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Background: Overweight (OW) and obesity (OB) are major health problems both in Mexico and the world. Because of the chronic low-grade inflammatory state that characterizes OW and OB, they are considered as cardiovascular risk factors. The leuko-glycemic index (LGI) is a ratio used as a prognostic factor to predict complications in patients with vascular diseases., Objective: To assess the utility of LGI index as an inflammatory and endothelial dysfunction marker in patients with OW and OB., Material and Methods: Comparative cross-sectional study in 124 patients of Family Medicine Unit 80 of Mexican Social Security Institute. Young adults aged between 18 - 50 years old, and BMI between 18.5 and 40 kg/m2, without diagnosis of chronic diseases, auto immunities or immunodeficiencies were included. Bioelectrical impedance (weight, height, BMI, % body fat, lean mass) and blood sample (blood count, glucose, lipid profile, inflammatory, endothelial dysfunction markers) were assessed. Patients were grouped according to their BMI: OB, OW and normal weight (NW)., Results: LGI was found to be significantly elevated in OB and OW patients vs. NW. LGI correlated positively with inflammation and DE markers: IL-6, TNF-α, vWF. A value ≥ 405 was estimated with ROC curves as cut-off point for LGI to predict the likelihood of inflammation and ED in OW and OB patients., Conclusions: ILG is relevant as a predictive marker of cardiovascular disease by reflecting inflammation and endothelial dysfunction in patients with OW and OB., (Licencia CC 4.0 (BY-NC-ND) © 2024 Revista Médica del Instituto Mexicano del Seguro Social.)

Backgrounds and Purposes: Patients with chronic kidney disease (CKD) have higher risk of developing cardiovascular disease. In CKD patients the mechanisms involved in, endothelial damage and the role of different drugs used on these patients are not completely understood. The aim of this work is to analyze the effect of statins and platelet antiaggregant (PA) on endothelial microvesicles (EMVs) and other markers of endothelial dysfunction., Experimental Approach: Cross-sectional study of 41 patients with CKD 3b-4 and 8 healthy volunteers. Circulating levels of EMVs, vascular endothelial growth factor (VEGF), and advance oxidized protein products (AOPPS) were quantified and the correlation with different comorbidity variables and therapeutic strategies were evaluated., Results: EMVs are increased in CKD patients as compared with controls (171.1 vs. 68.3/μl, P<.001). It was observed a negative correlation between age and EMVs. Statins and PA were associated with a reduction in EMVs and VEGF levels, independently of the serum total cholesterol levels (TC). The levels of AOPPS and VEGF were not different in CKD vs. controls., Conclusion: CKD is associated with a change in EMVs, VEGF and AOPP levels. The treatment with statins and PA normalizes these values to almost the observed in controls and this effect is independently of the prevailing TC level. These findings explain the existence of the pleiotropic effects of statins and PA which deserve further studies., (Copyright © 2019 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

Objectives: Psoriasis is associated to endothelial dysfunction, which causes impaired vascular functioning. TNF-α blockers have shown the ability to improve vascular functioning in psoriasis. The nailfold vessel resistance index (NVRI) assesses microvascular functioning at nailfold. The objectives of the study is to assess the effect of the TNF-α inhibition with adalimumab on NVRI., Material and Methods: Quasi-experimental study. Fifteen patients with moderate-severe psoriasis received adalimumab 40mg sc according to label information. Participants were assessed at baseline and at 12, 24 and 52 weeks after study intervention., Results: A reduction of -0.09±0.02 (P<.01) in NVRI and a -11.2±2,41ng/ml (P<.001) in E-selectin was observed at week 52., Conclusions: Adalimumab could produce a progressive and sustained reduction of vessel resistance at nailfold and E-selectin in patients with psoriasis., (Copyright © 2017 Elsevier España, S.L.U. All rights reserved.)

Vitamin D deficiency is a serious public health problem worldwide that affects not only skeletal health, but also a wide range of acute and chronic diseases. However, there is still skepticism because of the lack of randomized, controlled trials to support association studies on the benefits of vitamin D for non-skeletal health. This review was based on articles published during the 1980-2015 obtained from the Cochrane Central Register of controlled trials, MEDLINE and PubMed, and focuses on recent challenges with regard to the definition of vitamin D deficiency and how to achieve optimal serum 25-hydroxyvitamin D levels from dietary sources, supplements, and sun exposure. The effect of vitamin D on epigenetic fetal programming and regulation of genes that may potentially explain why vitamin D could have such lifelong comprehensive health benefits is reviewed. Optimization of vitamin D levels in children and adults around the world has potential benefits to improve skeletal health and to reduce the risk of chronic diseases, including some types of cancer, autoimmune diseases, infectious diseases, type 2 diabetes mellitus, and severe cardiovascular disorders such as atherothrombosis, neurocognitive disorders, and mortality., (Copyright © 2017 SEEN. Publicado por Elsevier España, S.L.U. All rights reserved.)

Background and Objective: The pathophysiology of gestational diabetes itself causes hyperstimulation of adipose tissue and of the placenta cells increasing the production of inflammatory cytokines, which cause changes in the tissues exposed such as the placenta and foetus. Therefore, the objective of this study was to compare metabolic markers and endothelial dysfunction in umbilical cord blood, as well as to determine the presence of atherosclerosis in the placentas of newborn infants of patients with gestational diabetes and in patients with normally progressing pregnancies., Patients and Method: An analytical cross-sectional study was carried out in 84 patients, obtaining data such as age, smoking and weight gain in pregnancy; the gestational age of the newborns was determined by Capurro, and their weight and destination subsequent to birth, the placentas were also collected in order to look for atherosclerosis through histological studies and glucose, insulin, VLDL-C, HDL-C, triglycerides, cholesterol, fibrinogen, PCR and markers of endothelial dysfunction (adiponectin, VCAM-1, ICAM-1 and IL-6) were determined in blood samples obtained from the umbilical cord., Results: Placental atherosclerosis presented in 28.94% of the group with gestational diabetes compared to 10.52% of the group with normally progressing pregnancies (P=.044); differences were found in glucose, cholesterol, triglycerides, fibrinogen, HOMA-IR, PCR-us, HDL-C, not in VLDL-C. Twenty-one point five percent of the newborns of the gestational diabetes patients required hospitalization, against 5.2% in the control group,, Conclusions: Pregnancies that involve diabetes have higher proportion of atherosclerosis, hospitalization of the newborn, insulin resistance, as well as elevation of markers associated with inflammation and endothelial dysfunction in umbilical cord blood., (Copyright © 2016 Elsevier España, S.L.U. All rights reserved.)

