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W Hort

Publications and source records attributed to W Hort.

At least 55 records · Page 3Linked to original sources
PubMed1989

[Pathologic-anatomic findings in sudden heart death].

Sudden cardiac death can be caused by a large variety of pathological conditions detected morphologically. In most cases it is the result of coronary sclerosis. A coronary thrombus is not only found in myocardial infarction, but also frequently occurs in unstable angina without infarction. In most instances these thrombi develop following rupture of an atheromatous plaque. A higher risk of sudden cardiac death is associated with abnormalities of the coronary ostia, most commonly an anomalous origin of the left coronary artery from the right sinus. HOCM is the most important cardiomyopathy causing sudden cardiac death in young athletes. Furthermore, myocarditis, pathological changes of the conduction system, and other rare conditions can lead to sudden cardiac death. A particular set of diseases contributes to sudden cardiac death in the young. Occasionally, disturbances in the texture of the ventricular septum can be found that have so far not been described in the literature. Acute arrhythmias hold a key position among the pathophysiological mechanisms leading to sudden cardiac death.

Cause of Death↗
PubMed1989

[Pattern of the coronary endothelium in the human].

The ultrastructural morphology of the endothelium of the normal human coronary arteries is equal to the endothelial cells of other locations in the macrovascular system. However, the patterns of the endothelial nuclei and the endothelial cell shape are consistent with unidirectional laminar blood flow conditions lacking secondary flow phenomena in this particular part of the arterial tree. On the other hand secondary flow probably occurs in areas of sclerotic plaques and a "cobblestone" pattern of the endothelial layer is often found at such places. In addition, multinuclear giant cells which might be of a heterogeneous origin, as well as other non-endothelial cells are a regular constituent of the endothelial layer of sclerotic lesions in the human coronary arteries.

Coronary Artery Disease↗
PubMed1989

[The endothelium and arteriosclerosis].

The endothelium is of great importance in the development of early atherosclerotic lesions, as suggested from animal experiments. Denudation of the endothelium may stimulate the proliferation of smooth muscle cells which are a major constituent of sclerotic plaques. Furthermore, injury of the endothelium causing no morphologic alterations may be enough to induce secretion of endothelial-derived growth factors or attachment of monocytes/macrophages at the endothelial surface. Recent immunohistochemical studies indicate that monocyte-derived cells can be included in the endothelial layer, but the function of such non-endothelial cells is not yet known. Endothelial cells at the surface of advanced sclerotic lesions are often structurally abnormal. The endothelial patterns at the shoulders of stenotic lesions indicate blood flow irregularities, but on the other hand, the endothelium of the stenotic channel is suggestive of an unidirectional laminar flow. Atherosclerosis in humans is the touchstone of experimental atherosclerosis.

Animals↗
PubMed1988

[Differential diagnosis and prognosis of primary and post-myocarditis cardiomyopathy in childhood].

It is still difficult to differentiate between the various stages of myocarditis and primary dilated cardiomyopathy (DCM). Hence, we analyzed the history, as well as the laboratory and virological data of 22 children with a dilated, poorly functioning left ventricle, aged 2 months to 16.7 years (m = 4.2 y), on whom we had performed endomyocardial biopsies about 4 months after the beginning of the illness. Specimens were investigated by light and electron microscopy and, in addition immunoserological (n = 15) and immunohistological investigations (n = 7) were performed. On the basis of cellular infiltration in the histological examination we diagnosed resolving/resolved myocarditis in 6 patients and DCM in 15 patients. Previous respiratory infection or sudden onset were found in 40-50% of patients in both groups. Antimyolemmal and antisarcolemmal antibodies showed no preference. Follow-up (3.1 +/- 2.8 years) of the patients showed equal mortality (33% vs. 38%) in the post-myocarditis and DCM group. Complete normalization of all findings in 3 patients of the DCM group makes the classification among the post-myocarditis group probable, which would, then give a lower mortality rate (22% vs. 46%) and a chance of restitution in 55% of cases. In any one specific case all the diagnostic methods do not allow undoubted distinction between both entities. The prognosis of myocarditis seems to be better than that of DCM in childhood.

