The Anti-Inflammatory Effects of Statins on Coronary Artery Disease: An Updated Review of the Literature

Diamantis, Evangelos; Kyriakos, Georgios; Quiles-Sánchez, Lourdes Victoria; Farmaki, Paraskevi; Troupis, Theodoros

doi:10.2174/1573403x13666170426104611

Cited by 166 publications

(126 citation statements)

References 70 publications

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“…We could not conclusively confirm in this trial if patients taking statins achieve worse post-booster immunogenicity since 15 patients represented too small a sample size and the power of test was lower than the usual 80%. This premise is, however, biologically plausible as numerous studies showed an ability of statins to modulate immuno-inflammatory processes [16]. One can assume that statins treatment can impact the vaccine-induced response in some way.…”

Section: Discussionmentioning

confidence: 99%

Factors Influencing Persistence of Diphtheria Immunity and Immune Response to a Booster Dose in Healthy Slovak Adults

et al. 2019

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We assessed the long-term persistence of humoral immunity against diphtheria in adults with childhood vaccination and the immunogenicity of a booster dose considering demographic, behavioural and vaccinating factors. We conducted a trial in 200 healthy Slovak adults aged 24–65 years, immunised against diphtheria in childhood and against tetanus at regular 10–15 year intervals, and receiving a dose of a tetanus-diphtheria toxoid vaccine. The response was determined by ELISA antibody concentrations of paired sera before and at 4 weeks post-vaccination. A seroprotection rate of 21% (95% confidence interval, CI 15.6–27.3%) was found in adults up to 59 years since the last vaccination with seroprotective levels of antibodies against diphtheria ≥0.1 IU/mL and a geometric mean concentration of 0.05 IU/mL. Conversely, seropositive levels ≥0.01 IU/mL were observed in 98% of adults (95% CI 95–99.5%). Booster-induced seroprotection was achieved in 78% of adults (95% CI 71.6–83.5%) clearly depending on pre-booster antibody levels correlating with age and time since the last vaccination. Moreover, only 54.2% of smokers and 53.3% of patients on statins exhibited seroprotection. Booster vaccination against diphtheria was unable to confer seroprotection in all recipients of only childhood vaccination.

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Section: Discussionmentioning

confidence: 99%

Factors Influencing Persistence of Diphtheria Immunity and Immune Response to a Booster Dose in Healthy Slovak Adults

et al. 2019

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“…In vitro and in vivo studies show that statins, inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and the most relevant drugs used to lower serum cholesterol levels, due to their pleiotropic effects decrease subclinical inflammation, oxidative stress, endothelial dysfunction, platelet aggregation, and activation [185][186][187][188][189], improving platelet sensitivity to NO [178], and aspirin [184], but not to GLP-1 [178]. The causes of the enhanced platelet hyperaggregability and the defective GLP-1 actions in dyslipidemia can be multifactorial, although the strong correlation with LDL underlines the role of cholesterol as a major determinant of platelet hyperreactivity with a putative role also in the impaired response to GLP-1.…”

Section: Role Of Dyslipidemia In the Impaired Platelet Reactivitymentioning

confidence: 99%

Influence of Cardiometabolic Risk Factors on Platelet Function

Barale

Russo

2020

IJMS

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Platelets are key players in the thrombotic processes. The alterations of platelet function due to the occurrence of metabolic disorders contribute to an increased trend to thrombus formation and arterial occlusion, thus playing a major role in the increased risk of atherothrombotic events in patients with cardiometabolic risk factors. Several lines of evidence strongly correlate metabolic disorders such as obesity, a classical condition of insulin resistance, dyslipidemia, and impaired glucose homeostasis with cardiovascular diseases. The presence of these clinical features together with hypertension and disturbed microhemorrheology are responsible for the prothrombotic tendency due, at least partially, to platelet hyperaggregability and hyperactivation. A number of clinical platelet markers are elevated in obese and type 2 diabetes (T2DM) patients, including the mean platelet volume, circulating levels of platelet microparticles, oxidation products, platelet-derived soluble P-selectin and CD40L, thus contributing to an intersection between obesity, inflammation, and thrombosis. In subjects with insulin resistance and T2DM some defects depend on a reduced sensitivity to mediators-such as nitric oxide and prostacyclin-playing a physiological role in the control of platelet aggregability. Furthermore, other alterations occur only in relation to hyperglycemia. In this review, the main cardiometabolic risk factors, all components of metabolic syndrome involved in the prothrombotic tendency, will be taken into account considering some of the mechanisms involved in the alterations of platelet function resulting in platelet hyperactivation.

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“…It is usually assumed that any beneficial effect of statins on coronary events is linked to their hypocholesterolemic properties. However, because mevalonic acid, intracellularly synthesized by HMG-CoA reductase, is the precursor of numerous metabolites, inhibition of HMG-CoA reductase has the potential to result in pleiotropic effects (62,63); hence, effects other than cholesterol reduction may help explain the anti-atherosclerotic properties of statins, such as improvement of endothelial function and reduction of platelet aggregation, increased number and activity of endothelial progenitor cells, inhibition of migration and A c c e p t e d M a n u s c r i p t proliferation of smooth muscle cells, stabilization of coronary plaques and atheroma regression (64)(65)(66).…”

Section: Statinsmentioning

confidence: 99%

Lipid lowering drugs and inflammatory changes: an impact on cardiovascular outcomes?

et al. 2018

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Inflammatory changes are responsible for maintenance of the atherosclerotic process and may underlie some of the most feared vascular complications. Among the multiple mechanisms of inflammation, the arterial deposition of lipids and particularly of cholesterol crystals is the one responsible for the activation of inflammasome NLRP3, followed by the rise of circulating markers, mainly C-reactive protein (CRP). Elevation of lipoproteins, LDL but also VLDL and remnants, associates with increased inflammatory changes and coronary risk. Lipid lowering medications can reduce cholesterolemia and CRP: patients with elevations of both are at greatest cardiovascular (CV) risk and receive maximum benefit from therapy. Evaluation of the major drug series indicates that statins exert the largest LDL and CRP reduction, accompanied by reduced CV events. Other drugs, mainly active on the triglyceride/HDL axis, for example, PPAR agonists, may improve CRP and the lipid pattern, especially in patients with metabolic syndrome. PCSK9 antagonists, the newest most potent medications, do not induce significant changes in inflammatory markers, but patients with the highest baseline CRP levels show the best CV risk reduction. Parallel evaluation of lipids and inflammatory changes clearly indicates a significant link, both guiding to patients at highest risk, and to the best pharmacological approach. Key messages Lipid lowering agents with "pleiotropic" effects provide a more effective approach to CV prevention In CANTOS study, patients achieving on-treatment hsCRP concentrations ≤2 mg/L had a higher benefit in terms of reduction in major CV events The anti-inflammatory activity of PCSK9 antagonists appears to be of a minimal extent.

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The Anti-Inflammatory Effects of Statins on Coronary Artery Disease: An Updated Review of the Literature

Cited by 166 publications

References 70 publications

Factors Influencing Persistence of Diphtheria Immunity and Immune Response to a Booster Dose in Healthy Slovak Adults

Factors Influencing Persistence of Diphtheria Immunity and Immune Response to a Booster Dose in Healthy Slovak Adults

Influence of Cardiometabolic Risk Factors on Platelet Function

Lipid lowering drugs and inflammatory changes: an impact on cardiovascular outcomes?

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