New insights by optical coherence tomography into the differences and similarities of culprit ruptured plaque morphology in non-ST-elevation myocardial infarction and ST-elevation myocardial infarction.

BACKGROUND: Plaque rupture is the most common pathology associated with non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI). However, limited data are available regarding ruptured plaque morphology and its relationship with the clinical syndrome. This study aimed (1) to provide a morphologic description of ruptured culprit lesions by optical coherence tomography (OCT) and (2) to investigate whether ruptured plaque morphology differs between NSTEMI and STEMI. METHODS: We included 84 consecutive patients with NSTEMI and STEMI undergoing OCT study of the culprit lesion. We identified patients with plaque rupture in the OCT study and used them as the study population. Qualitative and quantitative analysis of ruptured plaque morphology was then performed, followed by a comparison of the morphological characteristics in patients with STEMI and NSTEMI. RESULTS: Fifty-five patients (70.5%) with rupture, 25 with NSTEMI, and 30 with STEMI were used for analysis. Plaque was ruptured at the minimal lumen in 34.5% of the cases, whereas 69% of the ruptures occurred at the plaque shoulder. Ruptured cap thickness was ≤90 µm in 96% of ruptured plaques. Patients with NSTEMI had greater minimal luminal area (P < .001), less lipid content (P = .01), and lower rupture length (P < .001) and length of missing fibrous cap (P < .05) compared with patients with STEMI. CONCLUSIONS: Rupture of the plaque in myocardial infarction usually occurs in sites different than the minimal lumen and at the shoulder of areas with fibrous cap measuring ≤90 µm. Patients with STEMI have greater plaque disruption and smaller minimal lumen area than patients with NSTEMI.

The impact of new generation drug-eluting stent implantation on patients with chronic kidney disease and a single lesion in the proximal segment of the left anterior descending artery.

INTRODUCTION: The impact of drug-eluting stents (DES) has not been extensively investigated in patients with moderate to severe renal dysfunction, as these patients are consistently excluded from randomised studies. We sought to assess prospectively the effectiveness and safety of the new-generation DES in patients with moderate chronic kidney disease (CKD) and an isolated de novo lesion in the proximal segment of the left anterior descending artery (pLAD). METHODS: We evaluated 400 consecutive patients with a pLAD lesion. There were 96 patients with moderate CKD (estimated glomerular filtration rate 59 ml/min/1.73 m2) and 304 without CKD. Major adverse cardiac events (MACE) were defined as death, non-fatal myocardial infarction and target lesion revascularisation (TLR). Clinical or telephone follow up was performed. RESULTS: There was a significantly higher incidence of mortality in patients with CKD (n=4) as compared with non-CKD (n=2) (4.16% versus 0.65%, respectively, p=0.03). The rate of non-fatal myocardial infarction was similar in the 2 cohorts (p=0.59), as was the TLR rate (p=0.99). Overall, there were no significant differences regarding MACE between the 2 groups of patients (p=0.19) during the 13.62 ± 6.22 month follow-up period. The rate of angiographic stent thrombosis was 2.08% in the CKD group versus 0.98% in the non-CKD group (p=0.59). CONCLUSIONS: New generation DES implantation in patients with CKD and a pLAD lesion is effective and safe, with rates of TLR and stent thrombosis comparable to those in patients with normal renal function. However, the higher mortality in patients with CKD needs further evaluation.

Methionine-induced homocysteinemia impairs endothelial function in hypertensives: the role of asymmetrical dimethylarginine and antioxidant vitamins.

BACKGROUND: Nitric oxide synthase (NOS) inhibitor asymmetrical dimethylarginine (ADMA) is synthesized by the methylation of arginine as part of the methionine/homocysteine cycle. However, the mechanisms regulating ADMA synthesis in hypertension are unclear. METHODS: We investigated the role of ADMA and antioxidants in endothelial dysfunction during methionine-induced homocysteinemia in hypertensives. Thirty-nine hypertensives and forty-nine normotensive controls underwent methionine loading (100 mg methionine/kg BW), after being randomized to receive vitamin C (2 g) and E (800 IU) or placebo. Endothelium-dependent dilation (EDD) was evaluated by plethysmography (baseline and 4-h post-methionine loading (4-h PML)). RESULTS: Hypertensives had higher homocysteine at baseline (P < 0.001) and 4-h PML (P < 0.05), whereas methionine increased homocysteine in all groups. EDD was decreased in both vitamins and placebo groups in controls (P < 0.01 for both) and vitamins- and placebo-treated hypertensives (P < 0.05 and P < 0.01, respectively). In controls, ADMA was increased in both vitamin- and placebo groups (P < 0.01 for both) at 4-h PML. Hypertensives had higher ADMA at baseline (P < 0.01 vs. normotensive) and remained unchanged at 4-h PML (P = NS in placebo and vitamins treated). CONCLUSIONS: ADMA is elevated in hypertensives but remains unchanged after methionine loading, suggesting that ADMA plays an important role in endothelial dysfunction in hypertensives, but it is not responsible for homocysteine-induced endothelial dysfunction in these patients.