Adolescent↗
PubMed1988

Regression of cardiac hypertrophy: morphometric and biochemical studies in rat heart after swimming training.

There is currently little information about the morphological changes of the myocardium accompanying the reversal of cardiac hypertrophy. In this study the hypothesis was tested that myocardial alterations induced by exercise will regress within a short interval after the end of training. Rat hearts were examined using morphometric and biochemical methods at the end of a 9-week period of endurance training and also 7, 10 and 14 days after its termination. At the end of the training period the heart weight had increased by 65% but the weight ratio of the right and left ventricular wall remained unchanged. A decline in the DNA content by 27% as well as a decrease in the volume density of the interstitial space by 14% and in the number of interstitial cell nuclei by 32% against controls, are explained by a 30% increase in the width of myofibres. The capillary density was reduced by 22% but the volume density of capillaries remained nearly constant as a result of widening of the capillary diameter by 27%. The surface density of capillaries was diminished by 10%. Ultrastructurally an increase in the ratio of mitochondrial to myofibrillar volume density was observed in the myocytes of hypertrophied hearts as compared to controls (0.54 and 0.63, respectively). Fourteen days after termination of training, 80% of the increment in heart weight had regressed. At this time the width of the myofibres and the volume density of the interstitial space had nearly normalized, while the capillary to fibre ratio had significantly increased. The ratio of mitochondrial and myofibrillar volume density became nearly normal, and a confluence of intermyofibrillar mitochondria resulted in significantly longer organelles. The increased DNA content 10 days after the training, as compared to controls, is attributable to the genesis of non-myocardial cells during the hypertrophic growth and their persistence during regression. The study has shown that cardiac hypertrophy induced by physical training nearly completely regresses within 14 days after termination of conditioning. The increased capillary to fibre ratio indicates neoformation of transversely oriented capillary branches in hypertrophy which particularly becomes apparent in two-dimensional estimation in the regression period. In comparison with myofibres, regression of capillaries seems to be delayed. The decline of heart weight and a significantly diminished RNA content during the regression of hypertrophy suggest that reduced synthesis is responsible for the decrease in heart weight.

Animals↗
PubMed1988

Ultrastructural findings in endomyocardial biopsy of patients with Kearns-Sayre syndrome.

Kearns-Sayre syndrome is clinically defined by progressive external ophthalmoplegia, atypical retinitis pigmentosa and the potential occurrence of complete atrioventricular (AV) block. Right septal endomyocardial biopsy specimens from nine patients (four men and five women with a mean [+/- SD] [corrected] age of 36.3 +/- 14.4 years) with chronic progressive external ophthalmoplegia and mitochondrial skeletal myopathy were studied. Three patients had atypical retinal pigmentation. An atrioventricular or intraventricular conduction defect was observed in five patients. A pacemaker was prophylactically implanted in one patient because of abnormal conduction distal to the His bundle. Ultrastructural investigations revealed mitochondriosis in many heart muscle cells and an increased variability of mitochondrial form and size in all patients. In seven patients, 0.4 to 2.1% of all examined myocytes contained exclusively abnormal mitochondria. Three main types were observed: huge, mainly round mitochondria with concentric cristae; large, round or oval mitochondria with transverse or curved cristae; and small, vacuolated mitochondria. The volume density of myofibrils was reduced (41.9 +/- 11.1 compared with the normal value of 56.5 +/- 2.5 volume density [in percent], p less than 0.01) in these myocytes. Increasing numbers of vacuolated mitochondria correlated significantly with a reduction of myofibrils (r = -0.64, p less than 0.01). The data suggest that the ventricular myocardium of most patients with complete and even incomplete Kearns-Sayre syndrome is affected by disseminated mitochondrial cytopathy.

Adolescent↗
PubMed1988

[Growth of coronary artery branches--morphometric studies of corrosion preparations of the interventricular branch of the left coronary artery in the pig and piglet].

