Intimal Disruption Research Articles

Percutaneous transluminal angioplasty. Radiological-pathological correlation.

Radiological and pathological assessment of the degree and extent of arterial injury caused by balloon angioplasty was performed in 20 renal arteries obtained at autopsy. Intact arteries were studied angiographically before and after dilatation and then examined histologically. Both normal and diseased arteries were subjected to varying degrees of dilatation. Damage ranged from minimal intimal disruption to major tears of the muscular media. Equivalent dilatory force created greater damage in the distal (muscular) than in the proximal (elastic) portion of the renal artery. There was no evidence of plaque remodeling or compression.

Transluminal angioplasty: correlation of morphologic and angiographic findings in an experimental model.

The morphologic consequences of transluminal angioplasty of stenotic atherosclerotic coronary arteries are unknown. This study describes the production of aortoiliac atherosclerosis in rabbits and reports the morphologic changes after transluminal angioplasty of stenotic arterial lesions. Atherosclerotic lesions were evaluated angiographically before and after transluminal angioplasty and were studied histologically and by electron microscopy after angioplasty. Moderatley stenotic aortic segments showed denudation of endothelial cells and deposition of a carpet of platelets enmeshed in fibrin. Medial and intimal compression were not seen. Intimal plaque disruption and splitting of atheromatous plaques were observed in more stenotic vessels where dilatation during angioplasty is relatively greater. Transluminal angioplasty, therefore, acutely causes desquamation of endothelial cells and superficial plaque elements, splitting of atheroma and subsequent deposition of platelets and fibrin in the area of angioplasty. This experimental model may be useful to evaluate the morphologic changes after angioplasty and might be used in further studies to determine the long-term pathophysiologic changes after transluminal angioplasty.

Intraarterial Drug Injury

BUCKSPAN, G. S.; FRANKLIN, J. D.; NOVAK, G. R.; BENNETT, B. D.; LYNCH, J. B.; DEAN, R. H. Author Information

Evidence in favor of the vasospastic cause of coronary artery thrombosis

Evidence is presented which suggests that it is likely that vasospasm initiates coronary artery thrombosis. Spasm causes a violent constriction of the vessel and also produces stasis, and both factors are implicated in the thrombotic process. Spasm can occur in sclerotic segments, and intimal tears and plaque ruptures in arteriosclerotic plaques are attributed to spasm. The thrombus forms over the intimal disruption, abetted by the stasis of spasm. In arteries with mild or no intimal injury, continuing stasis over a period of time is considered as the major factor in thrombus formation. This ongoing stasis is attributed to an injury-spasm reaction to necrotic muscle, and probably is equivalent to the “no-reflow” phenomenon of infarction.

Intraarterial drug injury: studies of etiology and potential treatment

By utilizing the rabbit ear as a vascular bed and examining the sequential angiographic and morphologic alterations following intraarterial Pentothal injury, one can conclude that intraarterial Pentothal is cytotoxic, causing intimal disruption and vessel wall necrosis with subsequent vascular occlusion and tissue loss. Furthermore, this injury is intensified by angiography and not significantly altered by intraarterial Priscoline—reserpine and low-dose Decadron. In contrast, pharmacologic doses of Decadron significantly reduce the extent of cellular injury and subsequent tissue loss.

Evaluation of Trauma With Angiograph

To the Editor.— In two angiograms shown by Redman (237:2415-2418, 1977), spasm was diagnosed in a brachial artery (her Fig 1) and in an axillary artery (her Fig 2). The minimal narrowing in these two angiograms could have been due to hematoma or soft tissue swelling. It cannot be denied that large arteries may go into spasm because of their intrinsic musculature, but arterial spasm is a dangerous diagnosis to make when there is trauma. It is convenient but hazardous for the physician who does not feel pulses in an extremity distal to an injury or who notes pallor and coolness to conclude that these findings are due to arterial spasm. This is particularly true in blunt trauma. Spasm may also be diagnosed on an arteriogram, particularly in cases of blunt trauma, but in my experience there has been contusion or intimal disruption in all such cases rather than spasm.