The omentin is an adipokine, which role is due to the capacity of regulate metabolic (insulin sensitivity) and anti-inflammatory activities, thus conferring vascular protection during obesity and diabetes mellitus type 2. By this, it is important to know the mechanisms by which omentin confers cardiovascular protection, with the purpose of establish omentin a possible therapeutic target or molecule on this scenario., (Copyright © 2015 Instituto Nacional de Cardiología Ignacio Chávez. Publicado por Masson Doyma México S.A. All rights reserved.)

Introduction and Objectives: Diabetes mellitus is associated with an enhanced risk for cardiovascular disease and its prevalence is increasing. Diabetes induces metabolic stress on blood and vascular cells, promoting platelet activation and vascular dysfunction. The level of vascular cell activation can be measured by the number and phenotype of microparticles found in the circulation. The aim of this study was to investigate the effect of a platelet-inhibitory dose of aspirin on the number and type of microparticles shed to the circulation., Methods: Forty-three diabetic patients were enrolled in the study and received a daily dose of 100mg of aspirin for 10 days to cover the average platelet life-span in the circulation. Before and after the intervention period, circulating microparticles were characterized and quantified by flow cytometry., Results: Type 1 diabetic patients had about twice the number of tissue factor-positive circulating microparticles (derived both from platelets and monocytes) and endothelial-derived E-selectin positive microparticles than type 2 diabetic patients. Aspirin therapy significantly inhibited platelets since cyclooxygenase 1 derived thromboxane generation levels were reduced by 99%. Microparticles derived from erythrocytes, activated monocytes, and smooth muscle cells were significantly reduced after 10 days of aspirin administration., Conclusions: These results indicate that: a) vascular and blood cells in type 1 diabetic patients are exposed to more sustained stress shown by their specific microparticle origin and levels; b) aspirin therapy inhibits vascular wall cell activation and microparticle shedding, and c) the effects of aspirin are similar in type 1 and 2 diabetes., (Copyright © 2016 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.)

Introduction and Objectives: Long-term data on the relationship between endothelial dysfunction after ST-segment elevation myocardial infarction and future adverse clinical events are scarce. The aim of this study was to noninvasively assess whether endothelial dysfunction 4 weeks to 6 weeks after primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction predicts future clinical events., Methods: This prospective cohort study was performed in 70 patients of the RESPONSE randomized trial, who underwent noninvasive assessment of endothelial function 4 weeks to 6 weeks after primary percutaneous coronary intervention. Endothelial function was measured by the reactive hyperemia peripheral artery tonometry method; an index<1.67 identified endothelial dysfunction., Results: The reactive hyperemia peripheral artery tonometry index measured on average 1.90±0.58. A total of 35 (50%) patients had endothelial dysfunction and 35 (50%) patients had normal endothelial function. Periprocedural "complications" (eg, cardiogenic shock, total atrioventricular block) were more common in patients with endothelial dysfunction than in those without (25.7% vs 2.9%; P<.01). During 4.0±1.7 years of follow-up, 20 (28.6%) patients had major adverse cardiovascular events: events occurred in 9 (25.7%) patients with endothelial dysfunction and in 11 (31.5%) patients with normal endothelial function (P=.52). There was an association between the prevalence of diabetes mellitus at baseline and the occurrence of major adverse cardiovascular events during follow-up (univariate analysis: hazard ratio=2.8; 95% confidence interval, 1.0-7.8; P<.05), and even in multivariate analyses the risk appeared to be increased, although not significantly (multivariate analysis: hazard ratio=2.5; 95% confidence interval, 0.8-7.5)., Conclusions: In this series of patients who survived an ST-segment elevation myocardial infarction, endothelial dysfunction, as assessed by reactive hyperemia peripheral artery tonometry 4 weeks to 6 weeks after myocardial infarction, did not predict future clinical events during a mean follow-up of 4 years., (Copyright © 2016 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.)

Introduction: Metabolic syndrome is a constellation of disorders that includes insulin resistance, central obesity, arterial hypertension and hyperlipidaemia. These disorders can have implications for the genitourinary apparatus., Objectives: To conduct a review on the pathophysiological aspects that explain the relationship between metabolic syndrome and sexual dysfunction, lower urinary tract syndrome, prostate cancer and stone disease., Methods: We performed a qualitative, narrative literature review through a literature search on PubMed of articles published between 1997 and 2015, using the terms pathophysiology, metabolic syndrome, endothelial dysfunction, lipotoxicity, mitochondrial dysfunction, kidney stones, hypogonadism, erectile dysfunction, lower urinary tract syndrome and prostate cancer., Synthesis of the Evidence: Metabolic syndrome constitutes an established complex of symptoms, defined as the presence of insulin resistance, central obesity, hypertension and hyperlipidaemia. Endothelial dysfunction secondary to lipotoxicity generates an inflammatory state, which involves renal cell metabolism, vascularisation of the pelvis and androgen production. These facts explain the relationship between metabolic syndrome, nephrolithiasis, lower urinary tract syndrome, hypogonadism and erectile dysfunction in men., Conclusions: Strategies such as proper diet, regular exercise, insulin treatment, testosterone-replacement therapy, therapy with antioxidants and free-radical inhibitors and urological treatments classically used for lower urinary tract syndrome have shown promising results in this syndrome., (Copyright © 2015 AEU. Publicado por Elsevier España, S.L.U. All rights reserved.)

Vasculopathy in systemic sclerosis is a severe, in many cases irreversible, manifestation that can lead to amputation. While the classical clinical manifestations of the disease have to do with the involvement of microcirculation, proximal vessels of upper and lower limbs can also be affected. This involvement of large vessels may be related to systemic sclerosis, vasculitis or atherosclerotic, and the differential diagnosis is not easy. To conduct a proper and early diagnosis, it is essential to start prompt appropriate treatment. In this review, we examine the involvement of large vessels in scleroderma, an understudied manifestation with important prognostic and therapeutic implications., (Copyright © 2015 Elsevier España, S.L.U. All rights reserved.)

