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Biomedical subjects

W E Stehbens

Publications and source records attributed to W E Stehbens.

At least 19 recordsLinked to original sources
PubMed1997

The elusive local factor in atherosclerosis.

Recent evidence confirms that local haemodynamic stresses account for the initiation, topographical localization and complications of atherosclerosis. These causative stresses are vibratory and associated with pulse pressure and the lesser vibrations of greater frequency generated by blood flow at predilection sites. This bioengineering fatigue hypothesis is further substantiated by analogous effects of repetitive stresses on erythrocytes and in the musculoskeletal system. The mechanism underlying fatigue is cumulative molecular scissions of the mural constituents which ultimately result in failure of the wall as a whole. Free radicals and oxidation products are by-products of this molecular scission in atherogenesis. This theory which explains the progressive inexorable loss of mural cohesion, its pathogenesis and complications is completely substantiated by the iatrogenic and experimental reproduction of the disease by haemodynamic means.

Animals↗
PubMed1997

Mechanisms underlying arterial fragility and the complications of atherosclerosis.

The etiology of atherosclerosis must explain the development of primary pathological complications (intimal tears, ectasia, tortuosity, aneurysms and stenoses). They are interrelated and associated with destruction of mural architecture and concomitant loss of tensile strength (fragility) attributable to bioengineering fatigue. The complications become manifested clinically by ischemia, hemorrhage and pressure effects developing with greater frequency in association with hypertension, arteriovenous shunts or connective tissue disorders. Moreover they are produced experimentally and iatrogenically by hemodynamic means but are unexplained by other current etiological hypotheses.

Adult↗
PubMed1997

Observations on the development of mural thrombi in chronic experimental aneurysms in sheep.

Observations were made on mural thrombi in experimental venous pouch aneurysms in sheep. Thrombi associated with mural tears and dissection consisted predominantly of laminated fibrin masking the earlier platelet deposition and infiltrating the wall to some extent. Thrombus growth was associated with platelet masses of Zahn and secondary fibrin deposition. Intervening spaces contained a variable quantity of coagulated plasma, fibrin mesh, leucocytes, disintegrating red cells and platelets rather than red thrombus as often suggested. Periodic deposition of platelet masses with surface rippling, the whorling patterns of laminated fibrin and mechanical disruption of red cells indicated the importance of haemodynamics. Coarse macroscopic lamination of mural thrombi was attributed in part to recurrent dissections between the wall and the mural thrombus and of the thrombus itself. These accounted for growth of thrombus with expansion of the wall and interference with organization of the thrombus. The model has proved suitable for the study of thrombogenesis and thrombus behaviour in aneurysms.

Aneurysm↗
PubMed1996

Structural and architectural changes during arterial development and the role of hemodynamics.

Hemodynamics is a major determinant in the anatomical and mural architectural development of the arterial tree. Arterial intimal proliferation commences in utero at specific anatomical sites often appearing eccentric in transverse section and precedes more diffuse concentric thickening. Regarded as an inherent structural component of the wall or an adaptive mural response to increasing hemodynamic stresses concomitant with growth, its occurrence in utero and in lower animals, though generally supportive of this view, ignores qualitative changes. Further doubt derives from the retrogressive destructive nature of structural changes in the arterial wall in the young, individual differences and their continued progression after birth and maturation. It is postulated that concomitantly with arterial development the associated degenerative changes are attributable to hemodynamically induced bioengineering fatigue caused by longitudinal stretching and circumferential distensile effects of the pulse waves and by lesser vibrations generated by flow at sites of predilection for compensatory intimal thickening. This intimal proliferation is the compensatory reparative response to loss of tensile strength of mural constituents and of the vessel wall as a whole.

Animals↗
PubMed1995

The hypothetical epidemic of coronary heart disease and atherosclerosis.

Accurate usage of the term 'epidemic' is important scientifically and it should ideally be used to mean only contagious diseases, not used loosely or emotively to mean non-infectious diseases, particularly coronary heart disease, which is a non-specific complication of many diseases. It should not be used as a surrogate term for atherosclerosis of indefinite severity. An epidemic of atherosclerosis is impossible, there being no variation in prevalence because the disease is ubiquitous. Moreover, vital statistics are too unreliable to determine the existence of an increase or decline in coronary heart disease. A coronary heart disease epidemic could be due to an increase in non-atherosclerotic coronary heart disease or increased severity of atherosclerosis. The former has not been studied and the latter would cause a shift to the left in age distribution and is inconsistent with the fall in 'all cause' and stroke mortality rates whilst coronary heart disease mortality allegedly increased alarmingly. A coronary heart disease epidemic, having no scientific basis, negates any reason for the sustained search for a speculative causative environmental factor.

Arteriosclerosis↗
PubMed1995

Ultrastructure of the afferent arteries of experimental femoral arteriovenous fistulae in rabbits.

Using transmission electron microscopy, the aorta and ilio-femoral arteries of 12 normocholesterolemic rabbits with femoral arteriovenous fistulae were investigated (49 to 895 days post-operatively) to determine whether the fibrofatty lesions in arteries proximal to chronic fistulae were ultrastructurally consistent with human atherosclerosis. The contralateral ilio-femoral arteries from the same animals and the vessels of 4 additional rabbits (2 with femoral arteriotomies) served as control material for comparison. There were microfractures adjacent to complete tears of the internal elastic lamina which had abrupt margins. These tears were observed mostly in the ilio-femoral arteries proximal to the fistula. They were most numerous, extensive and associated with considerable intimal proliferation near the fistula. Further proximally the tears were associated with progression to severe atrophy of the wall, the media in places being reduced in width to no more than 2 or 3 smooth muscle cells without any evidence of cellular degeneration. Intimal proliferation near the fistula and the naturally occurring intimal thickenings at branching sites proximal to the fistula, not only extended peripherally and progressed with time post-operatively, but exhibited ultrastructural changes consistent with atherosclerosis. These changes comprised dystrophic basement membrane, granulovesicular degeneration (matrix vesicles) and necrosis of smooth muscle cells, disruption of the elastic laminae, the appearance of extracellular and to a lesser extent intracellular lipid, adherence of monocytes, accumulation of foam cells, intimal fibrin deposition and sub-endothelial hemorrhage. Such results indicate that augmented hemodynamic stresses associated with femoral arteriovenous fistulae are consistent with those of human atherosclerotic lesions.

