Aspirin Improves Endothelial Dysfunction in Atherosclerosis

Husain, Syed; Andrews, Neil; Mulcahy, David; Panza, Julio A.; Quyyumi, Arshed A.

doi:10.1161/01.cir.97.8.716

Cited by 238 publications

(159 citation statements)

References 53 publications

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“…Investigation of possible mechanisms, by which low-dose aspirin can influence on BP of patients with AH and hypercholesterolaemia Improvement of endothelial function was shown in acute studies, 28,29 while results of chronic trials are conflicting [30][31][32] Our study demonstrates that addition of low-dose aspirin in hypertensive and hypercholesterolaemic subjects on top of antihypertensive and statins improves endothelial function and reduces BP Homogeneity of the studied population. Demonstration of synergistic interactions between aspirin and statins on BP reduction via improvement of NOmediated endothelial function Small study.…”

Section: Low-dose Aspirin On Bp In Hypertensive Patientsmentioning

confidence: 72%

“…[23][24][25][26][27] It is of note that low-dose aspirin, at least in acute studies, improves endothelial function in patients with hypercholesterolaemia 28 and atherosclerosis. 29 Results of chronic trials are conflicting. [30][31][32] Since other COX inhibitors showed no beneficial vascular effects, aspirin might exhibit a vasculoprotective, COX-independent mechanism.…”

Section: Discussionmentioning

confidence: 99%

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Effects of low-dose aspirin on blood pressure and endothelial function of treated hypertensive hypercholesterolaemic subjects

et al. 2005

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The main objective of this study was to assess whether aspirin 100 mg QD can improve blood pressure (BP) control and endothelial function in subjects with arterial hypertension (AH) and hypercholesterolaemia. In total, 21 patients of both sexes (52.1711.5 years) with treated AH and hypercholesterolaemia on antihypertensive and statin therapy were included in the treatment group. In the control group, 20 matched patients of both sexes (51.3712.7 years), but without statin therapy, were recruited. Treatment group subjects received aspirin (100 mg QD) for a duration of 12 weeks at randomization (Treatment phase-1), followed by single blind matching placebo for 12 weeks (Placebo phase) and then again received aspirin (100 mg QD) for an additional 12 weeks (Treatment phase-2). The control group participated in Treatment phase-1, but did not continue Placebo phase and Treatment phase-2. At randomization and at the end of each study phase, mean 24-h systolic BP (SBP) and diastolic BP (DBP) were assessed by 24-h ambulatory blood pressure monitoring (ABPM) and endotheliumdependent (flow mediated, FMD) and -independent (nitroglycerin induced, NTG) vasodilatations of brachial artery were measured using high-resolution ultrasound. In Treatment phase-1, reduction of SBP and DBP (DSBP 5.772.6 mmHg, P ¼ 0.008; DDBP 3.871.7 mmHg, P ¼ 0.014) and improvement of FMD (4.170.6%, P ¼ 0.019), in Placebo phase an elevation of SBP and DBP (DSBP À6.272.9 mmHg, P ¼ 0.002; DDBP À4.271.9 mmHg, P ¼ 0.031) and worsening of FMD (À3.870.9%, P ¼ 0.027), and in Treatment phase-2 reduction of SBP and DBP (DSBP 4.972.3 mmHg, P ¼ 0.005; DDBP 4.171.3 mmHg, P ¼ 0.024) and improvement of FMD (4.571.3%, P ¼ 0.009) were observed in the treatment Group but not in the control group. Addition of low-dose aspirin to antihypertensive medications and statins in hypertensive and hypercholesterolaemic subjects can reduce both SBP and DBP by improvement of endothelial function.

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Section: Low-dose Aspirin On Bp In Hypertensive Patientsmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 99%

Effects of low-dose aspirin on blood pressure and endothelial function of treated hypertensive hypercholesterolaemic subjects

et al. 2005

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“…The subject of pharmacological treatment of endothelial dysfunction has been reviewed by myself and others recently (52,94,95). Suffice it to say, interventions associated with favourable cardiovascular outcomes have been associated with attenuation of endothelial dysfunction for the most part (96)(97)(98)(99)(100)(101). The notable exception to this is hormone replacement therapy, which has been associated with improvement in endothelium-dependent vasomotion, but not cardiovascular outcome.…”

Section: Relationship Of Endothelial Function To Risk Factors and Thementioning

confidence: 99%

Arterial stiffness or endothelial dysfunction as a surrogate marker of vascular risk

