Morphology after Transluminal Angioplasty in Human Beings

Block, Peter C.; Myler, Richard K.; Stertzer, Simon H.; Fallon, John T.

doi:10.1056/nejm198108133050706

Cited by 465 publications

(73 citation statements)

References 9 publications

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“…Pathological material obtained from three patients who died within 3 days of successful percutaneous transluminal angioplasty has shown significant fractures of the atheroma extending into the media. 14 The histological findings in these patients are identical to that noted in our Group 1 animals.…”

Section: + --Discussionsupporting

confidence: 84%

Acute effects of transluminal angioplasty in three experimental models of atherosclerosis.

Faxon¹,

Weber²,

Haudenschild³

et al. 1982

Arteriosclerosis

185

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T he development and clinical utilization of transluminal angioplasty has provided a nonsurgical treatment of atherosclerotic obstruction. In 1964, Dotter and Judkins 1 described a method for enlarging the lumen of stenotic peripheral vessels using a percutaneous catheter system. The development of a unique double balloon catheter system in 1973 has allowed successful nonsurgical treatment of peripheral, renal, coronary, and cerebral vascular disease in selected patients. 2 The results of peripheral percutaneous dilatation have been encouraging with an initial success rate of 80% and a patency rate of 73% after 2 years. 3 The use of transluminal angioplasty in

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Section: + --Discussionsupporting

confidence: 84%

Acute effects of transluminal angioplasty in three experimental models of atherosclerosis.

Faxon¹,

Weber²,

Haudenschild³

et al. 1982

Arteriosclerosis

185

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“…We must, therefore, attribute the increase in lumen area mainly to the stretching of the media and adventitia allowed by the release of the media from the noncompliant atherosclerotic plaque. Castaneda-Zuniga et al 1 and Block et al 2 have come to similar conclusions from observations on nonperfusion-fixed human postmortem specimens. Had these specimens been perfusion-fixed, it is likely that the dramatic changes in lumen contour resulting from angioplasty would have been apparent.…”

Section: Discussionsupporting

confidence: 66%

Vessel, plaque, and lumen morphology after transluminal balloon angioplasty. Quantitative study in distended human arteries.

Lyon¹,

Zarins²,

Lu³

et al. 1987

Arteriosclerosis

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We performed transluminal balloon angioplasty In 24 cadaver and nine amputated limb superficial femoral arteries under controlled experimental conditions. The cadaver arteries were excised, restored to in situ length, redistended, and maintained at 100 mm Hg Intraluminal pressure at 37° C throughout the anglographlc and dilation procedure and during fixation. The amputated limb arteries were dilated and pressure perfusion-flxed after dilation. Quantitative analysis of cadaver vessels revealed that arteries with prominent atherosclerotic lesions had the same internal elastic lamina (IEL) circumference (15.6 ± 1.0 mm) as those with little or no stenosis (16.8 ± 0.5 mm) but lumen area (8.8 ± 1 . 7 mm 2 ) was markedly reduced compared to nonstenotlc sites (20.0 ± 1.9 mm 2 , p < 0.01). Lesions occupied 49 ± 6% of the area circumscribed by the IEL In cadaver arteries with prominent plaques. After dilatation, lumen areas at stenotic sites were enlarged 43% on hlstologic sections (12.6 ± 1.8 mm 2 vs 8.8 ± 1 . 7 mm 2 , p < 0.

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“…9,10 Furthermore, mechanical endothelial injury has been reported to be a key feature in coronary arteries of patients after percutaneous coronary intervention (PCI) and, together with other forms of endothelial damage, has been implicated in arterial lesion formation in patients. [11][12][13] To better understand the effects of endostatin on reendothelialization and neointima formation, we overexpressed the endostatin gene in a mouse model of arterial injury. In this model, luminal endothelium-denuding injury was performed without disruption of the internal elastic lamina, leading to luminal endothelial regrowth and concurrent neointima formation.…”

mentioning

confidence: 99%

Decreased Reendothelialization and Increased Neointima Formation With Endostatin Overexpression in a Mouse Model of Arterial Injury

et al. 2003

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Background-Impaired endothelial regeneration contributes to arterial lesion formation. Endostatin is a specific inhibitor of endothelial cell growth and induces endothelial cell apoptosis. We examined the effect of endostatin overexpression on reendothelialization and neointima formation in a mouse model of arterial injury. Methods and Results-Mice underwent femoral arterial denudation and received recombinant adenovirus, expressing either murine endostatin (nϭ19) or control adenoviral vector (nϭ12), by jugular vein injection. Endostatin gene transfer resulted in high serum levels of endostatin. Strong adenoviral gene expression of ␤-galactosidase-expressing control vector was detected in liver tissue and was absent in the injured arterial wall at 1 week. Deposits of endostatin protein were detected along the denuded arterial wall and were not seen in the noninjured contralateral artery at 1 week. Endostatin deposits were also absent in the injured artery of control vector-treated animals. Overexpression of endostatin led to decreased reendothelialization and increased apoptosis of luminal endothelial cells 2 and 4 weeks after arterial injury (PϽ0.05). In addition, endostatin overexpression resulted in increased neointima formation (PϽ0.05). Endothelial apoptosis and neointima area correlated positively with endostatin serum levels, whereas the degree of reendothelialization correlated negatively with endostatin serum levels (PϽ0.05). Furthermore, poor reendothelialization correlated with increased neointima formation (PϽ0.05). Conclusions-In summary, decreased reendothelialization and enhanced endothelial apoptosis, in response to endostatin overexpression, were associated with increased neointima formation. These findings demonstrate that high serum levels of endostatin are capable of inhibiting endothelial regeneration and promoting arterial lesion growth in conditions of endothelial injury.

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Morphology after Transluminal Angioplasty in Human Beings

Cited by 465 publications

References 9 publications

Acute effects of transluminal angioplasty in three experimental models of atherosclerosis.

Acute effects of transluminal angioplasty in three experimental models of atherosclerosis.

Vessel, plaque, and lumen morphology after transluminal balloon angioplasty. Quantitative study in distended human arteries.

Decreased Reendothelialization and Increased Neointima Formation With Endostatin Overexpression in a Mouse Model of Arterial Injury

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