Restenosis after percutaneous transluminal coronary angioplasty. A histopathological study using autopsied hearts.

Morimoto, Shin-ichiro; Mizuno, Yasushi; Hiramitsu, Shinya; Yamada, Kenji; Kubo, Natsuko; Nomura, Masatoshi; Yamaguchi, Tetsu; Kitazume, Hidemasa; Kodama, Kazuhisa; Kohno, Hiroyuki; Shimizu, Youichi; Mizuno, K; Chino, Masamichi; Watanabe, Soichi; Ueda, Tetsuro; Toyoda, Mitsuyasu; Sekiguchi, Morie

doi:10.1253/jcj.54.43

Cited by 39 publications

(13 citation statements)

References 16 publications

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“…Restenosis after PTCA or DCA has been attributed to immediate elastic recoil, 17 arterial remodeling 18 and mural thrombus formation. [19][20][21] Migration of medial smooth muscle cells to the intima, with proliferation of the smooth muscle cells induced by the fragmentation of the internal elastic lamina, is also believed to play a role. [19][20][21] Arbustini et al observed a high percentage of smooth muscle cells in the fragments of restenotic lesions obtained by DCA, 14 a finding that we also found.…”

Section: Discussionmentioning

confidence: 99%

“…[19][20][21] Migration of medial smooth muscle cells to the intima, with proliferation of the smooth muscle cells induced by the fragmentation of the internal elastic lamina, is also believed to play a role. [19][20][21] Arbustini et al observed a high percentage of smooth muscle cells in the fragments of restenotic lesions obtained by DCA, 14 a finding that we also found. Ishiwata et al detected restenosis in 270 of 666 cases in which coronary angiography had been performed 6 months after PTCA.…”

Section: Discussionmentioning

confidence: 99%

“…Despite the similarity in the clinical manifestations, the underlying mechanisms differ, with the former attributable to plaque rupture and thrombus formation, and the latter attributable to arterial remodeling, mural thrombus formation, organization, and smooth muscle cell proliferation. [18][19][20][21] In the latter case, the fibrous cap is thick, so the role of plaque rupture and thrombus is minimal. Therefore, compared to unstable angina caused by de novo atherosclerotic lesions, the possibility of acute coronary artery occlusion is low, and the prognosis is relatively favorable.…”

Section: Discussionmentioning

confidence: 99%

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Histopathologic Evaluation of Coronary Artery Thrombi Obtained by Directional Coronary Atherectomy in Patients With Restenosis-Induced Unstable Angina Pectoris