Anderson

2006

Canadian Journal of Cardiology

151

113

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T he understanding of the pathophysiology of atherosclerosis and its vascular complications has increased dramatically over the past decade. Numerous measurable biomarkers play a role in the atherosclerosis process, and are associated with clinically important vascular events. Not only has their evaluation advanced our knowledge of the atherosclerotic process but it has also accelerated a search for new diagnostic tools to aid in risk stratification. Putative factors include soluble biomarkers and imaging assessments of vascular structure and function. The endothelium plays a key role in vascular homeostasis through the release of a variety of paracrine factors that interact with platelets, inflammatory cells and the vessel wall. The endothelium's central location allows it to sense and respond to a variety of perturbations. Endothelial dysfunction is an early marker of disease. Risk factors can also affect mechanical properties such as arterial stiffness, which is now recognized as a major contributor to systolic hypertension in elderly people. Methods of assessing endothelial function and arterial stiffness are available for clinical research and recent evidence suggests that these measures may provide important prognostic information. ATTRIBUTES OF A SURROGATE BIOMARKEREpidemiological studies, such as Framingham, have allowed longitudinal assessment of cardiovascular events and the development of simple scoring tables for risk calculation (1,2). These factors involved include blood pressure, lipid profile, smoking status and age. More recently, many factors thought to be associated with the atherosclerotic process have been studied. Some of these have been shown to correlate with clinical outcomes and have been deemed biomarkers (3,4). However, association does not necessarily imply causation and, due to a variety of limitations, most of these markers will not be useful for the clinical evaluation of risk or drug therapy (5). To become clinically important, a biomarker must fulfill the criteria for a surrogate marker. A surrogate substitutes for clinically important end points with respect to how an individual feels, functions or survives. Classic examples include blood pressure and low density lipoprotein cholesterol. These are targets of treatment. A surrogate should meet the following criteria:• Adds independent information above currently used criteria;• Is reliably and reproducibly measured;• Accounts for a significant proportion of disease risk;• Provides good predictive value;• Is reasonably associated with the underlying pathophysiology;• If it is to be used in risk prevention, is present before the clinical appearance of the outcome; and• Is available and practical for widespread application (5-8). ADVANCES IN VASCULAR BIOLOGY

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“…Anti-inflammatory therapies, including nonselective and selective COX inhibitors, have been reported to improve endothelial function in patients with risk factors and established atherosclerosis. For example, aspirin (Husain et al 1998) and the selective COX-2 inhibitor celecoxib (Widlansky et al 2003b) have both been shown to improve endothelium-dependent dilation. It is well established that cholesterol-lowering therapy also reduces systemic markers of inflammation, including CRP (Ballantyne et al 2003).…”

Section: Human Studies Of Systemic Inflammation and Endothelial Dysfumentioning

confidence: 99%

Effects of Systemic Inflammation on Endothelium-Dependent Vasodilation

Huang

Vita

2006

Trends in Cardiovascular Medicine

114

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The importance of inflammation in the pathogenesis of atherosclerosis is well established. The vascular endothelium contributes to and is affected by the inflammatory process. For example, a variety of cytokines have the ability to "activate" the endothelium and thereby promote expression of adhesion molecules and chemotactic factors that accelerate the inflammatory process and direct accumulation of leukocytes to specific sites in the arterial tree. In experimental systems, activation of endothelial cells is also associated with a loss of the biologic activity of endothelium-derived nitric oxide, an effect that accelerates the inflammatory process and also promotes local thrombosis and impairs local control of vasomotor tone. Consistent with these experimental studies, recent studies have provided evidence that inflammation is associated with an impairment of nitric oxide-dependent responses in human subjects. This article will review the experimental and clinical studies that support the relevance of inflammation to nitric oxide bioactivity in human atherosclerosis.It is now well recognized that atherosclerosis is an inflammatory disease (Ross 1999). Systemic risk factors induce a state of inflammation that contributes to all stages of atherosclerosis from the initiating events in lesion formation to the latest phase when plaques rupture, thrombose, and produce clinical syndromes such as myocardial infarction or stroke (Libby et al. 2002). The importance of inflammation in atherosclerosis is supported by recent studies showing that elevated levels of inflammatory markers identify individuals with increased risk for cardiovascular events (Pearson et al. 2003). In particular, the acute phase reactant C-reactive protein (CRP) shows promise as a clinically useful marker of cardiovascular risk (Ridker 2003).The vascular endothelium is both affected by and contributes to the inflammatory process that leads to atherosclerosis. For example, proinflammatory factors "activate" endothelial cells to promote an atherogenic phenotype. The activated endothelium, in turn, expresses adhesion molecules and chemotactic factors that accelerate and localize the inflammatory process. An important consequence of endothelial activation is loss of the biologic activity of endotheliumderived nitric oxide. Investigators have argued that a broad alteration of endothelial function, including loss of nitric oxide under proinflammatory conditions, might be a critical mechanism that links systemic states of inflammation to atherosclerosis (Vallance et al. 1997). This article will review the recent studies that support the relevance of systemic inflammation to nitric oxide bioactivity in human subjects. The Endothelium as a Regulator of Vascular HomeostasisThe endothelium regulates vasomotor tone, blood fluidity, growth of vascular smooth muscle cells, and local inflammation by elaborating a number of paracrine factors, including nitric oxide (Widlansky et al. 2003a). Endothelium-derived nitric oxide is a potent vasodilator and acts ...

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Aspirin Improves Endothelial Dysfunction in Atherosclerosis

Cited by 238 publications

References 53 publications

Effects of low-dose aspirin on blood pressure and endothelial function of treated hypertensive hypercholesterolaemic subjects

Effects of low-dose aspirin on blood pressure and endothelial function of treated hypertensive hypercholesterolaemic subjects

Arterial stiffness or endothelial dysfunction as a surrogate marker of vascular risk

Effects of Systemic Inflammation on Endothelium-Dependent Vasodilation

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