Effects of Ramipril on Coronary Events in High-Risk Persons

Dagenais, Gilles R.; Yusuf, Salim; Bourassa, Martial G.; Yi, Qilong; Bosch, Jackie; Lonn, Eva; Kouz, Simon; Grover, John W.

doi:10.1161/hc3001.093502

Cited by 153 publications

(34 citation statements)

References 13 publications

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“…Current therapies that limit aldosterone-mediated vascular injury, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone antagonists, are effective but have significant and often limiting side effects caused by inhibition of renal MR (hyperkalemia), off-target effects on non-mineralocorticoid steroid hormone receptors (gynecomastia), and aldosterone-independent alterations in renal filtration (renal failure) (1,2,47). The identification of PGF as a vascular MR-regulated gene involved in vascular remodeling suggests that inhibition of PGF and/or Flt1 receptor signaling may be effective and more specific targets to prevent vascular cell proliferation and fibrosis after vascular injury.…”

Section: Figurementioning

confidence: 99%

Placental growth factor mediates aldosterone-dependent vascular injury in mice

Jaffe¹,

Newfell²,

Aronovitz³

et al. 2010

J. Clin. Invest.

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Section: Figurementioning

confidence: 99%

Placental growth factor mediates aldosterone-dependent vascular injury in mice

Jaffe¹,

Newfell²,

Aronovitz³

et al. 2010

J. Clin. Invest.

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“…1 Conversely, chronic inhibition of angiotensin II (Ang II) formation by ACE inhibitors reduces the risk of cardiovascular events in patients with arteriosclerosis and after myocardial infarction, as shown in large-scale trials such as the Heart Outcomes Prevention Evaluation study. 2 We and others have recently demonstrated that the RAS is present in human arteriosclerotic lesions 3,4 and is associated with inflammation processes, thereby potentially influencing plaque rupture. 3 Ang II activates a multiplicity of signaling pathways, resulting in cell proliferation, matrix degradation, inflammation, and apoptosis.…”

mentioning

confidence: 96%

Expression of CYR61, an Angiogenic Immediate Early Gene, in Arteriosclerosis and Its Regulation by Angiotensin II

et al. 2002

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Background-The renin-angiotensin system is thought to be involved in development and progression of arteriosclerosis, thereby contributing to adverse cardiovascular events. To elucidate the role of angiotensin II (Ang II) at a cellular level, we analyzed the Ang II-induced gene expression profile. Methods and Results-Genes induced on Ang II stimulation (10 Ϫ7 mol/L, 45 minutes) in rat smooth muscle cells were analyzed by polymerase chain reaction selected subtraction. In addition to known genes, such as interleukin 6, leukemia inhibitory factor, and c-fos, we identified CYR61, an angiogenic immediate early gene. Northern blot analysis revealed a rapid 2.5-fold increase of CYR61 transcript levels by Ang II, peaking at 30 minutes, which was blunted by Ang II type 1 receptor blockade. Exposure of rat aortic rings to Ang II (30 minutes) revealed a 2-fold, and intraperitoneal injection of Ang II (30 minutes) in mice a 3-fold, increase of aortic CYR61 transcripts. In arteriosclerotic aortas of apolipoprotein E-deficient mice, CYR61 transcripts confirmed by in situ hybridization and proteins shown by immunohistochemistry were elevated, whereas they were hardly detectable in wild types. In human carotid atherectomies and arteriosclerotic coronary arteries, immunohistochemical analysis revealed expression of CYR61 within connective tissue in neointima, adventitia, and surrounding small capillaries and blood vessels, colocalized with ACE and Ang II. Normal human arteries showed no significant staining for CYR61. Conclusions-CYR61, an angiogenic factor, is induced by Ang II in vascular cells and tissue. The expression of CYR61, colocalized with Ang II and ACE, in small vessels of human arteriosclerotic lesions is consistent with the notion that the activated renin-angiotensin system may contribute to plaque neovascularization by enhancing regulators of microvessel formation and cell proliferation.

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“…One clinical trial of cholesterol lowering also observed reduced atherosclerosis progression in men who chose to consume high levels of ␣ -tocopherol supplements (39). Based on such suggestive observations, several randomized clinical trials have been conducted to determine whether supplementation with 50-800 IU ␣ -tocopherol reduces cardiovascular disease (CVD) (32,(40)(41)(42)(43) or risk factors for CVD (44)(45)(46)(47)(48).…”

mentioning

confidence: 99%

α-Tocopherol protects against diet induced atherosclerosis in New Zealand white rabbits

Schwenke

Rudel

Sorci‐Thomas

et al. 2002

Journal of Lipid Research

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In this study, we asked the question "does ␣ -tocopherol supplementation prevent an increase in total plasma cholesterol (TPC) concentration and reduce the deposition of cholesterol in arterial plaques of rabbits fed atherogenic diets?" Isocaloric diets containing 0.1% cholesterol to induce atherosclerosis were enriched in one of three fats: saturated fats (SAT), monounsaturated fats (MONO), or n-6 polyunsaturated fats (POLY). Half of each of the three diets were supplemented with 2,500 IU ␣ -tocopherol/kg-diet. Unsupplemented diets contained 25 IU ␣ -tocopherol/kg-diet. Rabbits supplemented with ␣ -tocopherol had plasma ␣ -tocopherol concentrations 10-fold higher and an average TPC concentration 31% lower, P ‫؍‬ 0.017, than rabbits fed unsupplemented diets. Among the three fat-fed groups, the difference was greatest for the POLY fat fed group (54%, P ‫؍‬ 0.041). POLY fat-fed rabbits without ␣ -tocopherol supplementation had plasma HDL cholesterol concentrations that were less than half that of rabbits fed other fats, P р 0.0001. In general, differences in mean esterified artery cholesterol concentrations among the three fat-fed groups, with and without ␣ -tocopherol supplementation, paralleled differences in TPC concentration among the groups.This study suggests that for rabbits fed high pharmacological doses of ␣ -tocopherol, atherosclerosis can be diminished in situations where the plasma cholesterol concentrations are also significantly lower. -Schwenke, D. C., L. L. Rudel, M. G. Sorci-Thomas, and M. J. Thomas. ␣ -Tocopherol protects against diet induced atherosclerosis in New Zealand white rabbits.

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Effects of Ramipril on Coronary Events in High-Risk Persons

Cited by 153 publications

References 13 publications

Placental growth factor mediates aldosterone-dependent vascular injury in mice

Placental growth factor mediates aldosterone-dependent vascular injury in mice

Expression of CYR61, an Angiogenic Immediate Early Gene, in Arteriosclerosis and Its Regulation by Angiotensin II

α-Tocopherol protects against diet induced atherosclerosis in New Zealand white rabbits

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