The dominant role of the systolic component of nondipping status on target-organ damage in never-treated hypertensives.

BACKGROUND: Blood pressure (BP) nondipping has been associated with target-organ damage (TOD) and adverse outcomes in hypertension. Diverse definitions of nondipping status appear in the literature, regarding the BP components taken into account. Aim of this study was to compare the effects of isolated nondipping of systolic, diastolic and combined systolic and diastolic BP on various indices of TOD. METHODS: From 630 consecutive subjects with never-treated essential hypertension stage I-II, we selected 279 subjects who were consistently isolated systolic nondippers (SND, n=76) isolated diastolic nondippers (DND, n=64) and combined systolic and diastolic nondippers (SDND, n=139) in two ambulatory BP monitoring sessions. All three subgroups were subjected to echocardiographic examination, carotid-femoral pulse wave velocity (PWV(c-f)) and albumin-to-creatinine ratio (ACR) determination. Metabolic profile was determined in a morning blood sample. RESULTS: SND compared to DND and SDND exhibited higher left ventricular mass/height(2.7) (42.4 ± 9.9 vs. 38.0 ± 9.1 vs. 40.9 ± 11.0 g/m(2.7), P < 0.05), higher log(10)(PWV(c-f)) (0.94 ± 0.07 vs. 0.86 ± 0.05 vs. 0.91 ± 0.07 m/s, P < 0.005), and higher log(10)(ACR) (1.2 ± 0.5 vs. 0.9 ± 0.3 vs. 1.1 ± 0.4 mg/g, P < 0.05). Isolated systolic BP nondipping was an independent determinant of all the studied indices of TOD whereas isolated diastolic BP nondipping was not. CONCLUSIONS: Isolated systolic as compared to diastolic and to combined systolic/diastolic BP nondipping is associated with higher left ventricular mass, stiffer arteries, and pronounced urinary albumin excretion.

Combined effects of atorvastatin and metformin on glucose-induced variations of inflammatory process in patients with diabetes mellitus.

BACKGROUND: Statin treatment improves survival in patients with atherosclerosis, but their effect on the glucose-induced variations of inflammatory markers, is unknown. We examined the effect of combined therapy with atorvastatin and metformin on glucose-induced variations of inflammatory molecules in patients with newly diagnosed diabetes mellitus type 2 (DM). METHODS: Thirty five subjects with newly diagnosed DM were randomized to receive metformin 850 mg/d (M, n=17) or metformin 850 mg/d+atorvastatin 10mg (n=18). All subjects underwent glucose loading (75 g oral glucose) at baseline and after 12 weeks of treatment. Blood samples were obtained at baseline and 3h post-loading, while serum tumor necrosis factor alpha (TNF-α) levels were determined at baseline and at 3h. RESULTS: Serum TNF-α remained unchanged in metformin at baseline (1.36±0.18 to 1.47±0.21 pg/ml p=NS) and after treatment (1.44±0.71 to 1.31±0.17 pg/ml, p=NS), while it was reduced in metformin+atorvastatin (2.3±0.3 to 2.0±0.4 pg/ml, p=NS at baseline and 1.80±0.2 to 1.65±0.2 pg/ml, p=0.03 after treatment). CONCLUSIONS: Interestingly, the combination of metformin and atorvastatin partly prevents the glucose-loading induced elevation of glucose levels (at 1 h), suggesting a better response to glucose intake than monotherapy with metformin. In addition, combined treatment with atorvastatin and metformin reduces the post-glucose loading levels of TNF-α compared to metformin monotherapy.

Association of resistin with urinary albumin excretion in nondiabetic patients with essential hypertension.

