Assessment of neutrophil and neutrophil/lymphocyte ratio in coronary collateral developed patients with acute coronary syndrome.

OBJECTIVE Inflammation-related markers provide diagnostic and prognostic information for coronary artery disease and acute coronary syndrome. We aimed to compare neutrophil count and neutrophil/lymphocyte ratio (NLR) in acute coronary syndrome patients with coronary collateral development in our study. METHODS A total of 426 patients (102 unstable angina pectoris (USAP), 223 non-ST-elevation myocardial infarction (non-STEMI), 103 ST-elevation myocardial infarction (STEMI) were compared regarding hemoglobin, platelet, lymphocyte, neutrophil count, and NLR. RESULTS Neutrophil count and NLR were significantly lower in USAP patients and higher in STEMI patients; 5.14± 1.79 vs. 7.21± 3.05 vs. 9.93±4.67 and 2.92±2.39 vs. 5.19±4.80 vs. 7.93±6.38, p <0.001. Other parameters, i.e., hemoglobin, platelet, and lymphocyte count, were not significantly different between the groups. CONCLUSIONS In our study, it was concluded that there may be a statistically significant difference in the number of neutrophil counts and NLR among the types of acute coronary syndromes with coronary collateral development.

Assessment of neutrophil and neutrophil/lymphocyte ratio in coronary collateral developed patients with acute coronary syndrome

SUMMARY OBJECTIVE Inflammation-related markers provide diagnostic and prognostic information for coronary artery disease and acute coronary syndrome. We aimed to compare neutrophil count and neutrophil/lymphocyte ratio (NLR) in acute coronary syndrome patients with coronary collateral development in our study. METHODS A total of 426 patients (102 unstable angina pectoris (USAP), 223 non-ST-elevation myocardial infarction (non-STEMI), 103 ST-elevation myocardial infarction (STEMI) were compared regarding hemoglobin, platelet, lymphocyte, neutrophil count, and NLR. RESULTS Neutrophil count and NLR were significantly lower in USAP patients and higher in STEMI patients; 5.14± 1.79 vs. 7.21± 3.05 vs. 9.93±4.67 and 2.92±2.39 vs. 5.19±4.80 vs. 7.93±6.38, p <0.001. Other parameters, i.e., hemoglobin, platelet, and lymphocyte count, were not significantly different between the groups. CONCLUSIONS In our study, it was concluded that there may be a statistically significant difference in the number of neutrophil counts and NLR among the types of acute coronary syndromes with coronary collateral development.

RESUMO OBJETIVO Marcadores relacionados a inflamação fornecem informações de diagnóstico e prognóstico para doença arterial coronariana e síndrome coronariana aguda. Nosso objetivo foi comparar o número de neutrófilos e razão neutrófilos/linfócitos (RNL) em pacientes com síndrome coronariana aguda com desenvolvimento de circulação colateral. MÉTODOS Um total de 426 pacientes [102 com angina de peito instável (APIN), 223 com infarto do miocárdio sem supradesnível de ST (IMSS), 103 com infarto do miocárdio com supradesnível de ST (IMCS)] foram comparados em relação a hemoglobina, plaquetas, linfócitos, neutrófilos e RNL. RESULTADOS O número de neutrófilos e RNL estavam significativamente mais baixos em pacientes com APIN e mais altos nos pacientes com IMCS; 5,14± 1,79 vs. 7,21± 3,05 vs. 9,93±4,67 and 2,92±2,39 vs. 5,19±4,80 vs. 7,93±6,38, p <0,001. Os outros parâmetros (hemoglobina, contagem de linfócitos e plaquetas) não foram significativamente diferentes entre os grupos. CONCLUSÃO No nosso estudo, concluiu-se que pode haver uma diferença significativa no número de neutrófilos e RNL entre os tipos de síndromes coronarianas agudas com desenvolvimento de circulação colateral.

