Trends in volume and risk profiles of patients undergoing isolated surgical and transcatheter aortic valve replacement.

BACKGROUND: Recent reports describe increases in the case volume of surgical aortic valve replacement (SAVR) after centers establish a transcatheter aortic valve replacement (TAVR) program. We investigate contemporary temporal trends in SAVR and TAVR case volumes and risk profiles at a high volume academic medical center. METHODS: We conducted a retrospective, descriptive evaluation of consecutive patients who underwent TAVR (n = 538) or SAVR (n = 657) in 2011-2016. The STS predicted risk of mortality (PROM) for isolated SAVR was used to calculate PROM for both SAVR and TAVR patients. Patients were stratified based on STS PROM as follows: low risk (<4%), intermediate risk (4-8%), and high risk (≥8%). Temporal changes in patient risk-profile were characterized descriptively. RESULTS: Median STS PROM for the study period was 6.3% and 2.0% for TAVR and SAVR cohorts, respectively (P < 0.001). Since 2011, TAVR volume consistently increased, while SAVR volume increased initially, peaking in 2013 and steadily declined. The STS PROM for SAVR remained stable during the entire study period, while that for TAVR showed a steady decline. The proportions of intermediate and low STS PROM patients undergoing TAVR increased. Proportions of each risk category in SAVR cohort remained stable over time. CONCLUSIONS: SAVR volume increased initially but declined eventually following the implementation of TAVR program. The distribution of the STS PROM in TAVR cohort changed dramatically with increasing proportion of patients in lower risk categories. These findings suggest the converging patient populations in TAVR and SAVR, which may be associated with the decline in the overall SAVR volume.

Ventricular septal rupture complicating acute myocardial infarction: Incidence, treatment, and outcomes among medicare beneficiaries 1999-2014.

OBJECTIVES: The present study was designed to assess whether the incidence and outcomes of VSR-AMI have changed in the era of timely primary PCI. BACKGROUND: Ventricular septal rupture (VSR) is a rare but frequently fatal complication of acute myocardial infarction (AMI). METHODS: We conducted a retrospective cohort study of all Medicare fee-for-service beneficiaries from 1999 to 2014 to examine trends in the incidence, surgical and percutaneous repair, and 30-day and 1-year mortality of VSR-AMI. RESULTS: The annual incidence of VSR-AMI hospitalization declined by 41.6% from 197 patients per 100,000 AMIs in 1999 to 115 patients per 100,000 AMIs in 2014 (P < 0.001). The 30-day VSR-AMI repair rate decreased from 49.9% in 1999 to 33.3% in 2014 (P < 0.001). In 2014, 82.9% of repairs were performed surgically and 17.1% percutaneously. VSR-AMI mortality rates were high (60.2% at 30 days; 68.5% at 1 year) and changed minimally over the study period with adjusted 30-day mortality per year Odds Ratio (OR) 0.99 (95% confidence interval [CI] 0.98-1.01) and adjusted 1-year mortality per year OR 0.98 (95% CI 0.97-1.00). Across the 16 years of data, unadjusted mortality rates were lower in patients undergoing repair than in unrepaired patients at 30 days (mean 51.7% and 65.7%, P ≤ 0.01) and 1 year (mean 62.0% and 72.8%, P < 0.01). CONCLUSIONS: In the era of increased timely primary PCI, the incidence of VSR-AMI hospitalization declined but its associated mortality rate remained high. Rates of VSR repair decreased from 1999 to 2014 despite increased use of percutaneous repair.

Circulating Erythrocyte Microparticles and the Biochemical Extent of Myocardial Injury in ST Elevation Myocardial Infarction.

