Biomedical subjects
Publications and source records attributed to W Hort.
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By modification of a miniaturized technique for transcatheter endomyocardial biopsy, it was possible to insert a bioptome through a 6 French catheter in 15 infants and children aged 40 days to 17 years and weighing 3.5 to 55kg. Eight right and 7 left ventricular biopsies were performed, and the specimens were examined by light and electron microscopy. In one child we failed to obtain a specimen. There were no complications. Diagnoses to be either proved or excluded were hypertrophic or dilated cardiomyopathy, endocardial fibroelastosis, glycogen and lipid storage disease, tumours and myocarditis. Morphological examination was diagnostic in 2 cases, helpful in 10 cases and of no help in 2 cases. by this technique it is possible to prove endomyocardial diseases with a high degree of reliability in infants and children without increasing risk or stress.
UNLABELLED: In order to study the etiology, the clinical course and the prognosis of patients with DCM, clinical, morphological (endomyocardial catheter biopsy), angiographic and hemodynamic data of patients with DCM were studied. The total number of patients was 396. In 258 patients definite DCM was diagnosed, in 138 patients DCM was suspected, e.g., because of an additional history of alcoholism. ETIOLOGY: In no case acute subacute or chronic myocarditis was found in myocardial biopsies (n = 114) and at autopsy (n = 18). However, from the history strong evidence was obtained for DCM being the late stage of diphtheric heart disease predominantly among patients with complete left bundle branch block. As far as the alcoholic etiology is concerned, the only significant difference between DCM and alcoholic heart disease was a higher proportion of women among patients with DCM (28% and 5%, resp.). Clinical course and prognosis: 221 patients were studied prospectively (mean follow-up time 3.1 +/- 2.3 years), 44% of patients died or deteriorated. However, in patients with normal cardiothoracic ratio this rate amounted only to 12%. The mean annual mortality rate was 9.8% and varied significantly in relation to different subsets of patients from 0% to 17%. A bad prognosis was significantly indicated by young age, high cardiothoracic ratio, pronounced elevation of enddiastolic volume index and of left ventricular enddiastolic pressure at rest and of mean pulmonary artery pressure at exercise, by severe morphologic changes of myocardial biopsies, severe ventricular arrhythmias, the absence of transient abnormal elevation of arterial blood pressure during follow up, of complete left bundle branch block and of a positive history of diphtheria. However, the wide scatter of data diminished the significance of them for the definite prognostic evaluation of individual case. The cumulative survival curves of patients with a history of alcohol abuse did not differ from that of patients with DCM. The data demonstrate that DCM in patients with the history of diphtheria together with left bundle branch block is possible caused by an inflammatory process. According to the analysis of the clinical course and the prognosis, DCM is one of the most severe heart disease. However, in different subsets of patients, the clinical course may be stable for long time and even normal longevity cannot be excluded.
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Different kinds of cell motility are reviewed in this paper with special regard to development and ultrastructure. The variety of animal cell motility types can be reduced to three principles : ciliary and ameboid movements and muscle contraction. The ultrastructure of all kinds of cilia is very similar from single cell organisms to highly specialized cells of the human body e.g., ciliary respiratory epithelium. As a rule, ciliary movement is caused by minimal sliding of the nine double tubules consisting of tubulin, a protein differing from myosin and actin. Ameboid movement and muscle cell contraction are based on the sliding filament mechanism of actin and myosin. Although the principles of this mechanism have not changed during evolution some differences in the structure and arrangement of actin and myosin filaments occurred. Obviously, the high degree of order of the myofibrils of vertebrate heart and skeletal muscle cells has developed from loose and rapid changing arrangement of contractile filaments in ameboid cells. There are some changes of residues in the actin and myosin molecules during the development of the intracellular contractile system. Finally, some peculiarities of the myocardium, its special arrangement of muscle cells and some disturbances of the contractile filaments under pathologic conditions are discussed.
Seventy-five livers with metastases were cut sagitally into 1 cm thick slices. A total number of 11,581 metastases sections was exactly mapped. There was an average of 154 metastases sections per liver. The average diameter of the metastases was 1 cm. 40% of the metastases reached to the hepatic surface, and 60% were invisible due to their deposition in the internal parenchyma. In 8% of the livers there were only superficial metastases (average 3.2 metastases), and in 12% were only deep metastases detected (average 2.6). The total number of superficial metastases increased with increasing diameter of the secondary tumors. An approximately homogeneous distribution of hepatic metastases within the liver parenchyma has been demonstrated.
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Postmortem coronary angiographies with a pressure of 100 mm Hg were performed on 50 human hearts with various degrees of coronary arteriosclerosis. The frequency and degree of narrowing of arterioles and small intramural arteries up to diameters of 400 mu were investigated by giant sections through the whole myocardium. The frequency of stenosing intimal lesions depended on the diameter of the arteries. Mostly (1.8%) small arteries with a diameter between 100 and 200 mu were affected. As a rule the degree of narrowing was unimportant. Only in 23% it surmounted 20%, in nearly 5% it exceeded 30% and only in 0.5% the level of 50% was surmounted. In the different layers of the left ventricular myocardium and of the ventricular septum no significant differences in the frequency of stenosing intimal lesions could be found. But in the right ventricular wall an evidently inferior frequency was determined. There was a significant increase of stenosing lesions with age but not with increasing heart weight. As a rule we observed an inversed correlation between the degree of coronary arteriosclerosis and the frequency of stenosing lesions of arterioles and small intramural arteries. Perhaps a severe coronary atherosclerosis protects the small intramural arteries against intimal lesions. We conclude from our results that only very seldom a stenosis of small intramural arteries and arterioles causes ischemic myocardial lesions.
