MicroRNAs in Cardiovascular Disease: Perspectives and Reality.

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.

Combined effects of fibrinogen genetic variability on atherosclerosis in patients with or without stable angina pectoris: focus on the coagulation cascade and endothelial function.

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.

The role of microRNAs in the initiation and progression of stable atheromatous plaque.

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.

Genetic variability of matrix metalloproteinase genes in cardiovascular disease.

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.

Inflammation in hypertension: current therapeutic approaches.

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.

Hepatitis B vaccination coverage levels among nurses in Greece: need for improvement.

OBJECTIVES: : The aims of this study were to estimate the hepatitis B vaccination coverage levels among nurses and understand the reasons for receiving or not receiving the preventive vaccination. METHODS: : This cross-sectional study was based on a self-reported questionnaire, which was administered to 788 nurses working in 17 hospitals in Greece. RESULTS: : Overall, 606 out of 784 participants (77.3%) completed the survey. Of these, 63.2% nurses reported that they were fully vaccinated. The majority of immunized nurses (66%) were female (P = 0.008), and 72.6% of the fully-vaccinated nurses were working in Intensive Care Units (ICUs). CONCLUSIONS: : This study showed that almost 40% of nurses are not protected against hepatitis B infection. There is a need for a more aggressive approach to increase the vaccination coverage among nurses.

Acute effects of different types of oil consumption on endothelial function, oxidative stress status and vascular inflammation in healthy volunteers.

Consumption of different types of oil may have different effects on cardiovascular risk. The exact role of maize oil, cod liver oil, soya oil and extra virgin olive oil on endothelial function, oxidative stress and inflammation is unknown. We evaluated the effect of acute consumption of these types of oil on endothelial function, oxidative stress and inflammation in healthy adults. Thirty-seven healthy volunteers were randomised to receive an oral amount of each type of oil or water. Endothelial function was evaluated by gauge-strain plethysmography at baseline and 1, 2 and 3 h after consumption. Oxidative stress status was determined by total lipid peroxides (PEROX), while inflammatory process was estimated by measuring the soluble form of vascular adhesion molecule 1. Serum levels of the two previous markers were measured at baseline and 3 h after oil consumption. Reactive hyperaemia (RH) was significantly decreased after maize oil consumption compared with controls (P < 0.05). However, the consumption of cod liver oil and soya oil induced a significant improvement of RH after 1 h, compared with controls (P < 0.05). There was no significant effect of any type of oil consumption on endothelium-independent dilatation, total lipid PEROX and vascular adhesion molecule 1 serum levels. Consumption of maize oil leads to impaired endothelial function, while soya oil and cod liver oil slightly improve endothelial function. However, all types of oils did not affect inflammatory process and systemic oxidative stress, suggesting that their effect on endothelial function may not be mediated by free radicals bioavailability.