Objective: Vascular endothelial inflammation and enhanced oxidative stress are important factors in the pathogenesis of obstructive sleep apnea syndrome (OSAS). The aim of this study was to determine the levels of heat shock protein (HSP) 27, HSP70, HSP90, L-arginine, and asymmetric dimethylarginine (ADMA) in patients with OSAS and determine their relationship with cardiovascular (CV) risk factors., Material and Methods: Forty patients with OSAS, comprising 26 with and 14 without traditional CV risk factors (obesity, hypercholesterolemia, diabetes, hypertension, and smoking), and 20 control subjects without OSAS were included. All patients underwent a full polysomnographic evaluation, and blood samples were obtained in the morning after the night the diagnostic study was performed., Results: No significant differences were found in serum HSP27 and HSP70 levels between the groups. HSP90 and ADMA levels increased significantly, whereas L-arginine levels decreased significantly in patients with OSAS, both with and without CV risk factors, compared with controls, but were not different among the subgroups. In all patients with OSAS, serum HSP70 levels were positively correlated with a percent time with saturation<90% (r=.349, P=.027). Serum L-arginine levels were negatively correlated with desaturation number (r=-.360, P=.022) and apnea-hypopnea index (r=-.354, P=.025) and positively correlated with mean oxygen saturation (r=.328, P=.039)., Conclusion: Serum levels of HSP90 and ADMA increased, whereas those of L-arginine decreased in patients with OSAS regardless of CV risk factors. These findings indicate the presence of oxidative stress and endothelial dysfunction in patients with OSAS., (Copyright © 2014 SEPAR. Published by Elsevier Espana. All rights reserved.)

Introduction: The pathophysiology underlying the association between migraine and other non-atherosclerotic vascular diseases is largely unknown. Endothelial dysfunction has been proposed as a common link. Besides, endothelial dysfunction is considered as a predictor of structural changes in the arterial walls., Aim: To review the current knowledge about the functional (endothelial dysfunction) and structural (arterial stiffness and atherosclerotic diseases) arterial properties associated with migraine., Development: Studies of biological markers of endothelial dysfunction in peripheral blood, systemic and cerebral vasoreactivity, arterial stiffness indexes and direct visualization of macroscopic changes in the arterial wall have shown differences between patients with and without migraine, as well as between the different migraine subtypes., Conclusions: Endothelial dysfunction, as a predictor of structural changes in arteries, has been proposed as an early marker for vascular pathology associated with migraine. In migraine patients there is an increase of biomarkers of endothelial dysfunction, but the correlation with vasoreactivity studies does not allow definite conclusions. Available data do not allow to conclude that migraine is associated with macroscopic alterations outside the cerebral arterial bed.

Background and Objective: Recent studies have found increased markers of endothelial activation in men with chronic spinal cord injury. This study was conducted to determine the effects of arm-cranking exercise on endothelial dysfunction in male adults with chronic SCI., Method: A prospective randomized study of 17 sedentary adult males with chronic SCI at or under T5 level. Nine performed a supervised exercise program at a moderate intensity (arm-cranking: 12 weeks, 3 sessions/week). Plasma levels of endothelin-1, soluble intercellular adhesion molecule type 1 (sICAM-1), and soluble vascular adhesion molecule type 1 (sVCAM-1) were assessed by ELISA. Outcome measurements also included physical fitness and total body fat mass percentage., Results: We observed both in the randomized and in the before-after studies a significant reduction of the levels of endothelin-1 and sICAM-1. Furthermore, significant improvements of both physical fitness and body composition were also found., Conclusion: Arm-cranking exercise improved endothelial dysfunction in adult males with chronic SCI. Long-term studies are still required to determine whether the correction of endothelial dysfunction improves the clinical outcomes of adults with chronic SCI., (Copyright © 2013 Elsevier España, S.L.U. All rights reserved.)

Haemolytic uraemic syndrome (HUS) is a clinical entity defined as the triad of nonimmune haemolytic anaemia, thrombocytopenia, and acute renal failure, in which the underlying lesions are mediated by systemic thrombotic microangiopathy (TMA). Different causes can induce the TMA process that characterizes HUS. In this document we consider atypical HUS (aHUS) a sub-type of HUS in which the TMA phenomena are the consequence of the endotelial damage in the microvasculature of the kidneys and other organs due to a disregulation of the activity of the complement system. In recent years, a variety of aHUs-related mutations have been identified in genes of the the complement system, which can explain approximately 60% of the aHUS cases, and a number of mutations and polymorphisms have been functionally characterized. These findings have stablished that aHUS is a consequence of the insufficient regulation of the activiation of the complement on cell surfaces, leading to endotelial damage mediated by C5 and the complement terminal pathway. Eculizumab is a monoclonal antibody that inhibits the activation of C5 and blocks the generation of the pro-inflammatory molecule C5a and the formation of the cell membrane attack complex. In prospective studies in patients with aHUS, the use of Eculizumab has shown a fast and sustained interruption of the TMA process and it has been associated with significative long-term improvements in renal function, the interruption of plasma therapy and important reductions in the need of dialysis. According to the existing literature and the accumulated clinical experience, the Spanish aHUS Group published a consensus document with recommendations for the treatment of aHUs (Nefrologia 2013;33[1]:27-45). In the current online version of this document, we update the aetiological classification of TMAs, the pathophysiology of aHUS, its differential diagnosis and its therapeutic management., (Copyright © 2015 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

We aimed to investigate the role of cathepsin D, an inflammatory and atherosclerotic mediator, in endothelial dysfunction in chronic kidney disease. The study included 65 patients with stage 2&ndash;4 chronic kidney disease (35 females, 30 males; mean age, 55.8&plusmn;15.6 years). Serum creatinine and cathepsin D levels and glomerular filtration rates (GFRs) were determined, and brachial flow-mediated dilation (FMD) percentage was measured by two-dimensional gray scale and color flow Doppler and vascular imaging. FMD &le;6% was considered to indicate endothelial dysfunction. Mean GFR, median creatinine levels, and median cathepsin D levels were 40.2&plusmn;11.2mL/min/1.73m2, 1.7mg/dL, and 819.75ng/mL, respectively. Endothelial dysfunction was present in 30 of the 65 patients (46.2%). There was a significant difference between groups with and without endothelial dysfunction in terms of cathepsin D (p=0.001) and creatinine (p=0.03) levels, and negative and significant correlations were found between brachial artery FMD% and cathepsin D (r=&minus;0.359, p=0.003) and creatinine (r=&minus;0.304, p=0.014) levels. Cathepsin D, which is known to be associated with atherosclerosis, may play a role in the process of endothelial dysfunction. Further studies are essential to determine the exact function of cathepsin D in endothelial dysfunction in chronic kidney disease and to determine its value as a tool for early diagnosis and target for treatment of cardiovascular diseases in patients with chronic kidney disease.