Preferential Atherosclerosis at the Aortic Junction of the Ligamentum Arteriosum: Clinical Significance and Pathological Correlation

Clinical experience with 5 patients who had complications of atherosclerosis within the aorta at the site of the obliterated ductus arteriosus suggested the occurrence of clinically significant preferential atherosclerosis at this location. To examine this hypothesis, the clinical findings in these patients (4 with saccular aneurysm and 1 with systemic emboli from an ulcerated plaque at this location) were correlated with postmortem examination of the aortic isthmus in 40 consecutive cadavers. The point of ductal closure was the area of most severe atheromatous involvement in 32 of the 40 cadavers, and 25 of the 40 specimens demonstrated ulcerated plaques at this location. Microscopical examination consistently demonstrated intimal irregularity or disruption and thinning of the aortic media in this area. These studies indicate that preferential atherosclerosis occurs at the aortic end of the obliterated ductus arteriosus and that these atherosclerotic changes can be a clinically significant development.

Morphologic studies in a patient with homocystinuria due to 5, 10-methylenetetrahydrofolate reductase deficiency.

Biochemical and morphologic studies on a patient with homocystinuria due to a deficiency of 5, 10-methylenetetrahydrofolate reductase (EC. 1.1.1.68) were performed. The concentrations of homocystine in the patient's plasma and urine were 2.97 mumol/dl and 44.67 mumol/24 hr, respectively. Activities of 5, 10-methylenetetrahydrofolate reductase (expressed as nanomoles of formaldehyde formed per hr per mg of protein) in cultured skin fibroblasts and liver tissue were 0.53 (control: 5.14) and 0.00 (control: 13.80), respectively. The major abnormalities were found in the arterial bed, consisting of intimal hyperplasia, fragmentation, and disruption of elastic lamellae and subcellular changes in the endothelial cells. Extensive thrombosis was observed. The brain and the liver also showed widespread pathologic changes. In the former, neuronal loss and cellular damage were prominent and extensive. Diffuse demyelination with moderate astrocytosis was found; but demyelination was out of proportion to the vascular changes. Hirano bodies in the cortical neurons and crystalline and lamellar bodies in the Purkinje cells were observed. In the liver, there were fatty change and mild to moderate portal fibrosis. Bizarre, giant mitochondria and membrane-bound multivesicular bodies were found. Mild pathologic changes were also observed in the striated muscles and the kidneys. Focal fragmentation, disruption, and smearing of the Z discs and disorganization of the myofilaments were found in the skeletal muscles. The kidneys showed shrunken glomeruli, thickened basement membranes, and swelling of epithelial as well as endothelial cells.

Atypical fibromuscular hyperplasia involving the carotid artery.

A case of atypical fibromuscular hyperplasia involving the carotid artery in a 38-year-old male is described. The lesion, with associated intimal disruption and subintimal hematoma, caused cerebral embolus and transient neurologic dysfunction. Segmental resection and autogenous graft reconstruction of the carotid artery were successful in removing the lesion and preventing subsequent symptoms.

Vascular jet collapse in selective angiocardiography.

Pressures exerted by the jet coming from an end hole catheter may be positive or negative, depending on the direction of measurement. Maximal positive pressure occurs if the catheter is in direct contact with the structure at a right angle position. Under such circumstances, the pressure in the injection syringe is transmitted, usually resulting in disruption of intima and media of the blood vessel.Negative forces may cause collapse of an injected blood vessel resulting in an angiographic artefact termed jet collapse. At effective injection pressures of 800 lb./sq. in. and more, vascular jet collapse is the cause of disruption of the vessel wall in animal experiments. Vascular jet collapse is more commonly seen in venography and arteriography in younger persons with elastic vessels. Vascular jet collapse is an important angiographic arte-fact, since it may be confused with organic narrowing or vascular spasm.