[Assessment of early atherosclerosis and decreased arterial elasticity to recognise the cardiovascular dysfunction in high-risk patients has gained importance in the past decade. Since 1990, more than 630 papers have been published in the adult and pediatric literature. Methods of early risk assessment in adults are well determined in international recommendations. The aim of the present work is to review the suggestions of the American Heart Association helping us to find the most appropriate method for the non invasive methods of cardiovascular assessment of young adults and children. Furthermore, multicentric studies should be conducted to create a Framingham like score system for pediatric patients, to render cardiovascular risk assessment much easier for the every day routine.]

[INTRODUCTION - An association of Chlamydia pneumoniae (C. pneumoniae) with coronary heart disease has been found with seroepidemiological methods. This organism was demonstrated in atheromatous plaques by electron microscopy, immunohistochemistry, and polymerase chain reaction. MATERIAL AND METHODS - To better understand the significance of the presence of C. pneumoniae in atheromatous plaques, we examined coronary artery segments from young adults (15-34 years) with and without atherosclerosis. 74 samples of left anterior descending artery were examined immunohistochemically for the presence of C. pneumoniae by the monoclonal antibody RR402. RESULTS - C. pneumoniae was identified in the atheroma in 11 of 17 cases (65%) and in preatheroma in 6 of 15 cases (40%), in fatty streak in 7 of 23 cases (30%) and in intimal thickening in 1 of 14 cases (7%). C. pneumoniae was not found in the intimal and medial layer of the normal-appearing coronary arteries. C. pneumoniae was detected in the adventitia in 51 cases (67%) of the coronary arteries: in the normal arteries and initial lesions in 27 of 42 cases (63%), and in the advanced lesions in 24 of 32 cases (75%). Correlation was observed between the C. pneumoniae positive cases and cigarette smoking. CONCLUSION - Our results suggest that C. pneumoniae may relate to the severity of atherosclerosis in the youth, thus may initiate atherosclerotic injury or facilitate its progression along with other risk factors.]

[Endothelial nitric oxide synthase enzyme is regulated through the phosphorylation of the Ser(1177) and the Thr(495) sites, which influence the biological availabilaty of nitric oxide. We examined the acute effect of cigarette smoke, which decreases nitric oxide production. Endothelial cells were treated with different concentrations and for different times with cigarette smoke buffer, then with reduced glutathione or different protein kinase inhibitors. We determined the total and the phosphorylated nitric oxide synthase levels with Western blot. Cigarette smoke increased phosphorylation in a concentration- and time dependent manner at the Ser(1177) site and more pronounced at the Thr(495) site. Besides, it also led to the dissociation of the active dimer form of the enzyme. Reduced glutathione inhibited these phosphorylations and prevented the dissociation of endothelial nitric oxide synthase enzyme. The inhibition of protein kinase A or B did not influence the effect of cigarette smoke. However, protein kinase C inhibitors increased the phosphorylation caused by cigarette smoke at Ser(1177), but decreased it at Thr(495) sites. Summarized, cigarette smoke shifts the phosphorylation of the enzyme towards an inhibitory state, further on, it leads to the dissociation of the enzymatically active form. This results in the decreased biological availabilaty of nitric oxide, in which protein kinase C may play an important role.]

[In the fight against atherosclerosis, statin therapy is one of the most important elements. On the basis of data from the past few years the clinical introduction of a more effective statin is not expected, however, in order to improve cardiovascular prevention further development of agents that reduce LDL-cholesterol levels more effectively than currently used statins is warranted. The need for the development of new cholesterol-lowering therapeutic options is also supported by the existence of statin intolerance. The currently available combination therapies do not provide additional mortality benefits compared with statin monotherapy. The new solutions include fourth-generation statin molecules that primarily aim to enhance the NO-donor capacity of statins, and to reduce their muscle toxicity. Certain compounds that affect cholesterol synthesis (squalene synthase inhibitors, MTP inhibitors, ACAT inhibitors) need to be further analysed because of the risk of side effects. The use of an antisense oligonucleotid that blocks the mRNA of apoB, the main protein on the LDL-particle and antibodies that inhibit the protein PCSK9 that promotes the intracellular breakdown of the LDL-receptor seems to be much more promising. Besides the lowering of LDLcholesterol level, studies have focused on the benefits of increasing HDL-cholesterol levels. Unfortunately, recently completed analyses show that new forms of the strong HDL-C increasing nicotinic acid have not provided any additional benefit when added to statin therapy. Similarly, the adverse effects associated with the promising CETP inhibitors and the lack of additional benefit when combined with statins question the significance of this drug class. The necessity for an absolute increase of HDL-cholesterol levels needs to be revised on the basis of new data, in other words, the exact role of the HDL particle in atherosclerosis needs to be further investigated.]

[The process of atherosclerosis nowadays plays an important role in the health care not just as a major cause of the most common cardiovascular diseases which lead to death, but also as a major factor in the loss of age-related elasticity in the blood vessels. Over the past two decades, large studies have shown that the treatment of high cholesterol levels can reduce the frequency of cardiovascular events and death and have confirmed the ability to reduce the already existing atherosclerotic plaque, which is almost unique in pharmacotherapy. Using lipid lowering therapy, if we do it properly, we can not only prevent vascular events, but can also cure atherosclerosis. Currently there are three drug groups (statins, ezetimibe and PCSK9- inhibitors), which have complete evidence that their use can reduce the number of cardiovascular events and plaque regression can be achieved. Despite many convincing clinical trials, lipid-lowering therapy is on the cardiovascular prevention palette in the just tolerated or forced applied category. In order to take advantage of its potentials at an appropriate level, as doctors, we have to approach to it by considering its importance. We should communicate to our patients that it’s about a life-long treatment, which not only can reduce the possibility of cardiovascular events, but also can slow down the aging process of the arteries. ]