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The development of a cardiac hypertrophy depends on modulation of two parameters, such as the amount of increased work load imposed on the heart and the rapidity with which the work load is applied. A gradual development of cardiac hypertrophy is usually observed in humans; at variance, the induction of cardiac hypertrophy is quite a rapid process in animal experiments. The enlargement of cardiac muscle cells during hypertrophy is due not only to an increased synthesis of contractile proteins but also to an accumulation of other cell constituents parallelly involved in the hypertrophy process. The mechanism whereby new sarcomeres are formed during cardiac hypertrophy is not yet completely clarified. Once the stimulus producing overload is removed, cardiac hypertrophy can regress completely. The possible role of biological regulators in inducing cardiac hypertrophy was also discussed.
137 hears with 185 infarctions with a diameter of at least 2.5 cm were investigated. Sometimes the infarcted areas were supplied by two arteries. Altogether there were 198 arteries supplying infarcted areas (= IA) and 213 arteries supplying non-infarcted areas (= NIA). The cross-sectional area of most severe stenosis of each coronary artery was determined and expressed in per cent of the area surrounded by the lamina elastica interna. Only two groups of infarctions were formed: recent infarcts (without and with organization) and old infarcts (completely scarred). Regarding all IA and NIA there were highly significant differences between the mean values. The rest of the lumen amounted in the IA 7.48% and in the NIA 38.20%. In hearts with recent infarcts, IA were significantly smaller (4.13%) than in hearts with old infarcts 8.75%). This difference is due to recanalizations in the group of old infarcts. Differences between the degree of stenosis of sole and repeated infarcts were missed and there was no correlation between the weight of the heart and the cross-sectional area of IAs. The IA of hearts with transmural infarction were constricted more strongly than those of hearts with subendocardial infarcts. 21 IA were larger than one NIA of the same heart. Most of these hearts included old infarcts and it is most probably that during the origin of the infarctions almost all of these IA were smaller than the NIA. The findings strongly support the coronarogenic origin of myocardial infarctions.
36 consecutive patients with chest pain and/or severe ventricular dysrhythmias, but normal coronary arteries and normal left ventriculogram, underwent thallium-201 myocardial imaging at rest and during exercise. The myocardial scintigram was abnormal in 27 patients (group A) and normal in only 9 patients patients (group B). To answer the question, whether the scintigram was false positive or a correct expression of a myocardial disorder not detectable with angiocardiographic methods, we compared the scintigraphic results with the findings of resting and exercise ECG (n = 36), mean pulmonary artery pressure during exercise (n = 27), myocardial lactate extraction during highrate atrial pacing (n = 14) and light- and electronmicropic examination of right ventricular endomyocardial biopsies (n = 14). The resting ECG was abnormal in 7 of 27 patients of group A and 1 of 9 patients of group B, the exercise ECG in 20 of 27 patients of group A and 1 of 9 patient B. An abnormally elevated exercise pulmonary artery pressure was measured in 10 of 21 patients of group A and 1 of 6 patients of group B. High rate atrial pacing induced an abnormal myocardial lactate extraction in 3 of 13 patients of group A, but not in the single investigated patient of group B. All 12 examined patients of group A and 1 of 2 patients of group B had abnormal biopsy findings. The high incidence of abnormal findings in group A compared to the rare incidence in group B suggests, that the abnormal myocardial scintigrams in patients with chest pain and normal coronary arteries is likely not false positive but reflects a myocardial disorder not being recognized on angiography.
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In the hearts of 100 unselected adult autopsies (average age 65 years) the coronary arteries and their major branches were investigated. After opening the lumen, the vessels were measured, and the location of all sclerotic lesions was identified, including fatty streaks. The frequency of distribution of advanced sclerotic changes was similar to that of lipid and fibrolipid plaques. 1003 major coronary artery branches were studied. 25% of them showed sclerotic changes in contrast to 92% in the coronary arteries themselves. There was a good correlation between the sclerotic lesions in the coronary arteries and their branches: no changes were found in the branches the corresponding stems of which were unchanged. In contrast to that, sclerotic branches nearly always originated from sclerotic areas of the coronary arteries. Branches of the left anterior descending artery were more frequently affected by atherosclerosis (39%) than branches of the right coronary artery (17%). Contrary to the right coronary artery sclerotic changes of the proximal branches of the left anterior descending and the left circumflex artery were significantly more frequent than sclerotic lesions of the distal branches. The frequency of sclerotic lesions in the branches was similar to that in the coronary arteries; the proximal part was more frequently affected than the distal one. In addition, the peripheral decreasing frequency of sclerotic changes, which was found to be more pronounced in the left coronary arteries than in the right one, showed a similar behaviour in the corresponding branches. Our investigations indicate the vessel's diameter to be a significant (but not the only) factor in atherosclerosis development in coronary arteries and their branches. In case of a corresponding size of lumen, the frequency of sclerotic changes in the coronary arteries was approximately the same as in their branches.
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In a total of 21 mongrel dogs a comparison between intravital and postmortal coronary arteriograms was made so as to establish the difference in vessel diameter. Fresh postmortal hearts injected in situ showed an average increase in coronary vessel diameter of approx. 6 per cent. Examinations of 24 hour postmortal hearts which were removed from the animals showed a vessel diameter increase of barely 20 per cent in the mean. These 20 per cent correspond fairly well with literature information about the maximal widening of coronary vessels with nitroglycerin. Nerves which are still functioning, and humoral substances which may influence the still living muscle in vessel walls are supposed to be the reason for the smaller increase in fresh postmortal in situ illustrated coronary arteries. It must be stressed, that the measured differences between intravital and postmortal coronary artery diameters can only be representative of wall sections free of arterioslcerosis.