In corrosion casts of the left anterior descending coronary artery and its branches of higher anterior order, their length, diameter, and number of branches were examined in hearts of seven mature and seven young pigs. We systematically analyzed 95 branches in the corrosion casts of the mature pig hearts and 76 branches within the corrosion casts of the young pig hearts (left anterior descending coronary arteries and branches of 1st-5th order). The lengths of the branches of 1st order and the diameters of the branches of 1st and 2nd order had increased to the same degree as the lengths and diameters of the main trunk of the left anterior descending coronary artery and the linear measurements of the hearts. In the area of the more peripherally located branches, the differences showed a tendency to decrease. The number of branches differed only slightly between mature pigs' and young pigs' corrosion casts. These results show that during physiologic growth, no or only unremarkable new development of coronary artery branches occurs.

Animals↗
PubMed1987

[The combination of atrial myxoma and multiple skin myxomas: a characteristic symptom complex?].

In 1980, a then 7-year-old boy from Yugoslavia had an atrial myxoma removed. Since then there have been no abnormal cardiac signs or symptoms. Between 1982 and 1986 five cutaneous myxomas in the trunk region were removed. None of the tumours had histological signs of malignancy. These observations can be fitted into the symptom complex (described in 1985 by Carney et al.) of cardiac myxoma, cutaneous myxoma, changes in skin pigmentation, and abnormal endocrine functions--although not all signs need be present together. A disposition towards the development of myxomatous tumours is to be assumed in these patients. One should, therefore, always suspect an occult cardiac myxoma in the presence of multiple cutaneous myxomas. Appropriate diagnostic measures need to be taken before the typical and sometimes lethal consequences of a cardiac myxoma have occurred.

Child↗
PubMed1987

Dilated cardiomyopathy in childhood: problems of diagnosis and long-term follow-up.

Clinical profile and course of 13 infants and children (median age 2 years, range 2 months to 17 years) with dilated cardiomyopathy are presented. Endocardial fibroelastosis and myocarditis were excluded by transvascular endomyocardial biopsy. Elevated cardio-thoracic ratio (mean 0.67), depressed fractional shortening (mean 13%) and cardiac index (mean 2.52 l min-1 m-2) were the indicators of congestive heart failure. During a mean follow-up of 41 months (range 6 to 204 months) five patients died, four remained in a stable condition, four improved. The main complications were rhythm disturbances (23%) and thrombus formation (15%). We could not identify any predictors of survival.

Adolescent↗
PubMed1987

[Endomyocardial biopsy in childhood--experiences in 60 pediatric patients].

In 60 pediatric patients, aged from 1 month to 22 years (median 3.54) and a bodyweight of 3 to 67 kg (median 12.6 kg) transvascular endomyocardial biopsy was performed from the right (35 patients) or left ventricle (30 patients). The specimens were investigated by light and electron microscopy. Immune serological investigations were performed in 22 patients, immune histological examinations in eight. There were three indications for biopsy: a. 29 children had a poorly functioning, dilated left ventricle. Of these, seven suffered from endocardial fibroelastosis, 16 from dilated cardiomyopathy, six (plus one control-biopsy) from healing/healed or chronic myocarditis. b. 17 children showed inadequate left ventricular hypertrophy. Of these, ten suffered from HCM, four from secondary hypertrophy, three from storage diseases. c. Various questions were answered in eight children - four with hypoxic, two with cytotoxic myocardial damage. There were five misindications, retrospectively. We observed no serious complications. Evaluation of biopsy revealed diagnostic findings in 11.7%, was helpful in 71.7% and of no help in 16.6%. Hence, even in childhood, endomyocardial biopsy is a diagnostic tool which can contribute useful information on the etiology or pathogenesis of the underlying myocardial disease.

Adolescent↗
PubMed1986

Cardiac amyloid deposits in endomyocardial biopsies. Light microscopic, ultrastructural, and immunohistochemical studies.