OBJECTIVES: Red blood cell microparticles (RBCm) have potential adverse vascular effects and they have been shown to be elevated in ST elevation myocardial infarction (STEMI). The purpose of this study is to investigate their relationship with biochemical infarct size. METHODS: RBCm were quantified with flow cytometry in blood drawn from 60 STEMI patients after a primary angioplasty. The creatine kinase-myocardial brain fraction (CK-MB) was measured at predefined time points and the area under the curve (AUC) was calculated. RESULTS: RBCm count was correlated with CK-MB AUC (Spearman's ρ = 0.83, p < 0.001). The CK-MB AUC values per RBCm quartile (lower to upper) were: 3,351 (2,452-3,608), 5,005 (4,450-5,424), 5,903 (4,862-10,594), and 8,406 (6,848-12,782) ng × h/ml, respectively. From lower to upper quartiles, the maximal troponin I values were: 42.2 (23.3-49.3), 49.6 (28.8-54.1), 59.2 (41.4-77.3), and 69.1 (48.0-77.5) ng/ml (p = 0.005). In multivariable analysis, RBCm remained a significant predictor of CK-MB AUC (standardized ß = 0.63, adjusted p = 0.001). CONCLUSIONS: Erythrocyte microparticles appear to be related to the total myocardial damage biomarker output. The exact pathophysiologic routes, if any, for this interaction remain to be identified. However, these results suggest that erythrocytes may be a - thus far virtually ignored - player in the pathogenesis of ischemic injury.

Anti-Inflammatory Treatment With Colchicine in Acute Myocardial Infarction: A Pilot Study.

BACKGROUND: Inflammatory processes have been identified as key mediators of the deleterious effects of ischemia/reperfusion in ST-segment-elevation myocardial infarction. Colchicine is a substance with potent anti-inflammatory properties, suitable for safe use in patients with cardiovascular disease. The purpose of this study was to test the hypothesis that a short course of colchicine treatment could lead to reduced infarct size. METHODS AND RESULTS: Patients presenting with ST-segment-elevation myocardial infarction ≤12 hours from pain onset (treated with primary percutaneous coronary intervention) were randomly assigned to colchicine or placebo for 5 days. The primary outcome parameter was the area under the curve of creatine kinase-myocardial brain fraction concentration. A subset of patients underwent cardiac MRI with late gadolinium enhancement 6 to 9 days after the index ST-segment-elevation myocardial infarction. One hundred fifty-one patients were included (60 in the MRI substudy). The area under the creatine kinase-myocardial brain fraction curve was 3144 (interquartile range [IQR], 1754-6940) ng·h(-1)·mL(-1) in the colchicine group in comparison with 6184 (IQR, 4456-6980) ng·h(-1)·mL(-1) in controls (P<0.001). Indexed MRI-late gadolinium enhancement-defined infarct size was 18.3 (IQR, 7.6-29.9) mL/1.73 m(2) in the colchicine group versus 23.2 (18.5-33.4) mL/1.73 m(2) in controls (P=0.019). The relative infarct size (as a proportion to left ventricular myocardial volume) was 13.0 (IQR, 8.0-25.3) % and 19.8 (IQR, 13.7-29.8) %, respectively (P=0.034). CONCLUSIONS: These results suggest a potential benefit of colchicine in ST-segment-elevation myocardial infarction, but further clinical trials are necessary to draw secure conclusions, especially considering the fact that the present study was not powered to assess clinical end points. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01936285.

Effect of Angiotensin converting enzyme inhibitors on soluble tumor-necrosis-factor-related apoptosis-inducing ligand levels - association with neointimal hyperplasia in drug eluting stents.

OBJECTIVE: To test the hypothesis that angiotensin converting enzyme inhibitors (ACEi) affect soluble tumor-necrosis-factor-related apoptosis-inducing ligand (sTRAIL) and this interaction is associated with less in-drug-eluting-stent (DES) neointimal hyperplasia following percutaneous coronary intervention (PCI). METHODS: From our database of patients with elective PCI and baseline intravascular ultrasound (IVUS) evaluation of the implanted DES, we randomly selected 60 patients who were prescribed an ACEi and 60 matched controls, who did not receive an ACEi following PCI. All patients underwent coronary angiography and IVUS. sTRAIL was measured in samples from the stented coronary artery and a peripheral vein. RESULTS: sTRAIL concentration was higher in the ACEi group, both in coronary and peripheral samples: 104 [78-139] pg/ml versus 63 [45-100] pg/ml (P < 0.001) and 99 [73-135] pg/ml versus 69 [49-103] pg/ml (P = 0.002), respectively. There was an inverse association (standardized beta -0.760; P < 0.001) between sTRAIL and lumen area loss in both treatment groups. In the multivariable analysis, log(sTRAIL) was an independent negative predictor of lumen area loss (standardized beta -0.660, adjusted 95% confidence interval -0.722 to -0.466). CONCLUSIONS: Treatment with ACEi was associated with higher sTRAIL levels and lower lumen area loss in the IVUS evaluation of implanted DES. sTRAIL levels were negatively associated with in-stent neointima hyperplasia in these post-PCI patients.