Animals↗
PubMed1995

The ultrastructure of arteries proximal to chronic experimental carotid-jugular fistulae in rabbits.

The afferent arteries from 11 normocholesterolemic rabbits with carotid-jugular arteriovenous fistulae ranging in duration from 107 to 718 days were examined by transmission electron microscopy to determine long term effects of an arteriovenous shunt on the afferent artery. Extensive tears and fragmentation of the internal elastic lamina of the elastic common carotid arteries were observed in all animals. Fragmentation and loss of elastic tissue as well as loss of muscle in the media accompanied progressive mural atrophy and tortuosity. Close to the fistula and in regions of tortuosity, fibromusculoelastic intimal proliferation was superimposed on the atrophic medial changes. The accumulation of matrix vesicles (cell debris), bizarre shaped smooth muscle cells, irregularly thickened multilaminated and reticulated basement membrane material beneath the endothelium and about smooth muscle cells, and abnormal shaped collagen fibrils were observed in the intima. Lipid was frequently found in the extracellular matrix and within smooth muscle cells while monocytes and lipid-laden macrophages were a feature of the more advanced intimal changes. These experiments confirm that in the absence of hypercholesterolemia the hydraulic stresses associated with an arteriovenous shunt cause severe mural atrophy and proliferative changes in the intima similar in nature to those of atherosclerosis.

Animals↗
PubMed1995

Atypical cerebral aneurysm in a young child.

Autopsy findings are described of an atypical aneurysm of a large cerebral artery in a young child. The lesion is believed to have been an infective (mycotic) aneurysm. Antibiotics were administered at the time of the first leakage which had been thought to be due to a sinus infection. The sac wall exhibited a subacute pleomorphic inflammatory cell response indicative of a resolving infective aneurysm, and appearance that is likely to be encountered more often in the future.

Aneurysm, Infected↗
PubMed1994

Ultrastructural changes in arteries proximal to short-term experimental carotid-jugular arteriovenous fistulae in rabbits.

The afferent arteries of 10 carotid-jugular arteriovenous fistulae in rabbits were examined by transmission electron microscopy to determine the early ultrastructural changes in the vicinity of haemodynamically induced tears of the internal elastic lamina. No significant changes appeared to precede the development of the tears but radially orientated partial fractures were observed adjacent to some major tears. The elastic tissue tears became more numerous, extended proximally along the artery and with time involved the innermost medial elastic laminae. Endothelial discontinuities were present over only a few early tears and the small size suggested repair was rapid. Endothelial cells overlying the elastic tissue tears increased in density and thickness. They were adherent to the underlying matrix and eventually to the thickened and multilaminated basal lamina. In the floor of the tears between the edges of the torn internal elastic lamina there were some smooth muscle cells of the synthetic type, degenerative and necrotic muscle cells and areas devoid of matrix with scarce proteoglycan material suggestive of oedema. Sixteen days post-operatively the smooth muscle cells in the floor of the tears were all of the contractile variety with thickened basal laminae overlaid by a relatively normal endothelial layer. There was no suggestion that inflammatory cells were responsible for the elastic tissue tears. The abrupt edges and the adjacent microfractures are consistent with the concept of mechanical failure of the elastic tissue.

Animals↗
PubMed1993

The quality of epidemiological data in coronary heart disease and atherosclerosis.

There are inherent difficulties in the use of indirect observations in the epidemiology of a chronic ubiquitous disease such as atherosclerosis. Such difficulties do not condone basic errors in epidemiological methodology, the use of low quality data, a lack of precision in measurements, invalid extrapolations and inappropriate use of terminology and coronary heart disease as a surrogate or synonym of coronary atherosclerosis and bias in the interpretation of data. These errors reveal a lack of rigorous and scientific standards in the epidemiology of coronary heart disease. Analysis cannot launder such data. Independent scientists must evaluate the data in respect of precision, logic and truth.

Arteriosclerosis↗
PubMed1993

Endothelium in the aorta and ilio-femoral arteries proximal to femoral arteriovenous fistulae in rabbits.

The endothelium and underlying internal elastic lamina of the aorta and ilio-femoral arteries from 15 rabbits with femoral arteriovenous fistulae (2 to 92 days postoperatively) and 3 rabbits with control femoral arteriotomies were examined using the en face technique and scanning electron microscopy. The rapidity of development of the tears in the internal elastic lamina of the muscular ilio-femoral arteries was greater than in fistulae involving the elastic common carotid artery. The elastic tissue tears appeared to have a predilection for certain anatomical regions possibly related to regions of specific hemodynamic stress. A few tears were observed in the aorta near the origin of the renal arteries. Initially the elastic tissue tears in the afferent ilio-femoral arteries were longitudinally orientated and the endothelium overlying the elastic tissue tears soon exhibited increased cell density relatively restricted to the floor of the tears. This cellular pattern was similar to that in the carotid-jugular fistulae. With time the endothelium assumed a more conventional morphology.

Animals↗