In four patients with unexplained, abnormal thickening of the interventricular septum as demonstrated by echocardiography, right ventricular endomyocardial biopsy revealed unexpected cardiac amyloid deposits that resulted in increased myocardial thickness and rapidly progressive heart failure. Light microscopically, amyloid was observed in the subendocardial layer, interstitium, and walls of the intramural arterioles. Electron-microscopically, the amyloid fibrils were adjacent to the basement membranes of the heart muscle cells and the vascular smooth muscle cells. Immunohistochemical typing with specific antibodies against different amyloid fibril proteins on glutaraldehyde-fixed paraffin sections revealed different amyloid types. In two patients with generalized idiopathic amyloidosis and in two others with amyloidosis in multiple myeloma, the A-lambda form was diagnosed. In a fifth patient, AA-amyloidosis was found in familial Mediterranean fever with cardiac manifestation without thickening of the interventricular septum. The amyloid deposits were located almost exclusively within the walls of the myocardial arterioles. The amount of amyloid as observed in the myocardial biopsies correlates with the rapidly progressive cardiac failure. It is suggested that in patients with abnormal thickening of the interventricular septum of unknown origin the diagnosis should be clarified by endomyocardial biopsy.

Adult↗
PubMed1986

[Morphologic studies following coronary thrombolysis and PTCA].

Compared with those of other species human coronary arteries show a particularly marked diffuse thickening of the intima. Superimposed on this diffuse thickening local sclerotic changes develop. In early stages they contain plenty of lipids which are mainly stored in modified smooth muscle cells, partly also in cells of monocytic origin. Normally ruptures of arteriosclerotic plaques are responsible for thrombotic occlusions in extensive transmural myocardial infarctions. They are caused by ruptures of the fibrous layer covering the necrotic core of the plaque. By thrombolytic therapy platelet thrombi can be dissolved but the causal stenosing plaques remain. Arteriosclerotic stenoses can be dilated by PTCA. In doing so tears in the area of the plaque can be observed. Often there is partial detachment of the intima from the media, sometimes even extensive dissection. Proliferation of smooth muscle cells is important regarding healing of these tears. They build up a neointima and can cause restenoses in cases of massive proliferation. So far it is unknown how often platelet thrombus formations and their successive stages are involved in causing restenoses. In addition it is not yet clear how far stretching of the media and the collagenous fibers of the adventitia contributes to a permanent dilatation of the lumen after PTCA.

Angioplasty, Balloon↗
PubMed1985

The distribution of liver metastases from colonic cancer. A quantitative postmortem study.

54 livers of patients with colonic cancer were investigated in a postmortem study. 26 livers contained metastases from colon carcinoma. Assessment of the number, size and location of metastases was made. The possible interdependence of the site of the colonic primary and the location of its secondaries in the liver was examined. Results suggest an approximately homogeneous distribution of metastases from colonic cancer in the hepatic parenchyma, irrespective of the location of the primary tumour.

Colonic Neoplasms↗
PubMed1985

[Light and electron microscopy findings in early and late stages of heart failure. Studies of endomyocardial biopsies of patients with latent (LCM) and dilated (DCM) cardiomyopathy].

Right-ventricular myocardial biopsies were obtained from 28 patients with LCM (EF 72 +/- 10.4%) and 36 patients with DCM of different degrees (EF 45 +/- 15%). Using paraffin sections and electron micrographs, 16 structural variables were semiquantitatively evaluated. Hypertrophy of myofibres, and nuclear and mitochondrial alterations were significantly more pronounced in patients with DCM. A score of 9 selected variables was found to be significantly higher in the DCM-group as compared with the LCM-group. The diameter of the myofibres was significantly thicker in DCM (17.5 +/- 2.2 microns) than in LCM (14.6 +/- 0.95 microns), but no significant difference of the volume density of myofibrils and of mitochondria could be determined. In the myocytes of DCM the mitochondria were significantly smaller than in LCM. The EF correlates with the myofibre thickness, with the semiquantitative score, and with the size of the mitochondria, but no significant correlation was seen with the volume density of myofibrils or mitochondria. The study has shown: At present no alterations in myocardial biopsies are known to be diagnostic for LCM or DCM. The findings support the concept of a diffuse myocardial disease in LCM. Only one patient out of 28 exhibited a myocardium without any pathologic changes. There is no evidence for small vessel disease in LCM. From the morphological point of view DCM and LCM are different only in quantity, but not in quality of their structural alterations.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy↗
PubMed1984

[Dilated cardiomyopathy in childhood: intravital differentiation of endocardial fibroelastosis using transvascular endomyocardial biopsy].