Cellularity and structure of fresh human coronary thrombectomy specimens; presence of cells with markers of progenitor cells.

Acute coronary syndromes and acute myocardial infarctions are often related to plaque rupture and the formation of thrombi at the site of the rupture. We examined fresh coronary thrombectomy specimens from patients with acute coronary syndromes and assessed their structure and cellularity. The thrombectomy specimens consisted of platelets, erythrocytes and inflammatory cells. Several specimens contained multiple cholesterol crystals. Culture of thrombectomy specimens yielded cells growing in various patterns depending on the culture medium used. Culture in serum-free stem cell enrichment medium yielded cells with features of endothelial progenitor cells which survived in culture for a year. Immunohistochemical analysis of the thrombi revealed cells positive for CD34, cells positive for CD15 and cells positive for desmin in situ, whereas cultured cell from thrombi was desmin positive but pancytokeratin negative. Cells cultured in endothelial cell medium were von Willebrand factor positive. The content of coronary thrombectomy specimens is heterogeneous and consists of blood cells but also possibly cells from the vascular wall and cholesterol crystals. The culture of cells contained in the specimens yielded multiplying cells, some of which demonstrated features of haematopoietic progenitor cells and which differentiated into various cell-types.

Inverse association of coronary soluble tumor necrosis factor-related apoptosis inducing ligand (sTRAIL) levels to in-stent neointimal hyperplasia.

OBJECTIVES: Soluble tumor necrosis factor-related apoptosis inducing ligand (sTRAIL) has been shown to exert protective action against atherosclerosis. The aim of this study was to investigate potential associations of coronary sTRAIL levels with indices of in-stent neointimal hyperplasia. METHODS: 67 patients who underwent percutaneous coronary intervention with drug-eluting stent were followed up at approximately 12 months with determination of coronary sTRAIL concentration, angiography and intravascular ultrasound evaluation of the stent sites. RESULTS: Mean sTRAIL concentration was 72.2 ± 2.8 pg/ml. sTRAIL was negatively correlated to indices of neointimal hyperplasia and positively correlated to in-stent minimum lumen area (p < 0.001). Neointimal obstruction and maximal in-stent cross-sectional neointima burden in patients in the upper sTRAIL quartile were 3.8 ± 1.2 and 12.6 ± 3.3%, respectively, versus 14.0 ± 0.7 and 49.8 ± 2.7% in the lower quartile (p < 0.001 for both). sTRAIL levels were significantly lower in patients with binary restenosis (48.7 ± 3.0 vs. 75.2 ± 2.9 pg/ml; p < 0.001). In the multivariate analysis, sTRAIL was an independent predictor of neointimal hyperplasia. CONCLUSION: This study demonstrates a negative association of sTRAIL to in-stent neointima formation. The potential pathophysiologic substrate of this effect implicates modulation of apoptosis in various cell types. These observations should prompt further evaluation of the link between sTRAIL and in-stent restenosis.

Antioxidant treatment in peripheral artery disease: the rationale is there, but what about clinical results?

Peripheral arterial disease is a major cause of morbidity and disability and has been consistently associated with an adverse overall prognosis. Oxidative stress has been linked to vascular disease, with several suggested pathogenetic mechanisms, leading to various insults of the arterial wall and, ultimately, to atherothrombotic disease. Considering that the pathophysiological background is quite compelling, attenuation of oxidative processes by means of various substances with antioxidant properties has been conceived as a promising therapeutic target. However, clinical results have been mostly disappointing and 'antioxidant' therapies are still far from being integrated into treatment algorithms for vascular disease.

Remote Ischemic Conditioning and Renal Protection.

