A definition of the intima of human arteries and of its atherosclerosis-prone regions. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association.

Stary, Herbert C.; Blankenhorn, David H.; Chandler, A. Bleakley; Glagov, Seymour; Insull, William; Richardson, Mary; Rosenfeld, Michael E.; Schaffer, Stephen Allan; Schwartz, Colin J.

doi:10.1161/01.atv.12.1.120

Cited by 340 publications

(217 citation statements)

References 92 publications

(37 reference statements)

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“…Both disorders have been associated with precocious and accelerated increase in vascular stiffness which, in turn, enhances the risk of cardiovascular diseases and mortality [3,4,5,6]. Peripheral pulse pressure (PP) is regarded as a surrogate measure of arterial stiffness in adult subjects older than 50 years, but not in the young [7, 8,] and in the general population it has been shown to correlate with cardiovascular morbidity and mortality [9, 10].…”

Section: Introductionmentioning

confidence: 99%

Pulse Pressure and Mortality from Cerebrovascular Diseases in Type 2 Diabetic Patients: The Verona Diabetes Study

Zoppini

Verlato²,

Zamboni³

et al. 2006

Cerebrovasc Dis

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Background/Objective: Previous studies conducted both in the general and diabetic population have shown that pulse pressure (PP) can predict mortality from cardiovascular diseases. The aim of the present study was to investigate the relationship between PP and specific cardiovascular mortality, i.e. from cerebrovascular and ischemic heart diseases, in a well-characterized cohort of type 2 diabetic patients. Methods: A cohort of 1,128 known type 2 diabetic patients 56 to 74 years of age with at least 2 blood pressure measurements for each year between 1984–1986 was followed-up for ten years to assess specific causes of death. The analyses were carried out by using the mean and the coefficient of variation (CV) of PP. Results: By the end of the 10-year follow-up period, 375 patients (178 male, 197 female) had died (33%). The mean PP resulted as an independent predictor of all causes and cardiovascular mortality. Remarkably, the mean PP, but not the CV of PP, was highly predictive of mortality from cerebrovascular diseases. The risk of cerebrovascular mortality rose by 86% with a 10 mm Hg increase in mean PP. PP turned out to be the most important predictor of cerebrovascular mortality among various pressure indexes (mean, systolic and diastolic pressure). Conclusion: The mean pulse pressure, but not the coefficient of variation is a strong predictor of cardiovascular mortality, mainly from cerebrovascular diseases, in type 2 diabetic patients.

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Section: Introductionmentioning

confidence: 99%

Pulse Pressure and Mortality from Cerebrovascular Diseases in Type 2 Diabetic Patients: The Verona Diabetes Study

Zoppini

Verlato²,

Zamboni³

et al. 2006

Cerebrovasc Dis

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“…By positioning a non-occlusive, soft silicone collar around the rabbit carotid artery, a neo-intima develops within seven days via smooth muscle cell infiltration into the subendothelium (Kockx et al, 1992). A neo-intima can be considered as a site of predilection for atherosclerosis (Wilens, 1951;Stary et al, 1992). Previously, it has been demonstrated that the nitric oxide synthase: guanosine 3':5'-cyclic monophosphate (cyclic GMP) system remains intact in neo-intima-bearing vessels, but that muscarinic endothelium-dependent relaxation becomes selectively impaired (De Meyer et al, 1991;Arthur & Dusting, 1992).…”

Section: Introductionmentioning

confidence: 99%

Vasoconstrictor responses after neo‐intima formation and endothelial removal in the rabbit carotid artery

Meyer¹,

Bult

Üstünes

et al. 1994

British J Pharmacology

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1 The present study examined the responses of the rabbit carotid artery to five vasoconstrictors after neo-intima formation induced by perivascular collar treatment and evaluated the role of constitutive and inducible nitric oxide (NO) synthase and endothelial cells (ECs). 2 Ring segments of the rabbit carotid artery were mounted in organ chambers for isometric tension recording. Neo-intima-bearing vessels developed less force (Em,.) in response to KCl, the thromboxanemimetic U-46619 and 5-hydroxytryptamine (5-HT), but not to angiotensin I and II. 3 The collar-treatment increased the sensitivity to 5-HT, and decreased the sensitivity to angiotensin II. The sensitivity to U-46619 and angiotensin I remained unchanged. 4 Mechanical removal of ECs and inhibition of NO biosynthesis by N0-monomethyl-L-arginine (L-NMMA) and N0-nitro-L-arginine (L-NOARG) increased the sensitivity to 5-HT in sham and collartreated segments to the same extent. The effects of collar-treatment and endothelial removal or treatment with inhibitors of NO biosynthesis were additive. Inhibition of NO biosynthesis failed to augment sensitivity to 5-HT after endothelial denudation. L-NOARG increased the force development to KC1 in sham and collar-treated segments to the same extent. However, L-NMMA and L-NOARG failed to augment the contractile responses of neo-intima-bearing vessels to 5-HT and KCl after endothelial removal. 5 The responses to angiotensin I were not altered, either by the neo-intima or by endothelial removal. In arteries with a neo-intima the sensitivity to angiotensin II was decreased. Removal of the endothelium or incubation with L-NOARG counteracted this rightward shift and increased Em|. 6 Our results demonstrate that contractions to 5-HT, angiotensin II and KCl are modulated by NO in both sham and neo-intima-bearing vessels. Inhibition of NO biosynthesis and collar treatment resulted in additive effects on the EC50 values, suggesting that the 5-HT and angiotension (AT) receptors on the smooth muscle cells are also modified by the formation of a neo-intima. Furthermore, the reduced contractile responses of segments with a neo-intima are not due to NO formed by an inducible NO synthase in those vessels.