Introduction: Endothelial dysfunction is an early event in the progression of atherosclerosis, and it appears in pathologies such as dyslipidemias. Certain pro-inflammatory enzymes are associated negatively with high-density lipoproteins (HDL) and positively with low-density lipoproteins (LDL). Calculating the atherogenic index greatly complements the study of these diseases. Lipid alterations have a high prevalence in Ecuadorian and Latin American populations. Better knowledge of which lipid alteration is the most prevalent would bring more attention to the subject, leading to early treatment. The goal of this study is to describe the complete lipid profile alterations in patients recently diagnosed with ischemic heart disease and find which of these is the most prevalent., Methods: We designed a cross-sectional, descriptive study that included patients from the Cardiology Service of the "Hospital Luis Vernaza" who presented with the first episode of ischemic heart disease between January 2012 and 2013. There were 220 patients with that diagnosis. One-hundred and thirty-one were excluded because they did not meet inclusion criteria. The final sample comprised 89 patients., Results: We found 41 (46.06%) patients with low HDL levels, 49 (55.05%) with high LDL levels, 28 (31.46%) with high triglycerides, 24 (26.96%) with high cholesterol levels, 25 (28.08%) with high VLDL levels, 26 (29.21%) had values over 5 in the Castelli index, and 32 (35.95%) had LDL/HDL values higher than 3., Discussion: It is of great importance to have a complete lipid profile from patients recently diagnosed with ischemic heart disease in order to work on secondary prevention. The most prevalent alteration found in our study was high LDL levels. The percentage of patients with low HDL was similar to other Latin American populations. More studies are needed to gain a more accurate idea of the status of the general population in this regard.

Heart failure is a complex syndrome that affects almost all organs and systems of the body. Signs and symptoms of organ dysfunction, in particular kidney dysfunction, may be accentuated or become evident for the first time during acute decompensation of heart failure. Cardiorenal syndrome has been defined as the simultaneous dysfunction of both the heart and the kidney, regardless of which of the two organs may have suffered the initial damage and regardless also of their previous functional status. Research into the mechanisms regulating the complex relationship between the two organs is prompting the search for new biomarkers to help physicians detect renal damage in subclinical stages. Hence, a preventive approach to renal dysfunction may be adopted in the clinical setting in the near future. This article provides a general overview of cardiorenal syndrome and an update of the physiopathological mechanisms involved. Special emphasis is placed on the role of visceral congestion as an emergent mechanism in this syndrome., (Copyright © 2014 Elsevier España, S.L. All rights reserved.)

Obstructive coronary artery disease is not detected in up to 14% of patients who present with acute coronary syndrome (ACS). Diagnosis of the underlying cause is usually not made and there is much controversy regarding prognosis. Those patients who develop ACS while having normal or near normal coronary arteries are more frequently young women and have fewer cardiovascular risk factors (CVRF). Its prognosis has typically been excellent. However, different results published in recent years show that these conditions are not always so benign. This might be explained by the different degrees of coronary obstruction, varied clinical presentation, biomarkers' mobilization or CVRF. It is necessary to determine the cause of ACS and stratify the risk of these patients in order to establish the appropriate treatment. This is especially relevant in those cases of coronary disease not detected by angiography, in which the absence of specific treatment can lead to poorer prognosis., (Copyright © 2012 Elsevier España, S.L. All rights reserved.)

Psoriasis and psoriatic arthritis are associated with increased risk of cardiovascular events and cardiovascular mortality. Alongside classic risk factors such as atherosclerosis, the severity of psoriatic skin disease also influences cardiovascular risk in these patients. In both cases, endothelial dysfunction and increased intima-media thickness in the carotid artery are indicators of subclinical cardiovascular disease. Active treatment of the psoriasis and management of traditional cardiovascular risk factors are essential in order to reduce cardiovascular morbidity in these patients. Clinical practice guidelines on the management of cardiovascular risk will define a new integrated approach to the care of patients with psoriasis and psoriatic arthritis., (Copyright © 2011 Elsevier España, S.L. and AEDV. All rights reserved.)

High altitude constitutes an exciting natural laboratory for medical research. While initially, the aim of high-altitude research was to understand the adaptation of the organism to hypoxia and find treatments for altitude-related diseases, over the past decade or so, the scope of this research has broadened considerably. Two important observations led to the foundation for the broadening of the scientific scope of high-altitude research. First, high-altitude pulmonary edema (HAPE) represents a unique model which allows studying fundamental mechanisms of pulmonary hypertension and lung edema in humans. Secondly, the ambient hypoxia associated with high-altitude exposure facilitates the detection of pulmonary and systemic vascular dysfunction at an early stage. Here, we review studies that, by capitalizing on these observations, have led to the description of novel mechanisms underpinning lung edema and pulmonary hypertension and to the first direct demonstration of fetal programming of vascular dysfunction in humans.

Background: Obesity derived from intra-abdominal fat deposition tends to increase hormonal and cytokine production, thus worsening insulin sensitivity and leading to endothelial dysfunction. Hyperinsulinemia is considered an independent risk factor for ischemic heart disease and cause of endothelial dysfunction in healthy individuals., Objective: To assess the impact of different degrees of insulin resistance, measured by HOMA-IR (Homeostasis Model Assessment of Insulin Resistance), on endothelial function in obese, non-diabetic patients without prior history of cardiovascular events and different metabolic syndrome components., Methods: Forty obese individuals were submitted to anthropometric measurements, BP measurements at office and ABPM and laboratory tests, in addition to non-invasive ultrasound assessment of endothelial function. Patients were divided into 3 groups according to the level of insulin resistance: patients with HOMA-IR values from 0.590 to 1.082 were assigned to Group 1 (n=13), from 1.083 to 1.410 to Group 2 (n=14) and from 1.610 to 2.510 to Group 3 (n=13)., Results: We found a significant difference in flow-mediated dilation in group 3 compared to group 1 (9.2 ± 7.0 vs 18.0 ± 7.5 %, p=0.006). There was a negative correlation between endothelial function and insulin, HOMA-IR and triglycerides., Conclusion: Our data suggest that mild changes in insulin resistance levels assessed by HOMA-IR may have an impact on vasodilatatory endothelial function in uncomplicated obese individuals with different cardiovascular risk factors.