The NLRP3 and CASP1 gene polymorphisms are associated with developing of acute coronary syndrome: a case-control study.

The protein products of NLRP3 and CASP1 genes are involved in the cleavage of pro-IL-1B and pro-IL-18 leading to the active cytokines, which play an important role in the development of the acute coronary syndrome (ACS). The aim of the present study was to evaluate whether NLRP3 and CASP1 gene polymorphisms are biomarkers of ACS susceptibility in Mexican population. Two polymorphisms of the CASP1 gene [G+7/in6A (rs501192) and A10370-G Exon-6 (rs580253)] and one of the NLRP3 gene [UTR'3 G37562-C (rs10754558)] were genotyped by 5' exonuclease TaqMan assays in a group of 617 patients with ACS and 609 control individuals. Under recessive model, the CASP1 G+7/in6A polymorphism was associated with an increased risk of developing ACS when compared to healthy controls (OR = 1.76, 95% CI 1.08-2.86, P Res  = 0.022). In the same way, under recessive model, the CASP1 A10370-G was associated with increased risk of ACS (OR = 1.75, 95% CI 1.07-2.85, P Res  = 0.025). Moreover, under co-dominant, dominant, over-dominant, and additive models, the NLRP3 UTR'3 G37562-C was associated with a decreased risk of ACS (OR = 0.45, 95%CI 0.22-0.92, P Co-dom  = 0.006; OR = 0.61, 95%CI 0.44-0.84, P Dom  = 0.002; OR = 0.67, 95%CI 0.48-0.94, P Over-dom  = 0.02; and OR = 0.65, 95%CI 0.50-0.94, P Add  = 0.02, respectively). In summary, this study demonstrates that the G+7/in6A and A10370-G polymorphisms of the CASP1 gene are associated with increased risk of developing ACS, whereas the UTR'3 G37562-C polymorphism of the NLRP3 gene is associated with a decreased risk of developing ACS in Mexican population.

Kounis syndrome and ziprasidone.

Kounis syndrome (KS), described by Kounis and Zavras in 1991, is the manifestation of an allergic reaction preceding and leading to an acute coronary syndrome (ACS). There are three variants of Kounis Syndrome. Here we describe a novel case report of a type 1 variant secondary to Ziprasidone.

Changes of circulating CD4(+)CD25(+)CD127(low) regulatory T cells in patients with acute coronary syndrome and its significance.

The aim of this study was to investigate the changes of circulating CD4(+)CD25(+)CD127(low) regulatory T cells (Treg) in patients with acute coronary syndrome (ACS) and its significance. The experiment was divided into three groups: ACS (48 patients), stable angina pectoris (SAP) (24 patients), and normal controls (24 subjects). The CD4(+)CD25(+)CD127(low) Treg cell counts were tested by flow cytometry, and the levels of high-sensitivity C-reactive protein (hs-CRP) and peripheral blood leukocytes (PWBCs) were determined in the peripheral blood of each group; comparisons were made among groups. The frequency of CD4(+)CD25(+)CD127(low) to CD4(+) cell in the ACS group (3.18 ± 1.76%) was significantly lower than those observed in control (5.64 ± 1.63%) and SAP (5.60 ± 1.56%) groups (F = 25.247, P < 0.01), while the hs-CRP and PWBC levels in the ACS group were significantly higher than those in the control group (P < 0.05). In addition, the reduced frequency of CD4(+)CD25(+)CD127(low) to CD4(+) cells was negatively correlated with the increased hs-CRP and PWBC counts by correlation analysis, and the related coefficients (r) were -0.518 and -0.311, respectively (P < 0.01). These findings indicate that the decrease of the frequency of Treg cells in the peripheral blood of patients with ACS might destroy the balance of tolerance of the peripheral immune system and might activate inflammation, thus participating in the occurrence and development of the pathological processes of atherosclerosis.

