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Biomedical subjects

E Falk

Publications and source records attributed to E Falk.

At least 91 records · Page 5Linked to original sources
PubMed1985

Non-epithelial basement membrane thickening in the urinary tract associated with phenacetin abuse.

In four cases of capillarosclerosis in the urinary tract associated with analgesic (phenacetin) abuse, the basement membrane (BM) thickening was not confined to the subepithelial capillaries, but was also found around the smooth muscle cells in the luminal part of the tunica muscularis. Electron microscopy confirmed that the changes in the BM around the smooth muscle cells were similar to those seen around capillaries. This non-vascular affection of BM in the urinary tract in patients with phenacetin abuse has not been reported previously. Thus, capillarosclerosis appears to be only part of a BM disorder, that clearly diminishes in intensity with increasing distance from the lumen. It is therefore suggested that the changes are caused by some agent (possibly a metabolite) in the urine diffusing from the lumen into the wall of the urinary tract.

Aged↗
PubMed1985

Embolization from angiographic catheter during angiography simulating vascular spasm. Report of a case with postmortem verification.

The initiating event in the pathogenesis of acute coronary thrombosis, especially the role played by vasospasm, remains controversial. Recently an angiographic sequence of events has been reported which should conclusively prove that spasm of a normal coronary artery might lead to occlusive thrombosis. The patient survived, and thus this conclusion was reached without morphological verification. The present report describes an almost identical angiographic sequence of events in a cerebral artery initially interpreted in the same way: spasm leading to thrombosis. The patient died, and an embolus derived from the angiographic catheter was found at postmortem examination exactly where angiography had shown "spasm". A "catheter embolus" simulating vascular spasm could as well explain the basic angiographic findings in the previously reported case. Thus, it still remains to be proved that spasm of a normal artery may lead to occlusive thrombosis.

Aged↗
PubMed1985

Uremic arterial disease in rabbits with special reference to the coronary arteries.

In rabbits with chronic renal failure of 9 months' duration, the distribution and morphological characteristics of uremic arterial disease were investigated, with special reference to the coronary arteries. All major systemic arteries were affected, large vessels more severely than smaller ones, and within each artery the changes were most pronounced in the proximal part of the vessel. The intimal lesions consisted primarily of smooth muscle cells without calcification or lipid accumulation. A reduction of the lumen exceeding 50% of the normal cross sectional area was not seen and mural thrombosis was not encountered. In the media, degenerative changes with increased amounts of proteoglycans and calcifications were prominent, but foci of increased cellularity were also seen. There was no evidence of lipid accumulation in the media either. Similar changes were found in the coronary arteries, but coronary angiography revealed no irregularities or stenosis. The calcified medial degenerative changes and intimal cellular lesions without lipid accumulation in non-cholesterol-fed rabbits distinguish uremic arterial disease from atherosclerosis.

Animals↗
PubMed1985

Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion.

Extensive microscopic examination of epicardial arteries and myocardium was performed in 25 cases of sudden death due to acute coronary thrombosis. Eighty-one percent of the thrombi had a layered structure with thrombus material of differing age, indicating that they were formed successively by repeated mural deposits that caused progressive luminal narrowing over an extended period of time. This episodic growth of the thrombus was accompanied by intermittent fragmentation of thrombus in 73% of the cases, with peripheral embolization causing microembolic occlusion of small intramyocardial arteries associated with microinfarcts. The period of unstable angina before the final heart attack was, in all but one of 15 patients, characterized by such an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation seemed to have alternated with intermittent thrombus fragmentation. The culmination of this "dynamic" thrombotic process in total vascular occlusion caused the final infarction and/or sudden death.

Adult↗
PubMed1984

Fatal atherosclerosis developed in less than 4 years in an aortocoronary vein graft in a hyperlipidemic patient.

It is generally believed that it takes decades to develop a complicated atherosclerotic plaque. This view is challenged by the present case describing a hyperlipidemic patient who died of vein graft atherosclerosis less than 4 years after otherwise successful coronary bypass surgery. Although the atherogenesis may be accelerated in autogenous coronary vein grafts compared with native coronary arteries, the present case illustrates that complicated atherosclerosis may develop in the course of only a few years if appropriate conditions prevail.

Adult↗
PubMed1983

Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis. Characteristics of coronary atherosclerotic plaques underlying fatal occlusive thrombi.

Ruptured atheromatous plaques were identified by step-sectioning technique as responsible for 40 of 51 recent coronary artery thrombi and 63 larger intimal haemorrhages. The degree of pre-existing luminal narrowing at the site of rupture was decisive for whether plaque rupture caused occlusive thrombosis or just intimal haemorrhage. If the pre-existing stenosis was greater than 90% (histologically determined) then plaque rupture nearly always caused occlusive thrombosis. Clearly indicating the primary role of plaque rupture in thrombus formation were the frequent finding of plaque fragments deeply buried in the centre of the thrombus and the nature of the thrombus at the site of rupture where it consisted predominantly of platelets. Thus, a severe chronic stenosis seems to be a prerequisite for occlusive thrombus formation, but the thrombotic process itself is triggered by an acute intimal lesion.