Objective: To assess the effect of postprandial lipemia on endothelial function, insulin resistance, and lipid profile in healthy subjects., Patients and Methods: A prospective', interventional study in 14 healthy young men aged 18-25 years who were given a high-fat meal. Endothelial function was measured using flow-mediated dilation (FMD) in the brachial artery, flow velocity, mean arterial pressure and serum nitrite/nitrate levels (NO(2)/NO(3)). Glucose, insulin, total cholesterol, and triglyceride levels were also tested. Insulin resistance was determined by calculating the HOMA-IR index (Homeostatic Model Assessment-Insulin Resistance)., Results: Baseline FMD was 5.9 ± 1.1%. Postprandial lipemia reduced endothelial function by approximately 50% in the first (3.3 ± 0.5%, p=0.03) and second (3.3 ± 0.4%, p=0.04) moment respectively. This finding was associated to an increased flow rate in the brachial artery and lower NO(2)/NO(3) levels (p<0.05). Higher cholesterol and triglyceride levels were found 1h and 2h postprandial (p<0.05). HOMA-IR was significantly increased 1h and 2h postprandial (p<0.05)., Conclusions: Postprandial lipemia causes changes in circulating lipid profile and induces endothelial dysfunction and higher insulin resistance., (Copyright © 2011 SEEN. Published by Elsevier Espana. All rights reserved.)

Brachial artery flow mediated dilation (FMD) is a validated, noninvasive physiological measure widely used as a research tool to quantify endothelial function. FMD is diminished in patients with several coronary risk factors, coronary artery disease, peripheral arterial disease, stroke, and is an independent predictor of cardiovascular events. FMD represents a useful method for identify asymptomatic atherosclerotic subjects with raised risk of developing atherothrombotic complications and improves with risk-reduction therapy such as antihypertensive or antidiabetic drugs, antiplatelet agents and statins. FMD could be a great usefulness in ischemic stroke such as stroke subtypes classification, prognostic significance in acute phase, and independent predictor for new-onset vascular event after first-ever stroke, but also in other disease such as cerebral haemorrhage, migraine or syncope. In this review article, brachial artery FMD and its role in experimental and clinical practice is extensively discussed.

Systemic diseases affect skeletal muscle, and inflammation and oxidative stress are some of the involved mechanisms. There is scarce information about the effects of essential hypertension on skeletal muscle. The soleus and extensor digitorum longus (EDL) muscles of spontaneously hypertensive rats (SHR) were studied compared to control Wistar Kyoto (WKY) rats. The levels of nitrite and nitrate in micromol/mg-protein; endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) nitric oxide synthases, nitrotyrosine and tumour necrosis factor alpha (TNF-alpha) in ng/mg-protein were determined. Compared with controls, the SHR showed increased levels of nitrotyrosine (soleus 24.4 +/- 5.0 vs. 3.3 +/- 0.3, p<0.001; EDL 20.2 +/- 4.3 vs. 4.5 +/- 0.4, p<0.0037), iNOS (soleus 26.6 +/- 3.7 vs. 8.3 +/- 0.9; EDL 21.3 +/- 3.7 vs. 11.0 +/- 0.8, both p<0.0001) and TNF-alpha (soleus 2.2 +/- 0.5 vs. 0.6 +/- 0.1, p<0.05; EDL 1.9 +/- 0.2 vs. 0.6 +/- 0.1, p<0.02). A decrease of eNOS was found in soleus muscle (20.6 +/- 1.4 vs. 30.3 +/- 1.2, p<0.00001); of nNOS (soleus 16.8 +/- 1.4 vs. 20.7 +/- 1.8, p< 0.05; EDL 13.6 +/- 1.3 vs. 21.9 +/- 1.8, p<.005) and nitrite in EDL (5.8 +/- 0.3 vs. 7.1 +/- 0.5, p<0.026).There was a positive correlation between TNF-alpha vs. nitrotyrosine in soleus (r=0.798; p<0.031) and a tendency in EDL (r=0.739; p=0.059); iNOS vs. nitrotyrosine (soleus: r=0.908; p<0.0001; EDL: r=0.707; p<0.01), a tendency between TNF-alpha and iNOS (EDL: r=0.736; p<0.059); and a negative correlation between eNOS vs. nitrotyrosine in soleus muscle (r=-0.816; p<0.0012). In conclusion, in skeletal muscles of SHR an inflammatory process was found evidenced by the increase in TNF-alpha, nitrotyrosine and iNOS. The decreased levels of constitutive synthases, together with the higher level of iNOS, are indicative of endothelial dysfunction.

Background: Mechanisms underlying vascular abnormalities in obesity remain to be completely clarified., Objective: L-arginine/nitric oxide pathway was evaluated on vascular response of high-fat diet-obese rats, focusing on endothelial and smooth muscle cells., Methods: 30-day-old rats were divided in two groups: control (C) and obese (OB, high-fat diet for 30 weeks). After 30 weeks, body weight, adiposity index, blood pressure, and metabolic and endocrine profiles of the animals were recorded. Curves to noradrenaline were obtained in absence and presence of nitric oxide synthase inhibitor (L-NAME, 3x10-4M) on intact and denuded thoracic aorta from C and OB rats., Results: Body weight, adiposity index, leptin and insulin levels were increased in OB, while blood pressure was unchanged. Obesity also produced glucose tolerance and insulin resistance. Reactivity to noradrenaline of intact aorta was similar in C and OB rats. L-NAME presence produced a similar increase in maximal responses, but a higher leftward shift of noradrenaline responses in intact aorta from C than in OB rats [EC50 (x10-7M): C = 1.84 (0.83-4.07), O = 2.49 (1.41-4.38); L-NAME presence C = 0.02 (0.01-0.04)*, O = 0.21 (0.11-0.40)**p < 0.05 vs respective control, p < 0.05 vs control plus L-NAME, n = 6-7]. None of the protocols altered the reactivity to noradrenaline of denuded aortas., Conclusion: High-fat diet-induced obesity promotes metabolic and vascular alterations. The vascular alteration involved an endothelial L-arginine/NO pathway improvement was probably correlated to diet-induced hyperinsulinemia and hyperleptinemia. The greater resistance to L-NAME effects in aorta of obese rats raises concerns about the lower cardiovascular vulnerability of obese individuals in the presence of associated pathologies that impair NO-system activity.

