Clinical Importance of Endothelial Function in Arteriosclerosis and Ischemic Heart Disease

Egashira, Kensuke

doi:10.1253/circj.66.529

Cited by 97 publications

(65 citation statements)

References 78 publications

(77 reference statements)

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“…24,25 We and others have demonstrated that 1 increased monocyte-mediated inflammation or MCP-1 expression is associated with greater neointima formation after stenting, 26,27 and 2 anti-MCP-1 gene therapy 15,28 -30 or administration of blocking antibody against the MCP-1 receptor 31 markedly reduces neointima formation after vascular injury. However, no previous study examined whether or not those inflammatory and proliferative changes after stenting depends on the AT 1 receptor.…”

Section: Discussionmentioning

confidence: 99%

“…21,22 These in vivo observations are also consistent with previously published in vitro data suggesting that proliferation and migration of smooth muscle cells are critically mediated by oxidative stress via AT 1 -mediated activation of NADPH oxidases. [23][24][25][26][27][28][29] Interestingly, treatment with ARB not only attenuated the levels of oxidative stress markers but also reduced the level of immunoreactive AT 1 . These data suggest the presence of a positive feedback loop in which activation of AT 1 further enhances expression and activity of the AT 1 receptor in vivo, as seen in the present study.…”

Section: Discussionmentioning

confidence: 99%

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Angiotensin II Type 1 Receptor Blockade Attenuates In-Stent Restenosis by Inhibiting Inflammation and Progenitor Cells

et al. 2006

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Abstract-The precise mechanism by which angiotensin II type 1 receptor blocker reduces in-stent restenosis in clinical trials is unclear. We, therefore, investigated the mechanism of in-stent neointima formation. Male cynomolgus monkeys and rabbits were fed a high-cholesterol diet and were allocated to untreated control and type 1 receptor blocker groups. Five days after grouping, multilink stents were implanted in the iliac artery. The type 1 receptor blocker reduced the development of in-stent neointima formation by Ϸ30% in rabbits and monkeys. To investigate potential mechanisms, we examined the expression of renin-angiotensin system markers, all of which increased in monocytes and smooth muscle-like cells in the neointima and media within 7 days. The type 1 receptor blocker attenuated increased oxidative stress, the enhanced expression of markers of the rennin-angiotensin system and monocyte chemoattractant protein-1, and macrophage infiltration. The effects of type 1 receptor blocker on the differentiation of peripheral blood mononuclear cells into vascular progenitor cells were also examined. Key Words: angiotensin II Ⅲ oxidative stress Ⅲ monocytes C oronary intervention with metal stent implantation is performed in Ͼ1.5 million patients with atherothrombotic lesions worldwide and has become the major revascularization technique. 1 The clinical benefits of this procedure are reduced by in-stent restenosis. In-stent restenosis results exclusively from neointima formation because of proliferation/migration of smooth muscle cells and inflammatory changes in response to stent-associated injury. 2 Recent clinical trials demonstrated great benefits of drug-eluting stents (containing sirolimus, paclitaxel, etc) in preventing restenosis and improving clinical outcomes. 3,4 However, systemic medical therapies for stentassociated thrombosis and for control of risk factors are essential therapy in addition to drug-eluting stents for the prevention of future coronary events. This notion is supported by recent reports showing multiple atherosclerotic plaque ruptures at sites other than the culprit lesion, as observed in acute coronary syndrome by intravascular ultrasound analysis. 5 The renin-angiotensin system (RAS) has been implicated in the pathogenesis of restenosis and acute coronary syndrome 6 -11 and, thus, may be a potential target for the prevention of in-stent restenosis and atherothrombotic events. Indeed, a recent, single-center VALsartan for Prevention of REstenosis after Stenting of Type B2/C lesions (Val-PREST) trial demonstrated that treatment with angiotensin II type 1 (AT 1 ) receptor blocker (ARB) reduces the incidence of restenosis and revascularization in selected patients with type B2/C lesions. 12 The same group compared valsartan with angiotensin-converting enzyme (ACE) inhibition after bare metal stent implantation in the VALsartan Versus ACE inhibition (VALVACE) trial and reported greater benefits from systemic valsartan treatment than from angiotensinconverting enzyme inhibitors in reducing r...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Angiotensin II Type 1 Receptor Blockade Attenuates In-Stent Restenosis by Inhibiting Inflammation and Progenitor Cells

et al. 2006

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“…Impaired endothelium-dependent vasodilation represents an early manifestation of atherosclerosis and ischemic vascular disease (Egashira, 2002).…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein B of low-density lipoprotein impairs nitric oxide-mediated endothelium-dependent relaxation in rat mesenteric arteries

Zhang

Edvinsson

et al. 2014

European Journal of Pharmacology

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“…A common early factor linking these disorders appears to be endothelial dysfunction, which paves the way for reduced vasoreactivity and vascular compliance, increased platelet activity, and inflammatory mechanisms that contribute to the development of atherosclerotic plaques. 1,2 Despite this apparent convergence, there is evidence that the pathophysiology underlying stroke may differ meaningfully from that of CAD. Starting around 1980, mortality rates from stroke in the United States have shown a leveling relative to the decline observed in preceding decades.…”

Section: Introductionmentioning

confidence: 99%

Medical prevention of secondary stroke: A cardiologist's perspective

Ezekowitz

2004

Clin Cardiol

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Summary: Post-stroke patients are at greatest risk from a second stroke rather than an event in another vascular bed. Thus treatment strategies must be aimed at preventing recurrent stroke. Recent evidence suggests that the pathophysiology underlying stroke may differ from that of coronary artery disease. Secondary events may replicate primary events, and treatment strategies for patients who experienced an initial stroke must therefore focus on preventing recurrent stroke. Medical strategies for secondary stroke prevention focus on four areas: control of hypertension, control of blood lipids, anticoagulant therapy, and treatment with antiplatelet agents such as aspirin, clopidogrel, and aspirin combined with extended-release dipyridamole, all of which the American College of Chest Physicians deems acceptable for first-line treatment for preventing secondary stroke.

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Clinical Importance of Endothelial Function in Arteriosclerosis and Ischemic Heart Disease

Cited by 97 publications

References 78 publications

Angiotensin II Type 1 Receptor Blockade Attenuates In-Stent Restenosis by Inhibiting Inflammation and Progenitor Cells

Angiotensin II Type 1 Receptor Blockade Attenuates In-Stent Restenosis by Inhibiting Inflammation and Progenitor Cells

Apolipoprotein B of low-density lipoprotein impairs nitric oxide-mediated endothelium-dependent relaxation in rat mesenteric arteries

Medical prevention of secondary stroke: A cardiologist's perspective

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