Over the course of the last 2 decades, the concept of remote ischemic conditioning (RIC) has attracted considerable research interest, because RIC, in most of its embodiments offers an inexpensive way of protecting tissues against ischemic damage inflicted by a number of medical conditions or procedures. Acute kidney injury (AKI) is a common side effect in the context of various medical procedures, and RIC has been suggested as a means of reducing its incidence. Outcomes regarding kidney function have been reported in numerous studies that evaluated the effects of RIC in a variety of settings (eg, cardiac surgery, interventions requiring intravenous administration of contrast media). Although several individual studies have implied a beneficial effect of RIC in preserving kidney function, 3 recently published randomized controlled trials evaluating more than 1000 patients each (Effect of Remote Ischemic Preconditioning in the Cardiac Surgery, Remote Ischaemic Preconditioning for Heart Surgery, and ERICCA) were negative. However, AKI or any other index of renal function was not a stand-alone primary end point in any of these trials. On the other hand, a range of meta-analyses (each including thousands of participants) have reported mixed results, with the most recent among them showing benefit from RIC, pinpointing at the same time a number of shortcomings in published studies, adversely affecting the quality of available data. The present review provides a critical appraisal of the current state of this field of research. It is the opinion of the authors of this review that there is a clear need for a common clinical trial framework for ischemic conditioning studies. If the current babel of definitions, procedures, outcomes, and goals persists, it is most likely that soon ischemic conditioning will be "yesterday's news" with no definitive conclusions having been reached in terms of its real clinical utility.

Peri-procedural Anticoagulation in Catheter Ablation for Atrial Fibrillation: A Review.

Catheter ablation for rhythm control in atrial fibrillation has been recognized as an established treatment. Patients with atrial fibrillation suffer from an increased risk of thromboembolic events. Long-term stroke risk and mortality have been shown to be reduced after catheter ablation, still the procedure per se is associated with an additive peri-procedural thromboembolic risk. Maintenance of the thrombotic - bleeding equilibrium in such patients during interventional procedures is compelling. Lack of data from randomized studies along with the recent introduction of novel oral anticoagulants in clinical practice has resulted in a wide variance of antithrombotic treatment approaches. Procedural interruption of anticoagulants, switching of anticoagulation scheme (i.e. from novel oral anticoagulants to vitamin K antagonists), bridging with heparin, timing of re-initiation of therapy and/or utilization of novel oral anticoagulants have all been points of dispute. In the present review we present the available data regarding optimal peri-procedural anticoagulation strategies in patients undergoing catheter ablation for atrial fibrillation.

Intra--and Intercellular Calcium Handling in Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH) is a serious life threatening disease that leads to right heart failure and death. Elevated pulmonary vascular resistance (PVR) is the main pathophysiological component that leads to elevated pulmonary arterial pressures and increased right ventricular afterload. Increased PVR is related to different mechanisms that include vasoconstriction, proliferative and obstructive remodeling of the pulmonary vessel wall and in situ thrombosis. Numerous molecular, genetic and humoral abnormalities have been proposed to play an important role in pulmonary vasoconstriction and remodeling. Of those, calcium (Ca(+2)) is a well recognized parameter involved in the pathogenetic mechanisms of PAH, because of its twofold role in both vasoconstriction and pulmonary artery smooth muscle cell (PASMC) proliferation. The aim of this review is to focus on Ca(+2) handling and dysregulation in PASMC of PAH patients.

Calcium Ions in Inherited Cardiomyopathies.

Inherited cardiomyopathies are a known cause of heart failure, although the pathways and mechanisms leading from mutation to the heart failure phenotype have not been elucidated. There is strong evidence that this transition is mediated, at least in part, by abnormal intracellular Ca(2+) handling, a key ion in ventricular excitation, contraction and relaxation. Studies in human myocytes, animal models and in vitro reconstituted contractile protein complexes have shown consistent correlations between Ca(2+) sensitivity and cardiomyopathy phenotype, irrespective of the causal mutation. In this review we present the available data about the connection between mutations linked to familial hypertrophic (HCM), dilated (DCM) and restrictive (RCM) cardiomyopathy, right ventricular arrhythmogenic cardiomyopathy/dysplasia (ARVC/D) as well as left ventricular non-compaction and the increase or decrease in Ca(2+) sensitivity, together with the results of attempts to reverse the manifestation of heart failure by manipulating Ca(2+) homeostasis.

Altered Calcium Handling in Reperfusion Injury.

