Distribution and composition of glycosaminoglycans in the left human coronary arterial branches under myocardial bridge

Shinjo, Samuel Katsuyuki; Prates, Nadir Eunice Valverde Barbato de; Oba, Sueli M.; Sampaio, Lúcia O.; Nader, Helena B.

doi:10.1016/s0021-9150(98)00323-2

Cited by 11 publications

(8 citation statements)

References 19 publications

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“…In this study, the statistical analysis allows us to assure that there are variations on the frequency of lesions present on the tunica intima of the left coronary artery branches, when prepontine and postpontine segments are compared to the pontine segment, as well as the non occurrence of significant variations on the appearance of these lesions between the males and females studied. Those results are consistent with those results from other authors 9,[11][12][13][14][15][16][17][18][19] , once all results assure that the lesion present at the tunica intima of these arteries along the pontine segment is smaller than those lesions observed on the other two segments. It was also possible to observe that when prepontine and postpontine segments are compared to each other, no significant difference on the lesion degree was found.…”

Section: Discussionsupporting

confidence: 93%

Ponte miocárdica associada a lesões cardiovasculares em bovinos adultos da raça Canchim

Santos¹,

Wafae²,

Beletti³

2012

Arq. Bras. Cardiol.

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Section: Discussionsupporting

confidence: 93%

Ponte miocárdica associada a lesões cardiovasculares em bovinos adultos da raça Canchim

Santos¹,

Wafae²,

Beletti³

2012

Arq. Bras. Cardiol.

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“…[19][20][21] It is not clear how much the underlying atherosclerotic plaques contribute to in-stent restenosis, but both the deep injury and the vessel stretch were shown to trigger the development of in-stent neointima in even normal coronary arteries. 22) Although maximum deployment pressures were not different between the two groups, an additional external force on the vessel wall might have caused a deeper injury in the MB group.…”

Section: Discussionmentioning

confidence: 99%

Angiographic Restenosis After Myocardial Bridge Stenting: A Comparative Study With Direct Stenting of De-Novo Atherosclerotic Lesions

et al. 2004

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SUMMARYData on restenosis after stent implantation in myocardial bridges (MB) are very limited. Six-month angiographic results for 12 symptomatic patients who underwent stent implantation for myocardial bridges were compared retrospectively with those of 39 patients who underwent direct stent implantation for de novo atherosclerotic lesions in the left anterior descending artery. Diameter stenosis decreased from 69 ± 8% to 4 ± 5% in the MB group and from 79 ± 8% to 7 ± 6% in the control group after stent deployment. Systolic narrowing was abolished in all patients with MB. In follow-up, quantitative angiography revealed late loss of 1.8 ± 1.3 mm in the MB group and 0.9 ± 0.9 mm in the control group (P = 0.025). The in-stent restenosis rate was also higher in the MB group compared to the control group (67% versus 28%; P = 0.037). Despite favorable immediate results, stent implantation in MBs may not be promising because of the higher in-stent restenosis rate compared to stenting in de novo atherosclerotic lesions. ( A myocardial bridge (MB) is an anatomical variation in which a part of a coronary artery (mostly left anterior descending artery (LAD)) courses under a segment of myocardium that compresses the lumen during systole despite a normal appearance during diastole. The reported incidence of MB varies over a wide range according to the method of diagnosis, changing from 0.5 to 2.5% in angiographic studies to 15 to 85% in autopsy series.1-3) Although known as a benign and asymptomatic condition in a majority of the patients, MBs may cause angina, myocardial ischemia, infarction, life-threatening cardiac arrhythmias, and even sudden cardiac death. [4][5][6][7][8] The clinical management of patients with symptomatic MB is not well established. On the basis of previous pathophysiological and clinFrom the

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“…The glycosaminoglycan (GAG) composition can influence the stability of atherosclerotic plaques [17], and hyaluronan and chondroitin sulfate accumulation is seen at their erosion centers. On the other hand, changes in the GAG composition can increase antithrombotic protection of vessel walls [18]. In myocardial arteries located beneath the intramyocardial bridge, where there are usually no thrombotic deposits or atherosclerotic lesions, have been found to show a 47% increase in GAG content as compared with the adjacent upstream and downstream segments of the vessel.…”

Section: The Cell Surface Layer -The Glycocalyx and The Extracellularmentioning

confidence: 99%

“…The dermatan sulfate content was increased 1.8-fold and the heparan sulfate content 1.6-fold. The latter was particularly emphasized by the authors as the cause of the elevated athrombogenicity of the vessel wall on deformation by the compressive forces of the fibers of the myocardial bridge during systolic pressure and during the development of atherosclerotic and thrombotic events [18]. The presence of these GAG contributes to vessel integrity and remodeling.…”

Section: The Cell Surface Layer -The Glycocalyx and The Extracellularmentioning

confidence: 99%

Effects of glycosaminoglycans in vascular events

Maksimenko

2008

Pharm Chem J

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In acute cardiovascular lesions, functional recovery of the myocardium occurs when adequate reperfusion of the infarct-related artery and an adequate level of microcirculation and tissue flow in the lesioned area are achieved. The major regulators of these effects are the glycosaminoglycan component of the endothelial cellular coating (glycocalyx, extracellular matrix, interstitial material) and its catabolic enzymes and their inhibitors. The causes and consequences of glycocalyx abnormalities in vascular lesions are considered, along with the potential for glycocalyx reconstruction. The glycoprotein environment of cells has been found to regulate the biomechanical properties of vessels, tissue assembly and repair; it was also able to bind low-and high-molecular-weight ligands. Hydration of glycosaminoglycans determines the development of tissue edema and mediates the anticoagulant activity of the extracellular matrix. Binding of chemokines, growth factors, other proteins, and lipoproteins to glycosaminoglycans has been noted in relation to execution of their regulatory functions. The existence of special structural biding sites for such reactants has been demonstrated, along with a relationship between the biological effects induced by glycosaminoglycans and their molecular weights. The involvement of glycosaminoglycans in the pathophysiological processes occurring in vascular lesions is reviewed, as are promising approaches to regulating the state of the pericellular coatings via the precise and effective control of the level of glycosylation of biological substrates. 553 0091-150X/08/4210-0553

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Distribution and composition of glycosaminoglycans in the left human coronary arterial branches under myocardial bridge

Cited by 11 publications

References 19 publications

Ponte miocárdica associada a lesões cardiovasculares em bovinos adultos da raça Canchim

Ponte miocárdica associada a lesões cardiovasculares em bovinos adultos da raça Canchim

Angiographic Restenosis After Myocardial Bridge Stenting: A Comparative Study With Direct Stenting of De-Novo Atherosclerotic Lesions

Effects of glycosaminoglycans in vascular events

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