[Inflammatory Markers and Their RoIe in Assessing Prognosis of patients With Stable Coronary Artery Disease After Coronary Stenting].

In recent years, expanded data have demonstrated the association between increased inflammatory markers and risk of adverse cardiovascular events in patients undergoing percutaneous coronary intervention (PCI) with stent implantation. Particularly, several studies have demonstrated association between increased C-reactive protein (CRP) level and various risk factors of cardiovascular diseases and their complications. The role of CRP in predicting restenosis after implantation of bare metal stents has been proven, but its role in predicting drug-eluting stents restenosis is still unproved. Significant association between increased white blood cells count and risk of development and severity of coronary artery disease and as well as poor prognosis after PCI has also been demonstrated. But erythrocyte sedimentation rate has been studied insufficiently in this regard. According to some studies, including those conducted in our institute, one can suggest an association between eosinophilic inflammatory response, progression of coronary atherosclerosis, and drug-eluting stents restenosis. Identification of factors affecting prognosis of patients with coronary heart disease after PCI will allow determining further strategy of patient management.

[Inflammatory Markers and Their Role in Assessing Prognosis of Patients With Stable Coronary Artery Disease After Coronary Stenting].

In recent years, expanded data have demonstrated the association between increased inflammatory markers and risk of adverse cardiovascular events in patients undergoing percutaneous coronary intervention (PCI) with stent implantation. Particularly, several studies have demonstrated association between increased C-reactive protein (CRP) level and various risk factors of cardiovascular diseases and their complications. The role of CRP in predicting restenosis after implantation of bare metal stents has been proven, but its role in predicting drug-eluting stents restenosis is still unproved. Significant association between increased white blood cells count and risk of development and severity of coronary artery disease and as well as poor prognosis after PCI has also been demonstrated. But erythrocyte sedimentation rate has been studied insufficiently in this regard. According to some studies, including those conducted in our institute, one can suggest an association between eosinophilic inflammatory response, progression of coronary atherosclerosis, and drug-eluting stents restenosis.

[Prognostic value of markers of inflammation in patients with stable ischemic heart disease after implantation of stents with drug covering at the background of long-term therapy with statins (inhospital period)].

The objective of this study was to examine the prognostic value of C-reactive protein, erythrocyte sedimentation rate (ESR), white blood count, phospholipase A2 in patients with stable ischemic disease on long-term statin therapy undergoing percutaneous coronary intervention (PCI) with drug-eluting stent implantation. In the interim analysis in- hospital outcomes were assessed a total of 602 patients from December 2009 through December 2010 underwent successful PCI with at least one DES implanted. They were prospectively followed before discharge. MACE (death, myocardial infarction [MI], stroke, stent thrombosis [ST] which did not lead to MI) occurred in 10,6% of the patients. There was no death or stroke before discharge. MI (including 0,3% of Q-MI) occurred in 10,3% of the patients. 6 patients had verified ST. Multivariate logistic regression identified ESR level before PCI and total length of stents implanted as independent predictors of MACE.

[Comparative transcriptome analysis of human aorta atherosclerotic lesions and peripheral blood leukocytes from essential hypertension patients].

One of the major cardiovascular risk factor which predisposes to and accelerates atherosclerosis is arterial hypertension (AH). To determine the molecular basis of the crosslink between AH and atherosclerosis for the development of new treatment strategies large-scale transcriptome analysis of the cells implicated in atherogenesis is needed. We used cDNA microarray technique for simultaneous analysis of gene expression in human abdominal aorta normal sites and atherosclerotic lesions of different histological types, as well as in peripheral blood leukocytes from patients with essential hypertension (EH) and donors. The microarray data were verified by quantitative RT-PCR (reverse transcription coupled with polymerase chain reaction) and immunohistochemical analysis. Differential expression of 40 genes has been found, among which twenty two genes demonstrated up-regulation and 18 genes demonstrated down-regulation in atherosclerotic aorta compared with normal vessel. New gene-candidates, implicated in atherogenesis, have been identified - FPRL2, CD37, CD53, RGS1, LCP1, SPI1, CTSA, EPAS1, FHL1, GEM, RHOB, SPARCL1, ITGA8, PLN, and COL14A1. These genes participate in cell migration and adhesion, phenotypic changes of smooth muscle cells, immune and inflammatory reactions, oxidative processes and extracellular matrix remodeling. We have found increased expression levels of CD53, SPI1, FPRL2, SPP1, CTSD, ACP5, LCP1, CTSA and LIPA genes in peripheral blood leukocytes from EH patients and in atherosclerotic lesions of human aorta. The majority of these genes significantly (p<0.005) positively (r>0.5) correlated with AH stage as well as with histological grading of atherosclerotic lesions.