et al. 2001

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variety of factors are involved in the development of unstable angina pectoris (UAP), including coronary plaque rupture and thrombus formation, 1-3 coronary spasm, 4 and abnormalities in the coagulationfibrinolysis system, 2 and of these, coronary plaque rupture and thrombus formation are thought to be a direct cause. Studies involving autopsy specimens, 5,6 coronary arteriography, 7 intracoronary endoscopy, 8-10 intravascular ultrasound imaging 11 and directional coronary atherectomy (DCA) [12][13][14][15] have demonstrated the presence of thrombus in many patients with UAP. Although thrombus is known to be involved in the development of acute coronary syndromes, the mechanism for the acute deterioration of angina pectoris, resulting from intimal proliferation after interventional therapy such as percutaneous transluminal coronary angioplasty (PTCA) or DCA, has not been adequately investigated. It is unknown whether thrombus plays a role in producing angina in this setting, so the present study determined the incidence of such thrombi by examining tissue specimens collected at the time of DCA. Japanese Circulation Journal Vol.65, June 2001 MethodsThe study group consisted of 14 patients (16 arterial branches) with angina pectoris in whom PTCA or DCA was performed and who developed UAP after restenosis at the same site, and who then underwent DCA for the restenosed lesion (R-UAP group) ( Table 1). With respect to drug therapy after PTCA or DCA, all patients received nitrates and/or diltiazem in addition to ticlopidine (200 mg/day) and aspirin (81 mg/day) as anti-platelet agents. After the development of UAP, patients were admitted and given heparin (16,000-20,000 units/day) for 1-2 days by continuous intravenous infusion, with an additional 10,000 units intravenously at the time of DCA. The control groups consisted of 94 patients with no prior history of PTCA or DCA, including a group with UAP (P-UAP group; n=29, 29 branches), a group with acute myocardial infarction (AMI group; n=34, 34 branches), and a group with stable angina pectoris (SAP group; n=31, 33 branches), who underwent DCA. Heparin was given to the P-UAP group in the same way as in the R-UAP group.The mean age was 66.1±7.4 years in the R-UAP group, 60.0±7.2 years in the P-UAP group, 58.7±10.6 years in the AMI group, and 61.2±9.2 years in the SAP group. The diagnosis of UAP was based on the definition proposed by the American Heart Association. 16 The degree of angiographic stenosis before and after DCA was measured using the direct caliber method by 2 experienced cardiologists who were blinded to the patients' clinical diagnoses.After DCA, the number of fragments and the tissue weight of the resected material were determined. After being fixed in 10% buffered formalin, the specimens were The pathogenesis of unstable angina pectoris (UAP) following percutaneous transluminal coronary angioplasty (PTCA) or directional coronary atherectomy (DCA) has not been adequately investigated, so the present study aimed to determine whether thrombi are present in...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Histopathologic Evaluation of Coronary Artery Thrombi Obtained by Directional Coronary Atherectomy in Patients With Restenosis-Induced Unstable Angina Pectoris

et al. 2001

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“…Since restenosis is a process due chiefly to growth into the lumen of ␣-actin-immunoreactive VSMCs (13,20,23) and a number of studies have demonstrated the key role of VSMCs in restenosis (8,18,21,27), we further hypothesized that the above phenotypic difference between Harlan and Sasco Sprague-Dawley rats was due to the intrinsic (namely, genetic) differences in responses of their VSMCs to growth and apoptotic stimuli. To test the hypothesis, we isolated carotid artery VSMCs (CAVSMCs) from Harlan and Sasco Sprague-Dawley rats and subjected them to molecular analyses.…”

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The critical role of the intrinsic VSMC proliferation and death programs in injury-induced neointimal hyperplasia

Mnjoyan

Doan

Brandon

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…In particular, how specimens from patients with acute coronary syndromes, such as acute myocardial infarction (AMI) and unstable angina pectoris (UAP), differ from those of patients with stable angina pectoris (SAP) or old myocardial infarction (OMI) in terms of the expression of cytokines and adhesion molecules, as well as how the pathogenesis of coronary atherosclerosis with organic stenosis or occlusion differs from restenosis (RS) incurred during the regeneration process following coronary intervention. 6,8,12 Recently, the results of a large prospective study indicated that the base-line concentration of C-reactive protein in plasma can predict the risk of future myocardial and ischemic stroke in healthy men. 13 Moreover, acute phase proteins such as C-reactive protein and serum amyloid A protein have been shown to have prognostic value in severe unstable angina.…”

mentioning

confidence: 99%

Expression of Cytokine and Adhesion Molecule mRNA in Atherectomy Specimens From Patients With Coronary Artery Disease

et al. 1999

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Restenosis after percutaneous transluminal coronary angioplasty. A histopathological study using autopsied hearts.

Cited by 39 publications

References 16 publications

Histopathologic Evaluation of Coronary Artery Thrombi Obtained by Directional Coronary Atherectomy in Patients With Restenosis-Induced Unstable Angina Pectoris

Histopathologic Evaluation of Coronary Artery Thrombi Obtained by Directional Coronary Atherectomy in Patients With Restenosis-Induced Unstable Angina Pectoris

The critical role of the intrinsic VSMC proliferation and death programs in injury-induced neointimal hyperplasia

Expression of Cytokine and Adhesion Molecule mRNA in Atherectomy Specimens From Patients With Coronary Artery Disease

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