Coronary Heart Disease (CHD) is the major mortality cause in the Western Hemisphere. Reinstituting blood flow in the acutely occluded coronary vessel became the standard intervention to prevent Myocardial Infarct (MI) progression. Ever since their conception, thrombolysis, Percutaneous Coronary Intervention (PCI) and Coronary Artery Bypass Grafting (CABG) have been at the forefront of CHD treatment, limiting MI size. However, it quickly became apparent that after a period of ischemia, reperfusion itself sets off a cascade of events leading to cell injury. It seems that cellular changes in the ischemic period, prime the cell for a loss of homeostasis once blood flow returns. Loss of calcium (Ca(2+)) regulation has been found to be a main culprit in both ischemia and reperfusion. Indeed, sarcoplasmic Ca(2+) overload during reperfusion is related to hypercontracture, proteolysis and mitochondrial failure--the so-called Reperfusion Injury (RI). Ca(2+) channels of the sarcolemma (SL) (L-Type Ca((2+)) Channels, Sodium / Calcium Exchanger) initiate Ca(2+) flux and those of the Sarcoplasmic Reticulum (SR) (Ca(2+) ATPase, Ca(2+) release channel) sustain the rise in intracellular Ca(2+) concentration. Ensuing interplay between Ca(2+), SR, mitochondria, myofilaments and proteolytic cascades i.e. calpain activation, results in cell injury. Novel insight about this interplay and details about the extent by which each of these players contributes to the RI, may allow scientists to devise and design proper interventions that ultimately reduce RI in clinical practice. The present article reviews the literature about key subcellular players participating in the sustained rise of cardiac myocyte cytosolic Ca(2+) during ischemia and reperfusion.

A balloon-expandable sheath facilitates transfemoral TAVR in patients with peripheral vascular disease and tortuosity.

OBJECTIVES: We sought to perform transcatheter aortic valve replacement (TAVR) via the transfemoral approach in patients with peripheral arterial disease (PAD), small caliber ileofemoral vessels and vascular tortuosity. BACKGROUND: For patients with increased surgical risk, TAVR is associated with a higher 1-year survival rate than surgical aortic valve replacement (SAVR). Transfemoral vascular access for TAVR results in superior outcomes versus procedures performed via other routes in terms of mortality, morbidity and healthcare economics. In many patients, the ability to safely perform the procedure via the transfemoral approach is limited by narrow, diseased and tortuous ileofemoral vasculature. METHODS: We employed the SoloPath Balloon Expandable TransFemoral Access System (Terumo Med. Corp., Tokyo, Japan) to perform transfemoral TAVR in five patients with PAD, small caliber ileofemoral vessels and vascular tortuosity. RESULTS: We report our experience using this balloon-expandable sheath during 5 cases of transfemoral TAVR in patients with inhospitable ileofemoral vasculature of mean diameter ⩽ 5.8 mm. The unexpanded sheath's malleable structure and hydrophilic coating permitted deployment despite severe stenoses and tortuosity. Subsequent inflation to 18 Fr facilitated successful TAVR. Postprocedural angiography demonstrated no significant vascular access complications. In one case, the entire procedure was performed percutaneously, without common femoral artery surgical cutdown. CONCLUSIONS: The SoloPath sheath system permits transfemoral TAVR in patients with PAD small caliber ileofemoral vessels and vascular tortuosity. The transfemoral balloon-expandable sheath allowed these patients to avoid the increased morbidity and mortality risks associated with direct aortic or transapical access.

Colchicine in Coronary Artery Disease: An Old Acquaintance in New Attire?

Colchicine has recently gained considerable attention in the field of cardiovascular research, after a number of studies showed that it may be of use in several settings of cardiovascular disease, including chronic coronary artery disease and following stent implantation. Its unique anti-inflammatory mechanism of action makes it safe to use in patients with cardiovascular disease, unlike most--if not all--currently available antiinflammatory agents. While its prophylactic and therapeutic value is well-established in certain conditions involving an acute inflammatory response, e.g. pericarditis, in other conditions, including coronary artery disease and heart failure, which are associated with a chronic low-grade inflammatory state, the evidence regarding its potential use remains sparse. In this concise review, we present key features of this drug and the rationale for colchicine therapy, in the context of acute and chronic coronary artery disease, as well as in ischemic heart failure and critically examine the evidence concerning a possible future role of colchicine treatment in these conditions.

A predictive score of radial artery spasm in patients undergoing transradial percutaneous coronary intervention.

