European Atherosclerosis Journal

Atherosclerosis associated with Chlamydia pneumoniae: Dissecting the etiology

Hasan Selcuk Ozkan, Meral Kayikcioglu — Sat, 31 Aug 2024 00:00:00 +0000

Chlamydia pneumoniae related infections and atherosclerosis are both common entities. Today, the literature presents an enormous amount of data regarding the role of C. pneumoniae in the development and sustainment of atherosclerosis and allowing us to comprehend the molecular mechanisms behind better. The implications of C. pneumoniae in atherogenesis include altered platelet function, hypercoagulability, macrophage dysfunction, vascular smooth muscle proliferation, and increased neutrophilic migration. Therefore, it would not be wrong to implicate that, C. pneumoniae plays important roles in almost every stage of atherogenesis. Furthermore, various serological markers suggestive of active or past C. pneumoniae infection are known to be associated with multiple clinical presentations, such as abdominal aortic aneurysms, subclinical atherosclerosis in the young individuals, aggravated atherosclerosis in heterozygous familial hypercholesterolemia. This review, as a result, aims to provide detailed insights into the pathophysiological mechanisms of atherogenesis associated with C. pneumoniae and its clinical implications.

MicroRNAs in the progression of atherosclerosis: rise and fall of the atherosclerotic plaque

Sat, 31 Aug 2024 00:00:00 +0000

Atherosclerosis is the main cause of mortality globally, being at the basis of most cardiovascular diseases. It is a multifactorial disease, arising from complex interactions comprising changes in lipid metabolism, inflammation and oxidative stress. These factors contribute to endothelial damage and dysfunction, the accumulation of immune cells and smooth muscle cells in the intima, ultimately leading to the formation of atherosclerotic plaques, which restricts blood flow through the vessels. Much progress has been made in the last decades in debunking the underlying mechanisms of atherosclerosis development, especially concerning the evaluation and prediction of plaque stability and the understanding of the roles played by each of the involved cell types. As yet, mechanisms that drive plaque development toward specific 'vulnerable' phenotypes remain undiscovered. Based on recent advancements in RNA therapeutics, this review aims to illustrate a comprehensive overview of miRNAs relevant to various aspects of atherosclerosis and emphasizes their theranostic potential, highlighting their dual role as both drug targets and biomarkers.

Atherosclerosis and cholesterol: What we should know

Alberico L. Catapano — Sat, 31 Aug 2024 00:00:00 +0000

The relationship between plasma cholesterol levels and the risk of cardiovascular events is well known. When analysing plasma cholesterol levels and integrating data from several studies, including the Pooling Project, the Framingham Heart Study and the Israeli Perspective Study, a consistent association was confirmed worldwide. This pattern was particularly evident in the Seven Countries Study.1 The observed variations in risk across different populations are largely due to the baseline risk values of these populations. For example, the Framingham Heart Study has shown that its results are applicable in any country by adjusting for baseline risk, suggesting a universal pattern in the relationship between cholesterol levels and cardiovascular risk. This has led to debate because the relationship has been oversimplified and presented as linear when it is not necessarily so. For example, an increase in total cholesterol of 0.5 mmol/L (about 20 mg/dL) correlates with a 12% change in mortality risk. In agreement with this observation, data from the Cholesterol Treatment Trialists' (CTT) Collaboration have shown that lowering low-density lipoprotein cholesterol (LDL-C) by 1 mmol/L reduces the risk of coronary heart disease by 22-23% reduction, which is consistent with data from clinical trials.

Novel approaches to lipid lowering

Maurizio Averna — Sat, 31 Aug 2024 00:00:00 +0000

The focus of this review are the novel and future approaches to reduce the cardiovascular (CV) residual risk by reducing the apoB-containing lipoproteins levels. We assume that in the clinical practice a combination therapy based on the use of high intensity statins, ezetimibe, bempedoic acid, mAbs anti PCSK9 or Inclisiran may reduce most of the cardiovascular risk associated with the apoB containing lipoproteins and may contribute to achieve the LDL-Cholesterol (LDL-C) goal in the majority of individuals at high and very high risk. However we can assume that a proportion of well treated patients will develop new cardiovascular events. Many factors such as the genetic background, the pre-existing burden of disease and the residual risk attributable to triglycerides, inflammation, coagulation and platelets may explain this recurrence of events. We discuss some novel options to reduce the residual risk due to the two main apoB-containing lipoproteins, LDL-C and Lp(a), that are:
-the newest-generation CETP inhibitor, Obicetrapib; the oral PCSK9 inhibition; the novel approaches to reduce Lp(a) plasma levels (antisense oligonucleotides-ASO; rna interfering-Sirna; assembly inhibition-; the PCSK9 gene editing.