Possibly due to the lack of clinical reports concerned with dilated cardiomyopathy in childhood, pediatric cardiologists may inadvertently designate the angiographic finding of a dilated left ventricle as endocardial fibroelastosis. We report historical and noninvasively-obtained data from twelve children, aged seven months to 17 years, with poorly-functioning dilated left ventricles, in whom no differentiation between the two diseases was enabled. Only by means of transvascular endomyocardial biopsies, performed during cardiac catheterization with a 6-F guide-catheter and a Machida bioptome for light and electron microscopal examination, was differentiation achieved among six patients with endocardial fibroelastosis and six with the nonspecific histological findings of muscular hypertrophy, interstitial fibrosis and marked degenerative changes. After exclusion of noxious and inflammatory etiologies, even in childhood, the diagnosis of primary dilated cardiomyopathy must be regarded as established. Since experience previously reported with endocardial fibroelastosis has not been based on histologic documentation of the diagnosis, questions with respect to natural history and prognosis remain unanswered.

Adolescent↗
PubMed1984

[Fibrinolysis in right ventricular thrombus].

After fracture of his toes, a 34-year-old male patient developed deep leg vein thrombosis and subsequent pulmonary embolism. Because of progressive heart enlargement, 2D-echocardiography was performed. A floating mass measuring 4.5 cm X 3.5 cm was found in the right ventricle. On account of the deep leg vein thrombosis and the lung perfusion deficits detected by scintigraphy, the floating mass was thought to be a thrombus. Because of the severity of the patient's state and the lack of success of a heparin therapy with 32,000 IU/d, fibrinolytic treatment with streptokinase was started. After initial improvement in pulmonary gas exchange the patient died about 7 hours later from progressive cardiopulmonary insufficiency. Necropsy revealed a smaller right ventricular thrombus than that seen by echocardiography. There were typical surface erosions caused by the fibrinolytic treatment. Many younger and older emboli which in part were fragmented could be shown in the pulmonary vessels. A fragmentation of the right ventricular thrombus and subsequent lethal occlusion of pulmonary vessels had to be considered. With respect to the course of the described case and some case reports in the literature we think fibrinolysis is more dangerous than surgical thrombectomy in right ventricular thrombosis.

Adult↗
PubMed1983

Differential diagnosis of hypertrophic cardiomyopathies: typical (subaortic) hypertrophic obstructive cardiomyopathy, atypical (mid-ventricular) hypertrophic obstructive cardiomyopathy and hypertrophic non-obstructive cardiomyopathy.

Previous clinical studies in patients with hypertrophic cardiomyopathies predominantly comprised patients with typical subaortic HOCM and in many other studies patients with 'hypertrophic' cardiomyopathies were investigated; i.e. no distinction was made between patients with the typical obstructive, the atypical obstructive and the non-obstructive forms of hypertrophic cardiomyopathy. In addition, in the more differentiated studies, the differential diagnosis between HOCM and HNCM was based mainly on the presence and absence of the subaortic pressure gradient. This is also true for the clinical characterization of both types of hypertrophic cardiomyopathy. Finally, diagnostic descriptions of atypical (mid-ventricular) HOCM exist only in the form of case reports, i.e. they are not based on observations in a large number of patients. Therefore a comparative study in 353 patients with hypertrophic cardiomyopathies was designed to characterize the clinical picture of patients with HNCM and with atypical HOCM in relation to typical HOCM with special reference to the differential diagnosis. The study revealed a profoundly different diagnostic profile of the three subsets of hypertrophic cardiomyopathies. The distinction between the three subsets may serve as a more differentiated basis for clinical studies related to diagnosis, therapeutic approaches, long-term follow-up observations and prognostic evaluation of patients with hypertrophic cardiomyopathies.

Adolescent↗