Association of the C-type lectin-like domain family-16A (CLEC16A) gene polymorphisms with acute coronary syndrome in Mexican patients.

The CLEC16A gene has an important role in the immune activation and regulation inflammatory. This gene encodes to C-type lectin domain that is involved in the recognition of DAMPS. The aim of this study was assess the CLEC16A gene polymorphisms in the risk of developing ACS in a group of patients. Four rs12708716, rs12917716, rs6498142 and rs9925481 (positions 146529 A>G, 155804 G>C, 47905 C>G and 64135 C>T, respectively) single nucleotide polymorphisms of CLEC16A gene were analyzed by TaqMan assays in a group of 452 patients with ACS and 456 healthy controls. The analysis was performed on the total group of individuals and then in groups of men and women separately. Under co-dominant model adjusted by cardiovascular risk factors the rs12708716 (146529 A>G) and rs12917716 (155804 G>C) polymorphisms were significantly associated with decrease risk of ACS in men (OR=0.16, PCo-dom=0.027 and OR=0.37, PCo-dom=0.016, respectively). In summary, our data suggests that two polymorphisms of the CLEC16A gene play an important role in the developing of ACS in men.

Correlation of serum high-sensitivity C-reactive protein and interleukin-6 in patients with acute coronary syndrome.

Serum high-sensitivity C-reactive protein (hs-CRP) is a sensitive indicator of inflammation, which is closely related with the progress of plaque formation. Interleukin-6 (IL-6) is one of the inflammatory markers of local coronary plaque and the peripheral blood cycle, promoting the occurrence of atherosclerosis development and plaque rupture. In this study, the correlation of hs-CRP and IL-6 was investigated in patients with acute coronary syndrome (ACS). Sixty cases of ACS, including 33 cases of acute myocardial infarction (AMI) and 27 cases of unstable angina pectoris (UAP), 45 cases of stable angina pectoris (SAP), and 45 healthy people (HG) were enrolled in study. The serum hs-CRP and serum IL-6 levels were tested by the immune turbidimetric method and enzyme-linked immunosorbent assay (ELISA), respectively. The differences among groups and their correlations were evaluated. Results showed that the serum hs-CRP and IL-6 concentrations of the AMI and UAP groups were significantly higher than those of the SAP and HG groups, respectively (P<0.01), and those of the AMI group were significantly higher than those of the UAP group (P<0.05). The serum hs-CRP and IL-6 levels of the ACS group were positively correlated (r=0.836). The serum hs-CRP and IL-6 levels could be used to determine the stability of plaque, and have some relevance in the ACS process, showing great value in judgments of ACS prognosis.

The MHC2TA 1614 C>G gene polymorphism is associated with risk of developing acute coronary syndrome.

BACKGROUND: Inflammation plays an essential role in the development and progression of atherosclerotic lesions. The major histocompatibility complex class II trans-activator (MHC2TA) is considered an important molecule in the inflammatory process regulation. The aim of the present study was to evaluate the role of MHC2TA gene polymorphisms as susceptibility markers for acute coronary syndrome (ACS). METHODS: Three polymorphisms (-168 A>G, 1614 C>G, and 2536 G>A) of the MHC2TA gene were analyzed by 5' exonuclease TaqMan genotyping assays in a group of 297 patients with ACS and 283 healthy controls. Haplotypes were constructed after linkage disequilibrium analysis. RESULTS: The 1614 C allele and CC genotype were associated with risk of developing ACS (PC=0.014, OR=1.37 and PC=0.006, OR=1.90, respectively). Based on Hosmer-Lemeshow Goodness of Fit test, the recessive model was selected to estimate risk between ACS patients and controls adjusted by cardiovascular risk factors using a multiple logistic analysis. In this case, the OR adjusted was 1.78 for the 1614 CC genotype (P=0.023). The analysis of linkage disequilibrium showed one risk haplotype (ACG) and one protective haplotype (AGG) for developing ACS (P=0.02, OR=1.5 and P=0.04, OR=0.72, respectively). CONCLUSION: The results suggest that MHC2TA 1614 gene polymorphism could be involved in the risk of developing ACS.

