorta, and no histologic component of the aortic media was observed in the aneurysmal wall. However, degenerative change of cystic and laminar medial necrosis were recognized near the ruptured site. Such localized degenerative change was considered to be caused by circulatory disturbance which originated from disruption of the vasa vasorum due to aortic rupture. Acta Pathol Jpn 42: 740–744, 1992.

Cardiac pseudoaneurysm caused by mitral ring calcification

A case of left ventricular pseudoaneurysm caused by mitral ring calcification (MRC) in a 71-year-old woman is reported. MRC was initially detected by two-dimensional echocardiography. Two months later, rupture of the posterior wall and pseudoaneurysm formation were diagnosed. Mitral value replacement and reconstructive surgery of the myocardial wall were performed. The patient died 46 days after the operation. At autopsy, there was no histopathological evidence of myocardial infarction, infective endocarditis, or other conditions affecting the cardiac endomyocardium. Pseudoaneurysm apparently resulted from left atrial and ventricular tears caused by MRC.