OBJECTIVE: Radial artery spasm may hinder completion of transradial angiography or PCI, leading to access site crossover, prolonged procedure times and complications. The aim of this study was to derive a radial artery spasm risk score in patients undergoing elective percutaneous coronary intervention (PCI), prospectively validate it, and apply it in a real-life clinical setting. METHODS: The study population consisted of 3 cohorts of patients undergoing elective PCI with transradial access: the derivation cohort (N=1006), the validation cohort (N=576) and the intervention cohort (N=140), consisting of patients with high risk score, in whom intensified spasm-preventive measures were applied. RESULTS: Multivariable analysis in the derivation cohort showed that 5 weighted factors could be used to construct a risk score for spasm: body-mass index, height, current smoking, hypertension and peripheral artery disease (c-statistic 0.945, with an optimal cut-off of 4). In the validation cohort, the cut-off of 4 predicted spasm with a sensitivity of 84.5% and a specificity of 74.7%. In the intervention cohort, which included only patients with a spasm-risk score of ≥4, the rate of spasm was drastically reduced (odds ratio 0.32, 95% confidence interval 0.17-0.61), compared to the corresponding high spasm risk subgroup of patients of the validation cohort. CONCLUSION: A spasm risk score can be used to predict radial artery spasm during elective transradial PCI. Using this score, a high spasm risk patient subgroup can be identified, where intensive spasm-preventive measures can lead to a significant reduction in the frequency of spasm.

Usefulness of colchicine to reduce perioperative myocardial damage in patients who underwent on-pump coronary artery bypass grafting.

The objective of the present study was to test whether a perioperative course of colchicine, in patients who underwent standard coronary artery bypass grafting, would result in reduced postoperative increase of myocardial injury biomarker levels. Patients were prospectively randomized to colchicine or placebo starting 48 hours before scheduled coronary artery bypass grafting and for 8 days thereafter (0.5 mg twice daily). The primary outcome parameter was maximal high-sensitivity troponin T (hsTnT) concentration within 48 hours after surgery. Secondary outcome measures were maximal creatine kinase-myocardial brain fraction (CK-MB) levels and area under the curve (AUC) of hsTnT and CK-MB concentrations; 59 patients were included. Maximal hsTnT was 616 pg/ml (396 to 986) in the colchicine group versus 1,613 pg/ml (732 to 2,587) in controls (p = 0.002). Maximal CK-MB was 44.6 ng/ml (36.6 to 68.8) and 93.0 ng/ml (48.0 to 182.3), respectively (p = 0.002). The median AUC for hsTnT was 40,755 pg h/ml (20,868 to 79,176) in controls versus 20,363 pg h/ml (13,891 to 31,661) in the colchicine group (p = 0.002). AUCs for CK-MB were 2,552 ng h/ml (1,564 to 4,791) in controls and 1,586 ng h/ml (1,159 to 2,073) in the colchicine group (p = 0.003). The main complaints associated with colchicine were, as expected, gastrointestinal, with 5 patients (16.7%) in the colchicine group reporting diarrhea versus 1 control (3.4%) (p = 0.195). In conclusion, a short perioperative course of colchicine was effective in attenuating postoperative increases of hsTnT and CK-MB compared with placebo. This finding, which needs confirmation in a larger clinical trial powered to assess clinical endpoints, suggests a potential role for this agent in reducing cardiac surgery-related myocardial damage.

Novel Inflammatory Biomarkers in Cardiovascular Therapeutics.

Inflammation has been established as an important determinant of cardiovascular disease progression. Currently, clinical examination, laboratory and imaging tests are invaluable for the diagnosis, prognosis and disease monitoring. Novel inflammatory biomarkers are also used to better restratify patients in risk groups but their potential to guide treatment decisions and management of patients has not been extensively evaluated. Therefore, in this review article we present the most recent data concerning the use of inflammatory biomarkers in cardiovascular therapeutics.

The Role and Predictive Value of Cytokines in Atherosclerosis and Coronary Artery Disease.

Atherosclerosis is currently regarded as a chronic inflammatory disease that is mediated by several types of cells and molecules. Emphasis has been placed on the role of cytokines and the way they act and interact to initiate and sustain inflammation in the microenvironment of an atherosclerotic plaque. Cytokines are invariably expressed by all cells involved in the pathogenesis of atherosclerosis, act on a variety of targets exerting multiple effects and are largely responsible for the crosstalk among endothelial, smooth muscle cells, leukocytes and other vascular residing cells. In the present paper our aim is to review current information on the role of the most commonly discussed cytokines in the process of atherogenesis and to discuss the prognostic significance of these cytokines in atherosclerosis and coronary artery disease.