Adaptive immunity is related to coronary artery disease severity after acute coronary syndrome in subjects with metabolic syndrome.

Metabolic syndrome (MetS) is an inflammatory state associated with high coronary disease risk. Inflammation and adaptive immunity modulate atherosclerosis and plaque instability. We examined early changes in anti-oxidized low-density lipoprotein (LDL) (anti-oxLDL) autoantibodies (Abs) in patients with MetS after an acute coronary syndrome (ACS). Patients of both genders (n=116) with MetS were prospectively included after an acute myocardial infarction (MI) or hospitalization due to unstable angina. Anti-oxLDL Abs (IgG class) were assayed at baseline, three and six weeks after ACS. The severity of coronary disease was evaluated by the Gensini score. We observed a decrease in anti-oxLDL Abs titers (p<0.002 vs. baseline), mainly in males (p=0.01), in those under 65 y (p=0.03), and in subjects with Gensini score above median (p=0.04). In conclusion, early decrease in circulating anti-oxLDL Abs is associated with coronary disease severity among subjects with MetS.

Interleukin 1 receptor antagonist polymorphisms are associated with the risk of developing acute coronary syndrome in Mexicans.

Inflammation plays an essential role in the development and progression of atherosclerotic lesions. Cytokines of the interleukin-1 family are central regulators in immunoinflammatory mechanisms. In the present work, the role of interleukin 1 (IL-1) and IL-1 receptor antagonist (IL-1RN) gene polymorphisms as susceptibility markers for acute coronary syndrome (ACS) was evaluated. Six polymorphisms in the IL-1 gene cluster members were genotyped by 5' exonuclease TaqMan genotyping assays in 289 ACS patients and 248 healthy controls. Haplotypes were constructed after linkage disequilibrium analysis. Statistically significant associations were found between three polymorphisms of the IL-1RA gene (rs419598, rs315951, and rs2234663) and the development ACS. The polymorphism RN.4T>C (rs419598) was associated with hypertension, previous myocardial infarction, and major adverse cardiac events. To establish the functional effect of the IL-1RN6/2 (rs315951) polymorphism (principal IL-1RN polymorphism associated with ACS in our study), monocytes were obtained from a group of 27 healthy individuals and the production of IL-1 receptor antagonist (IL-1Ra) was determined. Monocytes from individuals with rs315951 CC genotype showed similar production of IL-1Ra as individuals with GG and CG genotypes. The analysis of linkage disequilibrium of the IL-1RA polymorphisms showed four out of eight different possible allele combinations with differences between the studied groups. Patients with ACS showed increased frequency of "T1C" haplotype when compared to healthy controls. The results suggest that IL-1RN gene polymorphisms could be involved in the risk of developing ACS in Mexican individuals.

Anticorpos contra LDL-ox e síndrome coronariana aguda / Antibodies against OxLDL and acute coronary syndrome