[Drug-eluting stents: long-term safety].

The review concerns the problem of late thromboses of drug-eluting stents and their influence on late prognosis of the patients; presents long-term results of the trial of sirolimus-eluting stents implanted to patients with coronary heart disease; analyses mechanisms of development of late stent thrombosis, data from different meta-analyses and registers comparing long-term outcomes in patients with implanted sirolimus-eluting stents and metallic stents; suggests risk factors of late thromboses of drug-eluting stents; presents original evidence on 3.5-year follow-up of patients with implanted sirolimus-eluting stents and metallic stents.

[Assessment of the course of ischemic heart disease after placement of stents with drug covering and uncovered metal stents: data of 3 years follow-up].

The placement of sirolimus-eluting stents decreases the frequency of repeat revascularization procedures in patients undergoing percutaneous coronary intervention (PCI) in randomized clinical trials. However, there is uncertainty about the effectiveness of sirolimus-eluting stents, and increasing concern about their safety in routine clinical practice. From the prof. Samko PCI laboratory in Moscow, Russia, we identified 426 patients, who received either bare-metal stents alone or sirolimus-eluting stents alone during an index PCI procedure between March 1, 2002, and September 31, 2004.The primary outcomes of the study were the rates of target-lesion revascularization, myocardial infarction, death, late stent thrombosis. The 3-year rate of target-lesion revascularization was significantly lower among patients who received sirolimus-eluting stents than among those who received bare-metal stents (3.1% vs. 19 %, p=0.001). The 3-year mortality rate was not different between the bare-metal stent group and the sirolimus eluting stent group (5.9% vs. 7.2%, p=0.68), the 3-year rate of all ARC late stent thrombosis was similar in the two groups (5.9% and 7.2%, respectively; p=0.95). Sirolimus-eluting stents are effective in reducing the need for target-vessel revascularization without significantly increased rates of death, late stent thrombosis, myocardial infarction.

Altered gene expression pattern in peripheral blood leukocytes from patients with arterial hypertension.

The role of various inflammatory mechanisms and oxidative stress in the development of atherosclerosis and arterial hypertension (AH) has been increasingly acknowledged during recent years. Hypertension per se or factors that cause hypertension along with other complications lead to infiltration of activated leukocytes in the vascular wall, where these cells contribute to the development of vascular injury by releasing cytokines, oxygen radicals, and other toxic mediators. However, molecular mechanisms underlying leukocyte activation at transcriptional level in AH are still far from being clear. To solve this problem we employed cDNA microarray technology to reveal the differences in gene expression in peripheral blood leukocytes from patients with AH compared with healthy individuals. The microarray data were verified by a semi-quantitative RT-PCR method. We found 25 genes with differential expression in leukocytes from AH patients among which 21 genes were upregulated and 4 genes were downregulated. These genes are implicated in apoptosis (CASP2, CASP4, and CASP8, p53, UBID4, NAT1, and Fte-1), inflammatory response (CAGC, CXCR4, and CX3CR1), control of MAP kinase function (PYST1, PAC1, RAF1, and RAFB1), vesicular trafficking of molecules among cellular organelles (GDI-1 and GDI-2), cell redox homeostasis (GLRX), cellular stress (HSPA8 and HSP40), and other processes. Gene expression pattern of the majority of genes was similar in AH patients independent of the disease stage and used hypotensive therapy, but was clearly different from that of normotensive subjects.