Transluminal coronary angioplasty and early restenosis. Fibrocellular occlusion after wall laceration.

Essed, C. E.; Brand, Marcel van den; Ae, Becker

doi:10.1136/hrt.49.4.393

Cited by 291 publications

(32 citation statements)

References 11 publications

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“…The role of platelets in coating a damaged surface immediately after PTCA' 45 " 47 ] and that of thrombus organization' 42 ' has been demonstrated for restenosis in the animal model. Intimal proliferation of smooth muscle cells seems to be the main mechanism of recurrence in man' 40 " 41 " 43 '. It can be triggered by platelet-derived growth factors, but might also be provoked by the balloon injury itself independently of serum factors' 481 and thus even under antiplatelet or anticoagulant drugs.…”

Section: Pathology Of Restenosismentioning

confidence: 99%

Restenosis and its determinants in first and repeat coronary angioplasty

Rapold

David²,

Val³

et al. 1987

European Heart Journal

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KEY WORDS: PTCA, restenosis, repeat PTCA, PTCA outcome determinants. (PTCA) Since its introduction' 12 ' successful percutaneous long-term success of PTCA. Reported restenosis transluminal coronary angioplasty (PTCA) has rates (14-47%) vary, depending in part on the denbeen shown to relieve angina and myocardial nition used, but according to the larger series' 18 " 22 ', ischaemia as assessed by exercise electrocardiogone patient in three with successful PTCA must raphy 13 ', thallium scintigraphy* 3 ' 4 ', and measureexpect recurrence, most of them within 6-8 months ment of coronary blood flow and myocardial after the intervention. Repeat PTCA has been metabolism' 5 ' 6 '. The original indications' 2 ' have been done with a higher primary success rate and fewer expanded' 7 " 171 . But regardless of selection criteria, complications than the initial procedure. Nevertherestenosis with recurrence of myocardial ischaemia less, there remains a substantial rate of second and symptoms remains the major problem limiting recurrences' 23 " 251 . The presence of angina as an indicator for restenosis has a predictive accuracy of only 56% Submitted for publication on 23 June 1986 and in revised form 21 after first and 67% after Second PTCA according tO OctobCTl986 the NHLBI report" 8231 . One patient in four with For the period that this work was carried out, Dr Rapold was restenosis has no chest pain. In a population at high supported by a grant oftheSwisi National Science Foundation. Restenosis is the main problem limiting long-term success of percutaneous transluminal coronary angioplasty

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Section: Pathology Of Restenosismentioning

confidence: 99%

Restenosis and its determinants in first and repeat coronary angioplasty

Rapold

David²,

Val³

et al. 1987

European Heart Journal

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“…4 Last, autopsy studies of restenotic lesions have failed to show thrombus as the predominant material. [5][6][7] In only a minority of cases that show restenosis in the first few weeks after PTCA can thrombus or suboptimal initial dilatation or both be considered a primary mechanism. Although some degree of mural thrombus formation after PTCA may be an important initiating or contributing factor, thrombosis per se probably does not determine the final response in most cases.…”

Section: Proposed Mechanisms Of Restenosismentioning

confidence: 99%

Restenosis after coronary angioplasty. Potential biologic determinants and role of intimal hyperplasia.