FUNDAMENTO: A oxidação da lipoproteína de baixa densidade (LDL-ox) induz à formação de epítopos imunogênicos na molécula. A presença de autoanticorpos contra a LDL-ox tem sido demonstrada no soro de pacientes com doença arterial coronariana (DAC). Contudo, o papel desses autoanticorpos na fisiopatologia das síndromes coronarianas agudas (SCA) e o seu significado clínico permanecem indefinidos. OBJETIVO: Avaliar a associação entre autoanticorpos contra a LDL-ox e SCA. MÉTODOS: Os títulos de imunoglobulina G autoanticorpos contra a LDL-ox por cobre (antiLDL-ox) e contra o peptídeo sintético D derivado da apolipoproteína B (antipeptD) foram determinados por ensaio imunoenzimático (ELISA) em 90 pacientes, nas primeiras 12h de SCA (casos) e em 90 pacientes com DAC crônica (controles). RESULTADOS: Os resultados mostraram que os títulos de antiLDL-ox foram significativamente mais elevados (p = 0,017) nos casos (0,40 ± 0,22), do que nos controles (0,33 ± 0,23). Por outro lado, os títulos de antipeptD foram significativamente menores (p < 0,01) nos casos (0,28 ± 0,23) do que nos controles (0,45 ± 0,30). A diferença dos títulos de ambos anticorpos entre os dois grupos estudados foi independente de idade, sexo, hipertensão arterial, diabete melito, dislipidemia, índice de massa corporal, tabagismo, perfil lipídico, uso de estatinas e história familiar de DAC. CONCLUSÃO: Os resultados mostraram que os títulos de antiLDL-ox foram significativamente mais elevados nos pacientes com síndrome coronariana aguda quando comparados aos pacientes com doença arterial coronariana e podem estar associados à instabilidade da placa aterosclerótica.

BACKGROUND: The oxidation of low-density lipoprotein (oxLDL) induces the formation of immunogenic epitopes in molecules. The presence of autoantibodies against oxLDL has been demonstrated in the serum of patients with coronary artery disease (CAD). However, the role of these autoantibodies in the pathophysiology of acute coronary syndromes (ACS) and their clinical significance remain undefined. OBJECTIVE: To evaluate the association between antibodies against oxLDL and ACS. METHODS: Titers of IgG autoantibodies against oxLDL by copper (anti-oxLDL) and anti-D synthetic peptide derived from apolipoprotein B (antipeptD) were determined by Enzyme-linked immunosorbent assay (ELISA) in 90 patients, in the first 12 hours of ACS (cases) and in 90 patients with chronic CAD (controls). RESULTS: The results showed that the titers of anti-oxLDL were significantly higher (p = 0.017) in cases (0.40 ± 0.22) than in controls (0.33 ± 0.23). On the other hand, the titers of antipeptD were significantly lower (p < 0.01) in cases (0.28 ± 0.23) than in controls (0.45 ± 0.30). The difference in the titers of both antibodies between the two groups was independent of age, sex, hypertension, diabetes mellitus, dyslipidemia, body mass index, smoking, lipid profile, statin use and family history of CAD. CONCLUSION: The results showed that the titers of anti-oxLDL were significantly higher in patients with acute coronary syndrome as compared to patients with coronary artery disease and may be associated with atherosclerotic plaque instability.

Antibodies against oxLDL and acute coronary syndrome.

BACKGROUND: The oxidation of low-density lipoprotein (oxLDL) induces the formation of immunogenic epitopes in molecules. The presence of autoantibodies against oxLDL has been demonstrated in the serum of patients with coronary artery disease (CAD). However, the role of these autoantibodies in the pathophysiology of acute coronary syndromes (ACS) and their clinical significance remain undefined. OBJECTIVE: To evaluate the association between antibodies against oxLDL and ACS. METHODS: Titers of IgG autoantibodies against oxLDL by copper (anti-oxLDL) and anti-D synthetic peptide derived from apolipoprotein B (antipeptD) were determined by Enzyme-linked immunosorbent assay (ELISA) in 90 patients, in the first 12 hours of ACS (cases) and in 90 patients with chronic CAD (controls). RESULTS: The results showed that the titers of anti-oxLDL were significantly higher (p = 0.017) in cases (0.40 +/- 0.22) than in controls (0.33 +/- 0.23). On the other hand, the titers of antipeptD were significantly lower (p < 0.01) in cases (0.28 +/- 0.23) than in controls (0.45 +/- 0.30). The difference in the titers of both antibodies between the two groups was independent of age, sex, hypertension, diabetes mellitus, dyslipidemia, body mass index, smoking, lipid profile, statin use and family history of CAD. CONCLUSION: The results showed that the titers of anti-oxLDL were significantly higher in patients with acute coronary syndrome as compared to patients with coronary artery disease and may be associated with atherosclerotic plaque instability.

