Hemodynamic assessment in the medical treatment of acute myocardial infarction: the effects of various vasodilators and catecholamines.
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Biomedical subjects
Publications and source records attributed to M Hiroe.
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Electrocardiography (ECG), echocardiography, nuclear method, cardiac catheterization, left ventriculography (LVG) and endomyocardial biopsy (biopsy) were performed in 40 cases of cardiomyopathy (CM), 9 of endocardial fibroelastosis (EFE) and 19 of specific heart muscle disease (SHMD), and the usefulness and limitation of each method was comparatively estimated. In CM, various methods including biopsy were performed. The 40 patients were classified into 3 groups, i.e., 1) hypertrophic (17), 2) dilated (20) and 3) non-hypertrophic . non-dilated (3) on the basis of left ventricular ejection fraction (LVEF) and hypertrophy of the ventricular wall assessed by LVG and/or echocardiography. The hypertrophic group was divided into 4 subgroups: 9 septal, 4 apical, 2 posterior and 2 anterior. M-mode scan was useful for detecting hypertrophy at the site of the ventricular septum and posterior wall, but not at the site of the anterior wall and apex. The hypertrophy was detected in 18 out of 20 cases using nuclear method. The posterior wall was hypertrophic but the septum was normal in 2 cases. In 2 of 3 non-hypertrophic . non-dilated cases, the left ventricle was oval in shape by LVG, echocardiography was normal, but significant pathological changes were seen in the biopsy, and there were abnormal ECG findings. There was no correlation between the ECG findings and the site of ventricular hypertrophy. Left ventricular ejection fraction measured by LVG (Kasser) had a closer correlation to LVEF obtained by nuclear method (multigated blood pool scan; r = 0.97) than LVEF by echocardiography (Teichholz; r = 0.79), although LVEF obtained by nuclear method was slightly higher than LVEF obtained by LVG. Myocardial perfusion defect was found in 10 of 20 cases of dilated cardiomyopathy (DCM) and the site of relative hypokinesis coincided with the site of the defect in 6 of 7 cases. A semi-quantitative myocardial perfusion defect index (PDI) and histo pathological contractility failure index (HCFI) obtained by the biopsy were devised. HCFI is the score of myocardial degeneration, fragmentation and fibrosis. The PDI plus HCFI had a close correlation with LVEF (r = -0.898). In 9 cases of DCM, LVEF was more reduced than right ventricular ejection fraction. The perfusion defect was also found in 4 cases of EFE and 4 cases of SHMD, i.e., sarcoidosis, postmyocarditis, Kugelberg-Welander disease and cardiac tumor. We conclude that the nuclear study is useful in assessing the site of the abnormal ventricular thickening, perfusion defect and ventricular function. Echocardiography is most useful in detecting ASH. The biopsy gives the sole diagnostic clue, especially in non-hypertrophic . non-dilated cardiomyopathy. ECG is useful in all cases but correlation with the site of disproportional hypertrophy was not obtained.
A 48-year-old male with a history of progressive atrioventricular conduction disturbance and a peculiar diastolic regurgitant murmur was reported. The echocardiographic examination and cineangiography disclosed an aneurysm of the right coronary sinus of Valsalva ruptured into the interventricular septum, which bulged into the left ventricular outflow tract in diastole and moved toward the septum in systole. The intracardiac phonocardiogram revealed that an unperforated sac in the interventricular septum, protruded into the left ventricular outflow tract, caused an unusual regurgitant murmur. The patient underwent successful surgical repair of the perforated orifice.
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Through an approach employing endomyocardial biopsy, early diagnosis of acute idiopathic myocarditis is possible. The histopathological findings consisted of fragmentation of muscle bundles, degenerative changes with lysis of myocytes and interstitial mononuclear cell infiltration. The cells were irregular in size and shape and contained slightly basophilic cytoplasm or were mixed with small round cells. Early clinical symptoms consisted of flu-like symptoms, i. e., higher fever, myalgia, malaise and arthralgia. Initial ECG changes consisted of complete A-V block in 9, bifascicular block in 3, and intraventricular conduction disturbance in 4 cases. Serial biopsies were performed at the early (0--2 weeks), middle (2--4 weeks), and late stages (more than 4 weeks) in 6 cases. Two of these biopsies were performed in 6 cases and all 3 were performed in one case. The numerous interstitial cell infiltration had almost disappeared by the early stage. At the late stage, either a slight or moderate degree of interstitial fibrosis was observed. These observations coincided well with the improvement of the ECG findings. Characteristic laboratory findings consisted of high LDH, GOT, and serum amylase levels. Varieties of treatments such as temporary cardiac pacing, peritoneal or hemo-dialysis, vasodilator therapy effectively to relieve the grave clinical condition. It is concluded that acute myocarditis may heal with remarkable improvement when the appropriate treatment is applied at the early stage of the disease.
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The cellular localization of endothelin (ET), a novel vasoconstrictor peptide, was studied in human vascular tissues by immunohistochemistry. Distinct and diffuse staining for ET-like immunoreactivity was demonstrated in the cytoplasm of vascular endothelial cells, but not in smooth muscle cells or adventitial fibroblasts. The specificity was confirmed by the negative results following immunoabsorption. These findings suggest that human vascular endothelial cells function as an endocrine and/or paracrine cells for ET secretion.
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is characterized by fibrofatty replacement of the right ventricular myocardium. Recently, the myocardial loss in ARVC has been suggested to be related to apoptosis. However, it is still unknown whether this phenomenon is already established in the myocardium of pediatric cases with this disease. We examined the histopathologic characteristics of the ventricular myocardium in specimens obtained from 10 patients, including 3 children with ARVC, and investigated the occurrence of apoptosis in the myocardium by terminal deoxyribonucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) assay and agarose-gel electrophoresis of DNA. Endomyocardial biopsy specimens from the 10 cases and a necropsy sample from one adult case with ARVC were examined. Histopathologic examination of biopsy specimens from the pediatric cases revealed extensive fibrosis. Typical fatty infiltration was demonstrated in one of the 3 pediatric cases. These findings were similar to those in adult cases; the histopathologic index based on the severity of myocardial damage, including myocyte degeneration and fibrosis, was not significantly different from that in adult cases. TUNEL assay revealed positive reactivity of the myocardial cells. The apoptotic index was 1.4 +/- 0.4% in children and 1.6 +/- 0.5% in adults (difference not statistically significant). Agarose-gel electrophoresis of a DNA extract of the myocardial tissue of the autopsy case revealed DNA fragmentation. Cases with idiopathic ventricular tachycardia and control cases with a cardiac transplant (with no rejection) had minimal histopathologic findings and negative reactivity in the TUNEL assay. These results indicate that myocardial damage is already established in cases diagnosed as ARVC in childhood, and suggest that the myocardial damage is closely related to apoptosis in children, as well as in adults, in this disease.