Adult↗
PubMed1982

Coronary artery narrowing without irreversible myocardial damage or development of collaterals. Assessment of "critical" stenosis in a human model.

Postinfarction cardiac rupture is the result of thrombotic occlusion of a functional end artery with no previous myocardial damage in the perfusion area of the occluded artery. The pre-existing atherosclerotic stenosis at the site of thrombosis is thus"non-critical" in relation to development of collateral vessels and/or irreversible myocardial damage. Eleven cases of postinfarction cardiac rupture were studied by microscopy of cross-sections of the thrombosed segments. At the site of the thrombosis, pre-existing atherosclerosis had narrowed the lumen to 11% or less of its normal cross-sectional area. Maximal pre-existing narrowing of the proximal left anterior descending artery was found in a case with 97% stenosis (histologically measured cross-sectional area reduction) and an estimated residual lumen of 0.71 mm2. The prestenotic luminal area which is usually considered angiographically as "normal" was in all cases shown histologically to be severely narrowed by a diffuse intimal thickening. It is concluded that organic coronary stenosis must be far greater than 75% to be responsible for the development of collateral vessels and/or irreversible myocardial damage.

Aged↗
PubMed1981

Amyloid deposits in calcified aortic valves.

Thirty-nine severely calcified aortic valves surgically removed were studied for amyloid deposits using the alkaline Congo red stain. Amyloid deposits were found in all the valves, in such quantities that they could be demonstrated using screening magnification (x40). A close topographic relationship was found between amyloid and calcium deposits. In addition, histological evidence was found of prolonged fibroblast proliferation. In the light of more recent studies, which identify Congophilic cytofilaments in fibroblasts, as well as demonstrating fibroblast degeneration and decomposition in senile aortic valves, the following pathogenesis is suggested for "calcific aortic stenosis": Mechanical injury of malformed aortic valves leading to fibroblast proliferation; fibroblast degeneration and decomposition with extracellular accumulation of cellular degradation products (among others Congophilic cytofilaments); calcium deposits in the cellular degradation products resulting in "calcific aortic stenosis".

Adult↗
PubMed1980

Haemangiopericytoma of bone. Review of the literature and report of a case.

A case of intraosseous haemangiopericytoma of the humerus is described. Exarticulation at the shoulder joint was performed and the patient has been followed for 8 years, so far without developing a local recurrence or metastases. The 16 cases of intraosseous haemangiopericytomas on record are reviewed.

Aged↗
PubMedDate not supplied

The histology of myocardium in malignant hyperthermia: a preliminary report of 11 cases.

The preliminary results of a retrospective examination of the myocardium from 11 patients who responded to general anaesthesia with malignant hyperthermia are presented. Light-microscopical examination of the sections revealed no specific changes due to malignant hyperthermia. Contraction bands were demonstrated in 4 cases and it is concluded that the present investigation does not support the suggestion that a specific myofibrillar damage is responsbile for the arrhythmias seen in malignant hyperthermia.

Adult↗
PubMedDate not supplied

A case of sudden cardiac death in connection with Salmonella typhimurium infection.

A case of fatal myocarditis in a 24-year-old otherwise healthy man is described. It was possible to cultivate Salmonella typhimurium from the alimentary tract, the blood, the liver and skeletal muscles. The possibility of a solitary myocarditis with fatal outcome due to Salmonella typhimurium infection is discussed. Such a case seems not to have been mentioned previously in the literature. The problems concerning the statistical registration of such a death are briefly discussed.

Adult↗
PubMedDate not supplied

Thrombus organization plays no major role in late neointimal formation after angioplasty in porcine coronary arteries.

Thrombus organization has been suggested to play a major role in late neointimal formation after coronary angioplasty. We sought to describe the time sequence of lesion formation after angioplasty in porcine coronary arteries and to quantify the relation between early thrombosis and late neointimal formation. Deep vessel wall injury was induced by conventional balloon angioplasty in the circumflex (CX) and right coronary (RCA) arteries and by retraction of a chain-encircled balloon in the left anterior descendent artery (LAD). Lesions were assessed by histomorphometry at days 0, 1, 4, 7, 14, 28, and 56 after angioplasty. A response-to-injury index (lesion area/injury length) was determined for each artery. Angioplasty led to rupture/removal of media. Thrombus was present at the exposed adventitia at days 0, 1, and 4. From day 7, neointima was observed on the luminal side of the arterial wall. All thrombus had disappeared at day 28, at which only neointima was observed. Histomorphometry revealed that lesion formation after angioplasty was a gradually increasing process from day 0 to day 28 with no further growth from day 28 to day 56. Maximal thrombus size (day 4, RCA: 0.07+/-0.04 mm, CX: 0.23+/-0.16 mm, LAD: 0.15+/-0.11 mm) was significantly smaller than late neointimal formation (day 28, RCA: 0.68+/-0.18 mm, CX: 0.63+/-0.23 mm, LAD: 0.71+/-0.18 mm) in all three arteries (p < .03). Lesion formation after angioplasty is a gradually increasing process for 4 weeks. Maximal thrombus size is about four times smaller than late neointimal formation. Thus, thrombus organization plays no major role in late neointimal formation.

Angioplasty, Balloon, Coronary↗