Since the discovery of the first noncoding RNA decades ago, the transcriptomics evolution has made a great leap reaching to the detection and recognition of microRNAs (miRNAs) in the early 1990s. Thereafter, numerous miRNAs were reported in different species, with a great body of literature focusing on their role in human health and in pathophysiological processes. miRNAs play a significant role in the cardiovascular system, not only in physiology and normal development but also in disease processes and evolution. Further studies on miRNAs have highlighted their participation in several expressions of cardiovascular disease, such as atherosclerosis, acute and chronic syndromes of coronary artery disease, heart failure, and cardiac arrhythmias. To date, the challenge remains to understand the underlying mechanisms of miRNAs that drive their expression profile so as to use them as innovative diagnostic tools or therapeutic targets in cardiovascular disease.

Since the discovery of the first noncoding RNA decades ago, the transcriptomics evolution has made a great leap reaching to the detection and recognition of microRNAs (miRNAs) in the early 1990s. Thereafter, numerous miRNAs were reported in different species, with a great body of literature focusing on their role in human health and in pathophysiological processes. miRNAs play a significant role in the cardiovascular system, not only in physiology and normal development but also in disease processes and evolution. Further studies on miRNAs have highlighted their participation in several expressions of cardiovascular disease, such as atherosclerosis, acute and chronic syndromes of coronary artery disease, heart failure, and cardiac arrhythmias. To date, the challenge remains to understand the underlying mechanisms of miRNAs that drive their expression profile so as to use them as innovative diagnostic tools or therapeutic targets in cardiovascular disease.

Atherosclerosis is a chronic process related to several underlying mechanisms leading to the formation and evolution of atherosclerotic plaque. Of great interest are during the last years short, non-coding RNAs, called microRNAs and responsible for several aspects of homeostasis and disease. According to the available data microRNAs are expressed in the cardiovascular system and have key roles in normal states, as well as in disease development and progression. Moreover, it has been shown that they contribute to atherogenesis, coronary artery disease and myocardial infarction. Importantly, microRNAs circulate in the bloodstream, while they exist in tissues, affect plaque initiation and progression and seem to be essential biomarkers of atherosclerosis. Therefore, understanding the role of these molecules may be of great importance in the understanding of the pathogenesis of atheromatous plaque providing new evidence for diagnosis and treatment of atherosclerosis and its' clinical presentation.

Background Fibrinogen is a coagulation/inflammatory biomarker strongly associated with atherogenesis. Data have reported that the genetic variability on fibrinogen chains may affect the atherosclerotic process and the risk of coronary artery disease (CAD). We examined the combined effects of the G455A and the G58A fibrinogen genetic polymorphisms on prothrombotic profile, endothelial function and the risk of CAD in a Caucasian population. Methods We recruited 422 patients with angiographically documented CAD and 277 controls matched for age and gender. The two polymorphisms were genotyped by polymerase chain reaction and restriction endonuclease digestion. Fibrinogen and D-Dimers levels, as well as factors' (f) V, X activity were measured by standard coagulometry techniques. Endothelial function was assessed by the flow mediated dilatation (FMD) of the brachial artery. Results The two polymorphisms had no significant effect on the risk for CAD. Although the 58AA subjects had not significantly different levels of fibrinogen compared with the 58GG + GA in both groups (p = NS), we importantly found that the 455AA homozygosity was associated with increased fibrinogen levels not only in the control group (p = 0.035), but also in the CAD group (p < 0.001) compared to the G allele carriers. Moreover, both the 58AA (p = 0.016) and 455AA homozygotes (p = 0.022) presented with higher levels of D-Dimers in the CAD group. Interestingly, the 455AA homozygotes had increased fV activity in the CAD group (p = 0.048). However, no significant effects were observed on fX activity and FMD. Conclusions Both fibrinogen polymorphisms are capable to modify the atherosclerotic process via their effects on the coagulation cascade.

It is well established that matrix metalloproteinases (MMPs) contribute to the degradation of the extracellular matrix of coronary plaque and contribute to the thinning of the fibrous cap. As a result, the atheromatous plaque becomes unstable and prone to rupture with consequent clinical manifestations including acute coronary syndromes. Moreover, genetic polymorphisms of MMPs have been found to be associated with the concentration of circulating MMPs, and over the past decade, considerable efforts have been devoted to explore the relationships between MMPs polymorphisms and myocardial infarction risk among various populations. However, existing studies have yielded inconsistent results. Some observations have suggested that genetic variation that affects the expression of MMPs may contribute to the occurrence of myocardial infarction, whereas others reported no support for an association of MMPs polymorphisms with myocardial infarction susceptibility. Furthermore, the interpretation of these studies has been complicated by the use of different populations or different control sources. Therefore, further studies are required to evaluate the role of matrix metalloproteinases and especially the associated genetic polymorphisms in cardiovascular disease.