Proteinuria is common following kidney transplantation and affects more than 40% of kidney transplant patients per year. In general, the level of proteinuria is low (<500 mg/day) but even those levels significantly reduce graft and patient survival. This is why it is of vital importance to detect proteinuria quickly following transplantation and to investigate its cause. During the same year of the transplant, proteinuria may be caused by multiple factors, including glomerular disease, effects of anti-HLA class II antibodies and drugs such as mTOR inhibitors, tubulointerstitial disease of the graft, and significant functional discrepancy between the graft and the recipient. The relationship between proteinuria and graft survival is likely to be due to the factors that cause proteinuria. It is unknown why proteinuria and patient survival are related, but it could be due to a relationship between proteinuria and traditional cardiovascular risk factors or a relationship between proteinuria, endothelial function and inflammation. To treat proteinuria, three aspects should be considered: the cause of proteinuria, the non-specific reduction of proteinuria, and the reduction of the cardiovascular risk.

Nitric oxide (NO), primarily identified as an endothelium-derived relaxing factor, is a free radical that signals different biological processes. The identification of NO synthase (NOS) isoforms and the subsequent characterization of the mechanisms of cell activation of the enzymes permitted the partial understanding of both the physiological interactions and of the mechanisms of the diseases in which NO is involved. Mainly expressed in the vascular endothelium, the endothelial NOS isoform (eNOS) plays an important role in the regulation of vascular reactivity and in the development and progression of atherosclerosis. The purpose of this review is to contextualize the reader about the eNOS structure and its mechanisms of cell activation. In view of the advances in molecular biology, we will also address the known mechanisms of gene expression regulation and the role of variants on the genetic code of eNOS associated with cardiovascular phenotypes. Although the importance of NO as an atheroprotective molecule is recognized, our focus will be the review of the literature on NO and its participation in the modulation of the muscle vasodilatation phenotype.

The role of the endothelium was considered mainly as a selective barrier for the diffusion of macromolecules from the lumen of blood vessels to the interstitial space. During the last 20 years, many other functions have been defined for the endothelium, such as the regulation of the vagal tonus, the promotion and inhibition of neovascular growth and the modulation of inflammation, of platelet aggregation and coagulation. This finding is considered one of the most important concepts in modern vascular biology. Currently, atherosclerosis is the prototype of the disease characterized in all its phases by an endothelial dysfunction, defined as an insufficient offer of nitric oxide (NO), which predisposes the endothelium to oxidative stress, inflammation, erosion and vasoconstriction. In this sense, several experimental studies have demonstrated that physical exercise is capable of restoring and improving the endothelial function. The impact of exercise on the endothelium has been broadly discussed. Considering its vasodilating effect and the risk factors, the possibility of treating coronary artery disease and its outcomes without the inclusion of physical exercise became unconceivable. However, the literature is still controversial regarding the intensity of physical effort that is necessary to cause significant protective alterations in endothelial functions. Moreover, the association between intense physical exercises and increased oxygen consumption, with a consequent increase in free radical formation, is also discussed.

Background: The presence of thrombosis in preeclampsia suggests that endothelial function could play an important role in its pathogenesis., Objective: Determine the association between markers of genetic thrombophilia, endothelial activation and preeclampsia., Material and Method: Prospective study of cases and controls to determine the factor V Leiden existence, protrombin G20210A, methylenetetrahydrofolate reductase C677T, activated protein C resistance and levels of von Willebrand factor and the sFlt1 receptor were determined in 28 women with preeclampsia and 41 pregnant controls., Results: Methylenetetrahydrofolate reductase C677T had a high allelic frequency (0.50). Even in the absence of factor V Leiden, there were significant differences in the prevalence of activated protein C resistance and abnormal levels of sFlt1 between patients with preeclampsia homozygous for methylenetetrahydrofolate reductase C677T and controls (72 vs. 10%, p <0.008 and 63.6 vs. 10%, p < 0.05, respectively). Patients with two or more abnormal tests, including homozygousity for the C677T allele had an increased risk of preeclampsia than those with one or no abnormal test (OR: 3.15; CI: 1.1-9.02)., Conclusion: Methylenetetrahydrofolate reductase C677T has a high allelic prevalence and is associated with markers of thrombosis and endothelial activation in Mexican women with preeclampsia.

Background: The preeclampsia syndrome is associated with endothelial dysfunction and the differential diagnosis between pure preeclampsia (PE) and superimposed preeclampsia (SPE) can be only be attained 12 weeks after delivery., Objective: To compare the assessment of endothelial function through flow-mediated dilatation in pregnant women with pure preeclampsia and superimposed preeclampsia., Methods: The flow-mediated dilatation of the brachial artery was carried out according to the recommendations of the International Brachial Artery Reactivity Task Force in pregnant women with preeclampsia syndrome. PE (n=14) and SPE (n=13) were diagnosed in the postpartum period according to the definitions of the National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy., Results: The median of the flow-mediated dilatation (FMD) in SPE (6.0%; 1.9-10.3) was decreased in comparison with the PE (13.6%;4.4-17.1), an apparently relevant difference , but not statistically significant (p = 0.08). The FMD < 10% was detected in 30.8% of the PE cases and in 69.2% of the SPE cases (p = 0.057). Significant differences could not be detected in the morphology of the uterine arteries between the PE and SPE cases through the Doppler spectrum., Conclusion: The FMD of the brachial artery of patients with preeclampsia syndrome was not capable of differentiating between PE and SPE. However, the data suggest that SPE is associated with worse endothelial function I comparison to PE.

Obesity is becoming a global epidemic. Around 1.1 billion adults and 10% of the world's children are currently overweight or considered obese. Generally associated with risk factors for cardiovascular disease, such as Diabetes Mellitus and systemic arterial high blood pressure, the obesity has been more and more seen as an independent risk factor for Coronary Artery Disease (CAD). Coronary arteriosclerosis comprises a series of inflammatory responses at cellular and molecular level, whose reactions are stronger in obese patients. In the past, the adipose tissue was regarded as a mere fat deposition. Now it is seen from a totally different standpoint, as an active endocrine and paracrine organ that produces several inflammatory cytokines, such as the adipokines. This article aims to raise awareness about obesity as an increasingly significant public health issue over the past decades, as well as to relate the intense inflammatory process in obese individuals with an increased tendency for this group of individuals to develop CAD.

The endothelium plays an important role in the regulation of the intracellular fluid, vascular permeability, and modulation of vascular focal tone and angiogenesis. Endothelial dysfunction is manifested by the loss of the endothelium ability to modulate physiology changes in its vascular bed, and actually it is considered a prognostic marker of coronary artery disease. The relevance of assessing endothelial dysfunction relies in that it has been observed in different pathologies like DM, dyslipidemia, hypertension, tabaquism and in immunologic diseases like antiphospholipid syndrome and systemic lupus. PET is a non invasive method that allows the absolute quantification of myocardial blood flow during rest, stress and adrenergic stimulation, which allows to asses endothelial function. Therefore PET is a useful diagnostic technique to identify patients with endothelial dysfunction, and in the assessment of its response to administered therapy, allowing an optimal control and prevention of secondary adverse events of these diseases.