1989

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Restenosis after successful PTCA remains a major problem limiting the efficacy of the procedure. The pathophysiologic mechanism of restenosis has been enigmatic so far, but accumulated evidence strongly suggests that intimal hyperplasia is the major mechanism. Based on current understanding of the process of intimal hyperplasia, one unifying concept may be that there are at least two major local biologic determinants influencing this process, lesion characteristics and regional flow dynamics. Lesion characteristics include the plaque structure and the quantity of smooth muscle. These may provide the anatomic substrate that determines the extent of injury and the degree of smooth muscle cell proliferation. The amount of smooth muscle cells in the stenotic lesion activated by injury to undergo proliferation may determine the eventual bulk of the restenotic lesion. In addition, low wall shear stress could promote intimal hyperplasia and cause structural change of vessels to decrease the lumen, whereas high wall shear stress exerts the opposite effects. Intimal hyperplasia after balloon injury is a complex process involving platelets, growth factors, endothelial cells, smooth muscle cells, mechanical injury, wall shear stress, and probably other unknown factors. Platelets not only contribute growth factors such as PDGF but also cause organized thrombus. Different growth factors may be involved in initiating smooth muscle cell proliferation and may come from many different sources, including smooth muscle cells, endothelial cells, and macrophages. Intact confluent endothelial cells may produce heparin sulfates and inhibit intimal proliferation; however, regenerating endothelial cells may have the opposite effect. Thus, the proliferative potential of smooth muscle cells, endothelial recovery, extent of injury, wall shear stress, and other unknown factors may all influence this process. Based on these concepts concerning the biology of restenosis, some research directions concerning potential forms of therapy are proposed.

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“…The pathogenesis of lesion recurrence after initially successful percutaneous transluminal coronary angioplasty and alternative angioplasty procedures is not well defined, but neointimal cellular proliferation and thrombus formation have been im-plicated as components ofnew tissue growth (1)(2)(3)(4)(5)(6)(7). In addition, production ofextracellular matrix, principally collagen and glycosaminoglycans, within the neointima has been shown to be a prominent feature of the late phase of restenosis lesions, both experimentally and clinically (8)(9)(10).…”

Section: Introductionmentioning

confidence: 99%

Modulation by beta-aminopropionitrile of vessel luminal narrowing and structural abnormalities in arterial wall collagen in a rabbit model of conventional balloon angioplasty versus laser balloon angioplasty.

Spears

Zhan²,

Khurana³

et al. 1994

J. Clin. Invest.

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This study was designed to assess the potential relationship between the late loss of angiographic luminal diameter and biochemical abnormalities of arterial wall collagen in rabbits subjected to angioplasty, and to test the hypothesis that a-aminopropionitrile (#APN), an inhibitor of lysyl oxidase, would inhibit such changes when administered orally for 1 mo after angioplasty. Endovascular injury was induced in rabbit iliac arteries by ipsilateral balloon angioplasty (BA) and by contralateral balloon angioplasty accompanied by exposure to continuous wave neodymium: yttrium aluminum garnet laser radiation (LBA). Computer measurement ofangiographic luminal diameter demonstrated significant vessel narrowing at 1 and 6 mo after both procedures. By quantitative histology, the majority of the 1-mo loss in angiographic diameter could not be attributed to neointimal thickening. Analysis of collagen cross-linking by HPLC in collagen obtained from the LBA-injured segments of the arteries 1 mo after angioplasty revealed a significant increase, relative to values from uninjured arteries (P < 0.05), in the difunctional cross-link dihydroxylysinonorleucine (DHLNL). 6 mo after angioplasty, the content of hydroxpyridinium, the trifunctional maturational product of DHLNL, was significantly elevated in both BA-and LBA-treated arteries compared with values from uninjured arteries (P < 0.05). In animals administered ,fAPN, luminal narrowing at 1 mo, compared with controls, was attenuated (P < 0.01) and DHLNL content was decreased (P < 0.05) in arteries subjected to LBA, but not in arteries subjected to BA. The results suggest that lathyrogenic agents may be efficacious in favorably modulating LBA-induced alterations in vessel diameter and mural connective tissue. (J. Clin. Invest. 1984. 93:1543-1553

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Transluminal coronary angioplasty and early restenosis. Fibrocellular occlusion after wall laceration.

Cited by 291 publications

References 11 publications

Restenosis and its determinants in first and repeat coronary angioplasty

Restenosis and its determinants in first and repeat coronary angioplasty

Restenosis after coronary angioplasty. Potential biologic determinants and role of intimal hyperplasia.

Modulation by beta-aminopropionitrile of vessel luminal narrowing and structural abnormalities in arterial wall collagen in a rabbit model of conventional balloon angioplasty versus laser balloon angioplasty.

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