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“…Based on their structural differences at different stages of atherogenesis, atherosclerotic plaques are classified as early, intermediate, advanced, and complicated lesions (12)(13)(14). Recently, other variables of the advancing lesions have also been described and related to the structural differences of the plaques.…”

mentioning

confidence: 99%

Decrease in pH Strongly Enhances Binding of Native, Proteolyzed, Lipolyzed, and Oxidized Low Density Lipoprotein Particles to Human Aortic Proteoglycans

Sneck

Kovanen

Öörni

2005

Journal of Biological Chemistry

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Binding of low density lipoprotein (LDL) to proteoglycans and modification of LDL are key processes in atherogenesis. Recently, it has been demonstrated that during atherogenesis the extracellular pH of atherosclerotic lesions decreases. We have examined the effect of the decreased pH on the binding of LDL to human aortic proteoglycans. The binding of native, oxidized, proteolyzed (␣-chymotrypsin-treated), or lipolyzed (sphingomyelinase-or phospholipase A 2 -treated) LDL particles to proteoglycans were measured in microtiter well assays at pH 5.5-7.5. We found that the lower the pH, the higher the amount of binding of LDL to proteoglycans. At the lowest pH tested (pH 5.5), the amounts of proteoglycan-bound native, proteolyzed, sphingomyelinase-, and phospholipase A 2 -treated LDL were 20-, 23-, 30-, and 37-fold higher, respectively, than at pH 7.5. Interestingly, although oxidized LDL failed to bind to proteoglycans at neutral pH, there was significant binding at acidic pH. Binding of native and modified LDL to proteoglycans at pH 5.5 was blocked by 1 M NaCl, indicating that at neutral pH LDL binds to proteoglycans via ionic interactions. Inhibition of this binding by acetylation and cyclohexanedione treatment of LDL showed that the positively charged amino acids of apolipoprotein B-100, lysine, and arginine, respectively, mediated the ionic interaction. Taken together, our results suggest that in areas of atherosclerotic arterial intima where the extracellular pH decreases, retention of LDL by proteoglycans is enhanced, leading to extracellular accumulation of LDL and progression of the disease.Accumulation of cholesterol in the inner layer of the arterial wall, the intima, leads to the development of atherosclerotic lesions, the lesional cholesterol being mostly derived from circulating low density lipoprotein (LDL) 2 particles (1). Once LDL particles have entered the subendothelial space they are entrapped by the extracellular matrix, particularly by intimal proteoglycans (2-4), which form an organized, negatively charged, tight network (5, 6). The retention of LDL particles by proteoglycans is considered to have key role in the development of atherosclerosis (7,8). A role for LDL retention in experimental atherosclerosis has been directly demonstrated in mice expressing proteoglycan bindingdefective human apoB-100. In these transgenic mice, formation of early atherosclerotic plaques is significantly decreased (9, 10), but this modification does not prevent the development of atherosclerosis at later stages (10).Numerous hydrolytic enzymes and pro-oxidative agents are found in the arterial intima, especially in atherosclerotic lesions, and LDL particles that enter the arterial intima are susceptible to proteolytic, lipolytic, and oxidative modifications, which can lead to aggregation and fusion of the modified LDL particles (11). Indeed, intimal LDL particles show signs of proteolysis, phospholipolysis, and oxidation, and intimal lipid droplets have features that suggest they are formed from modified LDL part...

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A definition of the intima of human arteries and of its atherosclerosis-prone regions. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association.

Cited by 340 publications

References 92 publications

Pulse Pressure and Mortality from Cerebrovascular Diseases in Type 2 Diabetic Patients: The Verona Diabetes Study

Pulse Pressure and Mortality from Cerebrovascular Diseases in Type 2 Diabetic Patients: The Verona Diabetes Study

Vasoconstrictor responses after neo‐intima formation and endothelial removal in the rabbit carotid artery

Decrease in pH Strongly Enhances Binding of Native, Proteolyzed, Lipolyzed, and Oxidized Low Density Lipoprotein Particles to Human Aortic Proteoglycans

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