COPD is currently the fourth cause of death in our country; the main causal agent of the disease is tobacco whose effects on the bronchial tree are not limited to the lung parenchyma. The action of tobacco injures the endothelial wall, which could contribute to lung thrombosis, ischemic events or secondary pulmonary hypertension. Our work investigates the existence of a prothombotic state in these patients, characterized by the activation of clotting and endothelial injury, comparing the values of biochemical markers between COPD patients and healthy volunteers. Fifty-one patients with COPD and a group of 30 healthy volunteers of similar ages were selected and fibrinogen, D-dimer, factor VIII and von Willebrand factor (FvW:Ag and FvW:Rico) levels were compared. We found an increase of all markers in the patient group compared to the healthy control group. The differences found were statistically significant in all cases (p<0.05). COPD is characterized by a state of hypercoagulability and endothelial injury that they could contribute to the development of vascular complications such as lung thrombosis, ischemic events or secondary pulmonary hypertension.

A subclinical inflammation state was detected in the early step of diabetes, which increases the serum levels of cytokines that induce acute-phase protein synthesis as C-reactive protein (PCR) and fibrinogen (Fg), stimulating the endothelial disfunction of adhesion molecules. Thirty patients (15 boys, 15 girls) with type 1 diabetes (DT1), without vascular complications, were studied. Their mean age and duration of diabetes were 11.8 +/- 2.1 and 3.9 +/- 3.2 years, respectively. The laboratory parameters evaluated were: blood leukocytes count, globular sedimentation velocity, fasting glycemia, glycosylated hemoglobin (HbA1c), high sensitivity PCR (uPCR), plasma soluble E-selectin (sE-S), sVCAM-1 and microalbuminuria. Increased levels of uPCR, sE-S and VCAM-1 were found, compared with the control group control [0.60 (0.30-1.25) vs. 0.20 (0.20-0.65) mg/l, p = 0.013], [108 (60-150) vs. 68 (56-82) ng/ml, p = 0.0031] y [750 (708-826) vs. 721 (674-751) ng/ml, p = 0.039] respectively. When diabetic patients were grouped according to duration of disease (3 and > de 3 years), uPCR values were higher in the second group. uPCR levels were better correlated with sE-S (r = 0.44, p = 0.03) and VCAM-1 (r = 0.49, p = 0.02). These results suggest the presence of pro-inflammatory and endothelial activation states, which are strongly associated with DT1.

Background: A great number of HIV-infected patients using antiretroviral drugs develop endothelial dysfunction and atherothrombosis, which lead to a high medical and social burden. Thus, it is important to identify pathophysiological mechanisms involved with the endothelial function in these patients, so that early intervention can be made to avoid disease progression., Objective: To evaluate endothelial function using endothelium-dependent and independent vasodilation in HIV-positive patients and in a control group., Methods: A total of 27 HIV-positive patients and 16 controls were evaluated. Endothelium-dependent (reactive hyperemia) and independent (SL nitroglycerine) vasodilation of the brachial artery was used to evaluate the endothelial function., Results: HIV-positive patients receiving protease inhibitors (PI) showed significantly lower endothelium-independent vasodilation than the HIV-negative (p=0.020) and HIV-positive without PI (p=0.034) subgroups. The change in brachial artery diameter during active hyperemia was not statistically significant in any subgroup. Multiple linear regression analysis showed that only PI was associated with the relative delta of brachial reactivity to vasodilator in HIV-positive patients at 60s and 90s., Conclusion: HIV-positive patients receiving PI presented endothelium-independent dysfunction when compared to HIV-positive patients not receiving PI and to the control group.

Unlabelled: The purpose of this study was to determine the effect of treatment, with Metformin alone or with the combination of Glimepiride/Metformin, on coronary endothelial function in asymptomatic patients with recently diagnosed type 2 diabetes mellitus (DM) Methods: 16 asymptomatic patients with type DM2 and 15 healthy controls (HC) were studied. At baseline and after treatment, myocardial blood flow (MBF) was measured with 13N-ammonia Possitron Emission Tomography (PET) at rest, during cold pressor testing (CPT) and during pharmacologic stress with adenosine. The endothelial dependent vasodilation index (EDVI), myocardial flow reserve (MFR) and the percentage of the change between rest MBF and CPT MBF (%deltaMBF) were calculated as markers of endothelial function. MBF was normalized to the rate pressure product (RPP)., Results: EDVI and %deltaMBF were significantly lower in diabetic patients before treatment in comparison with HC demonstrating endothelial dysfunction in the former. Treatment with Glimepiride/Metformin significantly increased EDVI and %deltaMBF in diabetic patients from baseline, thus showing an improvement in coronary endothelial function.

HIV-infected patients share traditional cardiovascular risk factors with the general population. Moreover, HIV per se significantly increases the risk of cardiovascular disease. Consequently, control of HIV infection with highly-active antiretroviral therapy (HAART) helps to reduce vascular risk in HIV-infected patients. However, there is evidence that HAART increases cardiovascular risk and the use of abacavir, didanosine, lopinavir/ritonavir and indinavir has been associated with the development of acute myocardial infarction (AMI). However, the absolute risk of AMI in patients receiving HAART is very low in relation to the benefit obtained with antiretroviral therapy., (Copyright 2009 Elsevier España S.L. All rights reserved.)

Patients with HIV have an increased risk of cardiovascular events related to arteriosclerosis. The virus is able to replicate in the arterial wall, implying severe inflammatory dysfunction. When this inflammatory dysfunction is accompanied by the metabolic disorders associated with HIV infection and its treatment, progression of the atheroma plaque is accelerated. HIV shows high replication in CD4+ T lymphocytes, which accumulate in the subendothelial space. CD4+ T lymphocytes produce viral proteins such as Tat, which leads to synthesis of chemokines such as monocyte chemoattractant protein-1 (MCP-1) or vascular cell adhesion molecule-1. This combination will attract monocytes into the subendothelial space, which penetrate rapidly if infected. These monocytes will also infect the smooth muscle cells, producing the initiation of endothelial dysfunction. Dyslipidemia and insulin resistance will then provoke modification of lipoproteins, which will be phagocytized through CD36 receptors by macrophages of the subendothelial space. Reverse cholesterol transport will be damaged, since the Nef viral protein is able to block the ABCA1 receptor. These events will produce rapid cholesterol accumulation in the atheroma plaque nucleus. Subsequently, the plaque will become complicated, either by rupture or erosion. Then, a juxtalesional thrombus is formed, where the platelet is activated., (Copyright 2009 Elsevier España S.L. All rights reserved.)

