Virtual histology intravascular ultrasound (VH-IVUS) imaging is an innovative tool for the morphological evaluation of coronary atherosclerosis. Evidence for the effects of statin therapy on VH-IVUS parameters have been inconclusive. Consequently, we performed a systematic review and meta-analysis to investigate the impact of statin therapy on plaque volume and its composition using VH-IVUS. The search included PubMed, Cochrane Library, Scopus and Embase (through 30 November 2014) to identify prospective studies investigating the effects of statin therapy on plaque volume and its composition using VH-IVUS. We identified nine studies with 16 statin treatment arms and 830 participants. There was a significant effect of statin therapy in reducing plaque volume (standardized mean difference (SMD): −0.137, 95 % confidence interval (CI): −0.255, −0.019; P = 0.023), external elastic membrane volume (SMD: −0.097, 95 % CI: −0.183, −0.011; P = 0.027) but not lumen volume (SMD: −0.025, 95 % CI: −0.110, +0.061; P = 0.574). There was a significant reduction in fibrous plaque volume (SMD: −0.129, 95 % CI: −0.255, −0.003; P = 0.045) and an increase of dense calcium volume (SMD: +0.229, 95 % CI: +0.008, +0.450; P = 0.043), while changes in fibro-fatty (SMD: −0.247, 95 % CI: −0.592, +0.098; P = 0.16) and necrotic core (SMD: +0.011, 95 % CI: −0.144, +0.165; P = 0.892) tissue volumes were not statistically significant. This meta-analysis indicates a significant effect of statin therapy on plaque and external elastic membrane volumes and fibrous and dense calcium volumes. There was no effect on lumen volume, fibro-fatty and necrotic tissue volumes.

Introduction : Many studies have shown that oral supplementation with astaxanthin may be a novel potential treatment for inflammation and oxidative stress in cardiovascular diseases, but evidence of the effects on lipid profile and glucose is still inconclusive. Therefore, we performed a...

Proprotein convertase subtilisin/kexin 9 (PCSK9) is part of the proteinase K subfamily of subtilases and plays a key role in lipid metabolism. It increases degradation of the low-density lipoprotein receptor (LDL-R), modulates cholesterol metabolism and transport, and contributes to the production of apolipoprotein B (apoB) in intestinal cells. Exogenous PCSK9 modifies the activity of 3-hydroxy-3-methylglutaryl-coenzyme A reductase and acyl coenzyme A:cholesterol acyltransferase and enhances secretion of chylomicrons by modulating production of lipids and apoB-48. Statins increase PCSK9 messenger RNA expression and attenuate the capacity to increase LDL-R levels. Therefore, the inhibition of PCSK9 in combination with statins provides a promising approach for lowering low-density lipoprotein cholesterol (LDL-C) concentrations. This review will address new therapeutic strategies targeting PCSK9, including monoclonal antibodies, antisense oligonucleotides, small interfering RNAs, and other small molecule inhibitors. Further studies are still needed to determine the efficacy and safety of the PCSK9 inhibitors not only to decrease LDL-C but also to investigate the potential underlying mechanisms involved and to test whether these compounds actually reduce cardiovascular end points and mortality.

Atherosclerotic cardiovascular disease is the leading cause of death in many developed countries. It is characterized by complex endocrine, paracrine and juxtacrine interactions between immune and vascular cells, as well as several tissues and organs. Oxidative stress and inflammation have an important role in the promotion of atherosclerotic cardiovascular disease. Considering the complicated mechanisms and signals involved in atherosclerosis, research is focused on blood-based biomarkers, gene-based markers, metabolomics and other potentially interesting approaches for biomarker discovery. These biomarkers can be introduced as routine diagnostic tests if they prove to be cost-effective and to predict future cardiovascular events. Given the overlap of circulating inflammatory and oxidative stress biomarkers in atherosclerosis and rheumatic diseases, we aim to overview their potential to screen cardiovascular risk and also to predict the evolution of associated rheumatic diseases.

Abstract: Many pharmacological and non-pharmacological strategies have been used to increase high-density lipoprotein- cholesterol (HDL-C) levels, but the results obtained have not been consistently associated with effective cardiovascular risk reduction. Therefore, research is now focused to improve HDL functionality, independent of HDL-C levels. The quality of HDL particles can vary considerably due to its heterogeneity caused by various lipids, proteins, vitamins, hormones and small RNAs that are associated with HDL. These components could act as potential HDL-related biomarkers, which may guide effective therapeutic interventions. Evaluation of HDL functionality seems to be more relevant, given the current evidence of the pleiotropic potentially atheroprotective functions of HDL. It is relevant to understand which HDL-related properties involved in its cardioprotective functions, in order to develop pharmacological and nonpharmacological therapies to improve HDL functionality.