Collagenase Activity of the Human Aorta

Busuttil, Ronald W.

doi:10.1001/archsurg.1980.01380110105016

Cited by 210 publications

(26 citation statements)

References 11 publications

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“…due to arterial distention, or, a congenital deficiency of the elastic tissue which predisposes vessels to dilate when subjected to hypertension. Relevant to this dis cussion, Busuttil et al 30 detected collagenase activity in the vessel walls of patients with resected abdominal aortic aneurysms but not in the walls of atherosclerotic aortas. Abnormal persistence of this proteolytic en zyme may weaken vessel walls, predisposing to dila tion and elongation and secondary atherosclerotic changes.…”

mentioning

confidence: 76%

Fusiform basilar aneurysm as a cause of embolic stroke.

Steel¹,

Thomas²,

Strollo³

1982

Stroke

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SUMMARY Giant fusiform basilar aneurysms (dolicho-ectatic basilar anomalies) are rare and have not previously been reported to cause embolic infarction in territory distal to the aneurysm. They most commonly present as posterior fossa mass lesions with brainstem compression and cranial neuropathies. Originally considered atherosclerotic in etiology, recent authors feel that they may represent a unique arteriopathy characterized by loss of elastin in the vessel wall. We report a case which presented solely as an occipital lobe infarction. To our knowledge, this is the first case in which a fusiform basilar aneurysm presented with an embolic infarction as its only manifestation. Stroke, Vol 13, No 5, 1982 GIANT FUSIFORM BASILAR ANEURYSMS (doli cho-ectatic basilar anomalies') are aneurysmal dilations of the basilar artery and usually present clinically as posterior fossa mass lesions ( 5 Emboli arising from in tracerebral aneurysms are unusual 22 -23 and to our knowledge have not been reported originating from a fusiform basilar aneurysm. We report a case which presented solely as an embolic occipital lobe in farction.Case Report A 59-year-old man with mild hypertension and Type IV hyperlipidemia experienced abrupt onset of right periorbital headache accompanied by loss of vision in the left visual field. He had no previous history of transient ischemic attacks (TIAs) or stroke. Several weeks prior to the event, he noted frequent right peri orbital headachees lasting 45-60 minutes without neurologic symptoms. Nine years previously he under went surgery for repair of an abdominal aortic aneu rysm. His risk factors included a 20 year history of mild hypertension (highest recorded pressure 140/100 mg Hg), smoking, hypertriglyceridemia, and moder ate obesity. His general physical examination was normal ex cept for early retinal vessel sclerosis. Blood pressure was 130/84 mm Hg. There were no carotid bruits. Neurologic examination demonstrated a left superior _, quadrantanopsia, but was otherwise unremarkable.The following studies were normal: serum electro lytes, complete blood count, syphilis serology, urinal ysis, coagulation profile, echocardiogram, and lumbar puncture. Serum triglycerides were 261 mg/dl (nor mal, 30-150 mg/dl). The electrocardiogram demon strated borderline nonspecific ST-T wave changes and rare multifocal premature ventricular contractions.A computed tomographic (CT) scan of the head demonstrated a nonhemorrhagic right occipital lobe infarction ( fig. 1), and a large eccentrically positioned basilar artery, with calcification in its walls, extending well above the posterior clinoids ( fig. 2a). The contrast enhanced ( fig. 2b) and reformatted coronal ( fig. 3) images revealed the presence of incomplete thrombo sis in the aneurysm which measured up to 2 cm in diameter. Pancerebral angiography ( fig. 4) confirmed the diagnosis of a partially thrombosed giant fusiform basilar aneurysm and showed the lesion to be continu ous with an ectatic and elongated dominant right verte bral artery. In additio...

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confidence: 76%

Fusiform basilar aneurysm as a cause of embolic stroke.

Steel¹,

Thomas²,

Strollo³

1982

Stroke

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“…Because proteinase species may not be adequately released from endogenous substrates by aqueous extraction and because previous workers had reported that CL-like activities were found exclusively in particulate suspensions of diseased vascular tissue, 8 the resuspended tissue pellets of aqueous homogenates were assayed for CL activity. A maximum of 33 units/g was found in diseased aortas, consistent with the relatively low level of activity found in the cleared supernatants (data not shown).…”

Section: Aqueous Extraction Of Proteinases and Inhibitorsmentioning

confidence: 99%

Connective tissue proteinases and inhibitors in abdominal aortic aneurysms. Involvement of the vasa vasorum in the pathogenesis of aortic aneurysms.

Herron

Unemori

Wong

et al. 1991

Arterioscler Thromb

145

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T he development of irreversible dilations of the infrarenal aorta has been attributed to hemodynamic disturbances as well as to structural and metabolic changes within the vessel wall. 1 -2 Chemical and histological analyses have demonstrated significant decreases in the two major structural proteins, collagen and elastin, in dilated vascular tissue from patients undergoing corrective surgery for abdominal aortic aneurysm (AAA) disease. 34 Experimentally, it has been shown that circumferential arterial wall stress is borne primarily by elastin and that collagen maintains the integrity of the arterial wall, as enzymatic hydrolysis of collagen results in vessel rupture, whereas degradation of

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“…This change may reflect increased collagenolytic and elastolytic activity in atherosclerotic aneurysm wall (6,7). For example, type IV collagenase mRNA was detected in cells surrounding vasa vasorum within the plaque (8), and macrophage elastase may induce aortic aneurysm in rats (9).…”

Section: Introductionmentioning

confidence: 99%

Expression of fibrinolytic genes in atherosclerotic abdominal aortic aneurysm wall. A possible mechanism for aneurysm expansion.

Schneiderman¹,

Bordin²,

Engelberg³

et al. 1995

J. Clin. Invest.

131

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Expansion of atherosclerotic abdominal aortic aneurysm (AAA) has been attributed to remodeling of the extracellular matrix by active proteolysis. We used in situ hybridization to analyze the expression of fibrinolytic genes in aneurysm wall from eight AAA patients. All specimens exhibited specific areas of inflammatory infiltrates with macrophagelike cells expressing urokinase-type plasminogen activator (u-PA) and tissue-type PA (t-PA) mRNA. Type 1 PA inhibitor (PAM-) mRNA was expressed at the base of the necrotic atheroma of all specimens and also within some of the inflammatory infiltrates where it frequently colocalized in regions contining u-PA and t-PA mRNA expressing cells.However, in these areas, the cellular distribution of the transcripts for t-PA and u-PA extended far beyond the areas of PAT-i expression. These observations suggest a local ongoing proteolytic process, one which is only partially counteracted by the more restricted expression of PAT-i mRNA. An abundance of capillaries was also obvious in all inflammatory infiltrates and may reflect local angiogenesis in response to active pericellular fibrinolysis. The increased fibrinolytic capacity in AAA wall may promote angiogenesis and contribute to local proteolytic degradation of the aortic wall leading to physical weakening and active expansion of the aneurysm. (J. Clin. Invest. 1995. 96:639-645.)

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Collagenase Activity of the Human Aorta

Cited by 210 publications

References 11 publications

Fusiform basilar aneurysm as a cause of embolic stroke.

Fusiform basilar aneurysm as a cause of embolic stroke.

Connective tissue proteinases and inhibitors in abdominal aortic aneurysms. Involvement of the vasa vasorum in the pathogenesis of aortic aneurysms.

Expression of fibrinolytic genes in atherosclerotic abdominal aortic aneurysm wall. A possible mechanism for aneurysm expansion.

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