Serial analyses of C-reactive protein and myeloperoxidase in acute coronary syndrome.

BACKGROUND: C-reactive protein (CRP) and myeloperoxidase (MPO) are involved in the pathogenesis of atherosclerosis, mainly during periods of instabilization. This study aims to test the hypothesis that patients with acute coronary syndrome (ACS) maintain a persistent inflammatory state, and that this is associated with long-term mortality. HYPOTHESIS: We hypothesized that serum C-reactive protein and myeloperoxidase collected at the index event and later, could add to the prognostic information in patients with ACS. METHODS: In a prospective cohort of 115 consecutive patients with ACS, myeloperoxidase and C-reactive protein were measured at admission and 2 y later. Patients were followed-up for the occurrence of cardiac death and other major cardiac events. RESULTS: Levels of CRP decreased from 26 +/- 34 mg/L in the acute phase to 6 +/- 8 mg/L in the chronic phase (p < 0.001), and MPO levels decreased from 86 +/- 43 pM to 27 +/- 32 pM (p < 0.001). After 29 +/- 12 mo, 27% patients died, 39% had new episode of ACS, and 30% underwent revascularization procedures. Initial CRP levels above 10 mg/L were associated with higher long-term mortality (hazard ratio [HR]: 2.43; 95% confidence interval [CI]: 0.98 to 6.07; p = 0.048). MPO levels were not associated with death or other major events. CONCLUSIONS: Changes over time or absolute values in the chronic phase of both markers were not associated with clinical outcomes. CRP levels, but not MPO levels, in the index event were predictive of long-term cardiovascular mortality.

Interleukin-18: an independent predictor of cardiovascular events in patients with acute coronary syndrome after 6 months of follow-up.

BACKGROUND: Interleukin-18 (IL-18), a proinflammatory cytokine, has been associated with atherogenesis and plaque rupture in acute coronary syndrome (ACS). Recent studies suggest that IL-18 may have a long-term prognostic value. The aim of this study was to evaluate the relationship between IL-18 levels and major adverse cardiovascular events within 6 months of follow-up in post-ACS patients. METHODS: One hundred and twelve consecutive patients admitted to a university hospital with ACS were included in the study. IL-18 and C-reactive protein were measured within the first 24 h of admission. Six months after hospital discharge, the incidence of major adverse cardiovascular events (cardiovascular death, new episode of ACS, and need for unplanned revascularization) was assessed. RESULTS: Mean age of patients was 64 +/- 11 years, and 58 (52%) were male. During the 6 months of follow-up, 33 patients (31.4%) experienced major adverse cardiovascular events. Median IL-18 serum levels were higher among patients who had events than among those who did not: 271.7 pg/ml (interquartile range: 172.9-389.6) and 139.7 pg/ml (interquartile range: 99.9-265.7), respectively (P < 0.01). In the Cox multivariate analysis, after adjustment for clinical risk factors and serum troponin, elevated levels of IL-18 were associated with higher incidence of events (hazard ratio: 2.5; 95% confidence interval: 1.14-5.52; P = 0.023). In this population, C-reactive protein was of borderline significance for events. CONCLUSION: Serum IL-18 levels in ACS patients were independent predictors of long-term cardiovascular events. These findings support the association between inflammation and prognosis of ACS patients, as well as the clinical impact of this biomarker.

High circulating autoantibodies against human oxidized low-density lipoprotein are related to stable and lower titers to unstable clinical situation.