Coronary artery disease (CAD) is the leading cause of mortality in Western Societies and several developing countries. Recent evidence suggests that most detrimental clinical manifestations of CAD, such as acute coronary syndromes (ACS), are the outcome of inflammatory processes that lead to plaque formation and rupture and eventually to ischemia and potentially myocardial necrosis. Neither of the traditionally used biomarkers is thought to be the gold standard in detection of myocardial ischemia or necrosis. A biomarker that could detect quite early the ischemic myocardium as well as define the risk of a future event with high sensitivity and specificity is still lacking. Several biomarkers, implicated in the pathogenesis and clinical evolution of atherosclerosis, have emerged as potent biomarkers for early detection of myocardial ischemia. In the current review, we summarize recent evidence of the most promising biomarkers and discuss their potential role in clinical practice in patients suffering from ACSs.

The role of inflammation as crucial underlying process contributing to the initiation and the progression of atherosclerosis as well as its clinical manifestations is well established. Recent data have demonstrated also a strong association between essential hypertension and inflammatory process. In addition, several studies have shown that tissue expression and plasma concentrations of several inflammatory biomarkers/mediators are related to increased risk of hypertension. The determination of markers such as acute phase proteins (C-reactive protein), adhesion molecules such as vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and chemokines is crucial in determining therapeutic responses and clinical outcomes of hypertensive patients. In addition, several therapeutic approaches targeting blood pressure may have also beneficial effects in terms of inflammation and thus further clinical benefits. Although the available data are encouraging, further large scale studies are required to evaluate the reported anti-inflammatory effects in management and treatment of arterial hypertension.

Background/Objectives: Inter-cellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and tumor necrosis factor-α (TNF-α), are implicated in atherogenesis. In addition, several types of oil as part of different types of diet are associated with the initiation of atherosclerosis and consequently with the risk of cardiovascular disease. However, the exact role of oil consumption on vascular inflammation remains unknown. In this parallel study, we assessed the acute effects of extra virgin olive oil, soy oil, corn oil and cod liver oil on circulating soluble(s) forms of adhesion molecules and TNF-α. Subjects/Methods: In all, 67 healthy volunteers were randomized to receive 50 ml of oil. Soluble forms of VCAM-1, ICAM-1 and TNF-α were measured by enzyme-linked immunosorbent assay at baseline and at 3 h post oil consumption. Results: All types of oil had no significant effect on soluble VCAM-1 levels ( P =nonsignificant (NS) for all). On the contrary, all oil types decreased ICAM-1 levels ( P <0.01). Olive oil ( P <0.05), soy oil and cod liver oil ( P <0.01 for both) reduced TNF-α levels significantly, in contrast to corn oil, which induced a nonsignificant decrease ( P =NS). Moreover, there was a significant correlation between the absolute change in ICAM-1 and TNF-α levels ( ρ =0.379, P <0.05), but not between the absolute changes in VCAM-1 and TNF-α levels ( ρ =0.019, P =NS). Conclusions: Acute consumption of all types of oil decreased significantly ICAM-1 levels. In addition, olive oil, soy oil and cod liver oil decreased significantly TNF-α levels. Moreover, the absolute change in TNF-α levels was correlated with the absolute change in ICAM-1 levels. These findings indicate that acute consumption of specific types of oil is associated with specific significant anti-inflammatory effects.

A cute coronary syndromes (ACS) are often associated with the rupture of vulnerable atherosclerotic plaque, coronary thrombus formation, and abrupt limitation of blood flow, leading to adverse outcomes. The interaction between the vulnerable atherosclerotic plaque and thrombus formation, a process referred to as atherothrombosis, is the cornerstone of ACS. Vulnerable plaque, which is the substrate of this condition, is the target of many therapeutic approaches, including statins. Statins, or 3-hydroxy-3-methylgloutaryl coenzyme A reductase inhibitors, (HMG-coA inhibitors) form a class of hypolipidemic drugs used to lower cholesterol levels in people with or at risk of cardiovascular disease. They lower cholesterol by inhibiting the enzyme HMG-CoA reductase, which is the rate-limiting enzyme of the mevalonate pathway of cholesterol synthesis (Figure 1). Nowadays, statins seem to play a crucial role in modulating cardiovascular disorders such as ACS, not only by affecting lipids, but also by exerting a number of pleiotropic effects beyond lipid lowering, such as plaque stabilization. Invasive modalities for atherosclerotic plaque examination will further evaluate the beneficial effects of statins on atherosclerotic plaque development, progression and stabilization. In the clinical setting statins appear to have an impact on mortality, which remains the major endpoint following ACS. In this article we review the role of statins in ACS, focusing on mortality as well as other important aspects of their use.

Background: Inter-cellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and tumor necrosis factor alpha (TNF-a) are implicated in the pathogenesis of atherosclerosis. Ho...

Background: Adiponectin is an adipokine with beneficial effect on vascular function. Although adiponectin levels are decreased in patients with diabetes mellitus (DM), it is unclear whether impaire...