Evidence from experimental and observational studies suggests that HIV infection per se and the associated proinflammatory state can increase the risk of cardiovascular disease. HIV infection can activate several inflammatory pathways in the vascular wall with cytokine release and expression of endothelial adhesion molecules. Many of these alterations can be suppressed by highly-active antiretroviral therapy (HAART). The role of HIV in cardiovascular risk has been demonstrated in studies of treatment interruption, mainly in the SMART trial, in which greater cardiovascular mortality was observed in the group interrupting HAART. The abrupt change to a more proinflammatory state produced by sudden resumption of viral replication could induce an increase in platelet adhesion and migration of inflammatory cells with plaque instability. Some studies suggest that HIV can also produce endothelial damage; a decrease in markers of endothelial activation and improvement of endothelial function after initiation of HAART have been described, and these changes have been correlated with the decrease in HIV viral load. Finally, HIV can induce cardiovascular disease through its effect on high-density lipoprotein cholesterol, which can decrease in patients with uncontrolled infection. Although the association of HIV with cardiovascular risk is controversial, coinfection with hepatitis C infection has been associated with a higher frequency of insulin resistance and acute myocardial infarction in some cohorts., (Copyright 2009 Elsevier España S.L. All rights reserved.)

Introduction and Objectives: Both endothelial dysfunction and a proinflammatory state are present during the early stages of atherosclerosis. In this context, increased expression of cyclooxygenase-2 (COX-2) results in higher levels of vasoconstrictive and proinflammatory substances. The aim of this study was to investigate the influence of COX-2 activity on endothelial dysfunction associated with peripheral arterial disease (PAD)., Methods: Brachial artery flow-mediated dilatation (BAFMD), endothelin and high-sensitivity C-reactive protein (hsCRP) levels, and the lipid profile were assessed in 40 patients with intermittent claudication. Of these, 20 were randomly assigned to a group in which they received the selective COX-2 inhibitor celecoxib for 1 week (Group 1), while the other 20 served as controls (Group 2)., Results: In Group 1, BAFMD increased significantly both 3 hours after the first dose of celecoxib (3.33+/-4.11 vs. 6.97+/-3.27%; P=.008) and 1 week after (3.33+/-4.11 vs. 7.09+/-4.40%; P=.001). The endothelin level decreased significantly in Group 1 (2.92+/-1.87 vs. 1.93+/-1.07 pg/ ml; P=.018), as did the levels of hsCRP (4.78+/-2.73 vs. 2.95+/-2.11 mg/l; P=.023) and low-density lipoprotein cholesterol (106.38+/-18.89 vs. 90.8+/-28.58 mg/dl; P=.019). In Group 2, none of these parameters changed significantly., Conclusions: COX-2 products contribute to endothelial dysfunction and an inflammatory state in PAD. This study's findings provide evidence that these phenomena are implicated in the initiation of atherosclerosis and could prove a new means of investigating alternative approaches to the treatment of early-stage disease.

HIV-associated hypogonadism is known to be a prevalent endocrine disorder, with a multifactorial etiology. Low testosterone levels are associated with decreased muscle mass, exercise capacity loss, erectile dysfunction, cognitive impairment, depression and decreased quality of life. In the same way, hypogonadism in HIV-infected men is associated with decreased muscle mass quantity and function, changes in corporal fat mass distribution and quantity, secretion of adipocytokines and endothelial dysfunction. This combined effect renders the entire body less sensitive to insulin, promoting development of atherosclerosis and glucose metabolism disorders. The clinical presentation is non-specific and hypogonadism screening scales are not useful in this population. Diagnostic procedures must include determination of free testosterone (FTc) in any HIV-infected men at the time of first HIV diagnosis and periodically, because of the clinical implications and the absence of specific predictive disease factors. Substitutive hormonal treatment must be offered only for HIV-infected men with FTc under reference levels and when reversible causes have been ruled out. Metabolic impact of hypogonadism suggests the incorporation of low testosterone levels to the list of cardiovascular risk factor in HIV-infected men.

Atherosclerosis is an inflammatory disease of the arterial wall, where both cellular and humoral immunity mechanisms are involved. Vascular endothelial dysfunction and lipoproteins retention into the arterial intima have been reported as the earliest events in atherogenesis, promoting cytokines and chemokines releases; both responsible of leukocytes recruitment. Arterial proteoglycans retain and modify the lipoproteins, increasing their phagocytosis into macrophages through class A and class B scavenger receptors in the case of oxidized lipoproteins (LDLox), causing the production of cytokines like Tumoral Necrosis Factor (TNF)- alpha, Interleukin (IL)-1 beta, IL-6, IL-12 and IL-18, among others. This secretion generates T cells activation into T helper lymphocytes (Th1), able to recognize the LDLox and heat shock protein as autoantigens, amplifying the inflammatory response. Macrophages that have uptaken lipoproteins become foam cells and their accumulation produces the formation of fatty streaks, the first step into atherosclerosis. Due to the biological and clinical importance of these events, the purpose of the present review is to offer recent information on the inflammatory reactions that occur around the establishment of the atheromatous plaque, exhibiting experimental evidences of the physiologic role of leukocytes and their interaction with the extracellular matrix. Furthermore, to emphasize about the major inflammatory biomarkers on the prognosis of cardiovascular diseases.

Ageing is an important risk factor for many cardiovascular diseases with a common underlying circumstance: the progressive decline of endothelial function. This work summarizes the mechanisms involved in such dysfunction focusing our attention in the vasoactive substances released by the endothelium. The decrease of nitric oxide contribution, the enhancement of vasoconstrictor prostanoids and the modification of the action of either the endothelium-derived hyperpolarizing factor or the vasoconstrictor peptide endothelin are some of the manifestations that appear as the consequence of ageing in endothelial cells. The increase in oxidative stress, the higher production of reactive oxygen species and the proinflammatory phenotype of the vascular wall contribute to explain these facts. The role played by the senescence of endothelial cells and their progenitors is also revised.