BACKGROUND: Oxidized lipoproteins and antibodies anti-oxidized low-density lipoprotein (anti-oxLDL) have been detected in human plasma and in atherosclerotic lesions. However, the role of these autoantibodies in the maintenance of vascular health or in the pathogenesis of acute vascular insults remains unclear. We examined the relationship of human immunoglobulin G (IgG) anti-oxLDL antibodies with cardiovascular disease risk markers in stable subjects and in patients after an acute coronary syndrome (ACS). METHODS: Titers of human anti-oxLDL antibodies were measured in hypertensive subjects in primary prevention (n=94), without other risk factors, and in individuals after a recent ACS event who also had metabolic syndrome (n=116). Autoantibodies against copper ion oxidized LDL were measured by enzyme-linked-immunosorbent assay. RESULTS: Anti-oxLDL titers were higher in hypertensive patients and these subjects presented lower high sensitivity C-reactive protein (hs-CRP) than those with ACS (p<0.0001). We found significant correlations between anti-oxLDL and hs-CRP (r=-0.284), body mass index (r=-0.256), waist circumference (r=-0.368), apolipoprotein B (r=-0.191), glucose (r=-0.303), systolic blood pressure (r=0.319), diastolic blood pressure (r=0.167), high-density lipoprotein cholesterol (r=0.224) and apolipoprotein A1 (r=0.257) (p<0.02 for all). After multiple linear regression hs-CRP, fasting glucose and waist circumference remained independently and inversely associated with anti-oxLDL. CONCLUSIONS: Acute inflammatory and metabolic conditions decrease titers of human antibodies of IgG class against oxidized LDL, and that circulating anti-oxLDL antibodies could be associated with a protective role in atherosclerosis.

[Pro-inflammatory and anti-inflammatory markers in coronary artery disease and acute ischemic coronary syndrome]. / Marcadores pro y antiinflamatorios en la enfermedad arterial coronaria y el síndrome isquémico coronario agudo.

Inflammation plays an important role in the development of atherosclerotic lesions, affecting several stages of the atheroma's development going from the initial leukocyte recruitment to the eventual rupture of the unstable atherosclerotic plaque. The inflammatory reactions within coronary atherosclerotic plaques influence the clinical outcome of acute coronary syndromes and coronary artery disease. Recent studies suggest that inflammation markers may reflect different aspects of the atherothrombotic process in relation to the stages of acute coronary syndrome. These markers play an important role in the risk of developing coronary artery disease, and may correlate with its severity. Some cytokines, acute phase proteins, acute phase reactants proteins, and adhesion molecules released from the inflammatory cells may reflect the inflammatory process in atherosclerotic plaques. However, it remains to be determined whether these pro- and anti-inflammation markers may confer risk or protection for cardiovascular disease, or simply reflect the underlying disease process. The analysis of the markers may be useful for the development of new strategies for coronary disease prevention and treatment. Therefore, we need a well-designed evaluation of these markers before their use in the clinical practice.

Marcadores pro y antiinflamatorios en la enfermedad arterial coronaria y el síndrome isquémico coronario agudo / Pro-inflammatory and anti-inflammatory markers in coronary artery disease and acute ischemic coronary syndrome

Inflammation plays an important role in the development of atherosclerotic lesions, affecting several stages of the atheroma's development going from the initial leukocyte recruitment to the eventual rupture of the unstable atherosclerotic plaque. The inflammatory reactions within coronary atherosclerotic plaques influence the clinical outcome of acute coronary syndromes and coronary artery disease. Recent studies suggest that inflammation markers may reflect different aspects of the atherothrombotic process in relation to the stages of acute coronary syndrome. These markers play an important role in the risk of developing coronary artery disease, and may correlate with its severity. Some cytokines, acute phase proteins, acute phase reactants proteins, and adhesion molecules released from the inflammatory cells may reflect the inflammatory process in atherosclerotic plaques. However, it remains to be determined whether these pro- and anti-inflammation markers may confer risk or protection for cardiovascular disease, or simply reflect the underlying disease process. The analysis of the markers may be useful for the development of new strategies for coronary disease prevention and treatment. Therefore, we need a well-designed evaluation of these markers before their use in the clinical practice.