BACKGROUND: Evidence suggests that resistin, a recently described protein, is associated with subclinical atherosclerosis in different clinical settings. In this study, we investigated the relationship of increased resistin levels with urinary albumin excretion, expressed as the albumin-to-creatinine ratio (ACR), an established index of diffuse vascular damage, in hypertensives. METHODS: Our population consisted of 132 untreated nondiabetic subjects with stage I-II essential hypertension (49 males, mean age = 54 years, mean office blood pressure (BP) = 159/100 mm Hg). In all patients, ACR was determined as the average of three nonconsecutive morning spot urine samples, and venous blood sampling was performed for estimation of resistin concentrations. The distribution of resistin was split by the median (4.63 ng/ml), and accordingly, subjects were stratified into those with high and low values. RESULTS: Hypertensive patients with high (n = 66) compared to those with low resistin (n = 66) exhibited higher ACR values (21.8 + or - 15.3 vs. 10.3 + or - 3.8 mg/g, P < 0.01), even after adjustment for confounders. In the total population, resistin was associated with 24-h systolic BP (r = 0.244, P < 0.05), serum creatinine (r = 0.311, P = 0.007), and ACR (r = 0.499, P < 0.01). Multiple regression analysis revealed that age (b = 0.193, P = 0.02), body mass index (b = 0.237, P = 0.02), 24-h systolic BP (b = 0.338, P < 0.0001), 24-h heart rate (b = 0.169, P = 0.04), and resistin (b = 0.77, P < 0.01) were independently associated with ACR (R(2) = 0.471, P < 0.01). CONCLUSIONS: Hypertensive subjects with augmented resistin levels exhibit higher albuminuria, independently of established risk factors. Moreover, the association of resistin with ACR suggests a link between resistin and microvascular disease in the early stages of essential hypertension.

ADMA, C-reactive protein, and albuminuria in untreated essential hypertension: a cross-sectional study.

BACKGROUND: Asymmetric dimethylarginine (ADMA) and subclinical inflammation are associated with atherosclerosis progression, whereas microalbuminuria is an established index of hypertensive organ damage. STUDY DESIGN: Cross-sectional. SETTING & PARTICIPANTS: In an outpatient hypertensive unit, 296 nondiabetic and untreated participants with hypertension were studied. Participants with atherosclerotic cardiovascular disease, severe valvulopathy, congestive heart failure, presence of neoplastic or other concurrent systemic disease, atrial fibrillation, serum creatinine level > 1.5 mg/dL in men and > 1.4 mg/dL in women, and urinary albumin excretion > 300 mg/24 h were excluded. PREDICTORS: ADMA and high-sensitivity C-reactive protein (hs-CRP) levels. OUTCOME VARIABLE: Albuminuria assessed using albumin-creatinine ratio (ACR). MEASUREMENTS: Participants underwent ambulatory blood pressure monitoring, echocardiography, routine assessment of metabolic profile, ADMA, and hs-CRP, whereas ACR was determined as the mean of 3 values in nonconsecutive morning spot urine samples. RESULTS: 64 participants had an ACR of 30-300 mg/g. Stratification based on ADMA level showed that participants with hypertension in quartile [Q] 4 compared with those in Q3, Q2, and Q1 showed the highest ACRs (53.2 vs 31.2 vs 30.4 vs 16.7 mg/g; P < 0.008 for all). Moreover, stratification based on hs-CRP level showed that participants with hypertension in Q4 (69.8% had microalbuminuria) showed the highest ACRs (72.2 vs 25.6, 16.2, and 19.2 mg/g for Q3, Q2, and Q1, respectively; P < 0.008 for all). Stepwise regression analysis showed that age, 24-hour systolic blood pressure, hs-CRP level, ADMA level, and the interaction of hs-CRP with ADMA were independent predictors of ACR (R(2) = 0.674; P < 0.001). LIMITATIONS: Cross-sectional study. CONCLUSIONS: In patients with untreated essential hypertension, increased hs-CRP and ADMA levels are associated with microalbuminuria, suggesting the involvement of inflammation and endothelial dysfunction in vascular and kidney damage.

Impact of 6 weeks of treatment with low-dose metformin and atorvastatin on glucose-induced changes of endothelial function in adults with newly diagnosed type 2 diabetes mellitus: A single-blind study.

BACKGROUND: Statin treatment has been reported to improve survival in patients with atherosclerosis, partly by improving vascular endothelial function. Elevation of blood glucose concentrations impairs endothelial function and promotes atherogenesis, but the effect of statins on glucose-induced endothelial dysfunction is unknown. Endothelium-dependent dilation (EDD) measured by gauge-strain plethysmography in the forearm is considered to be a reliable marker of endothelial function in forearm resistance vessels. OBJECTIVE: This study examined the combined effects of metformin and atorvastatin treatment on glucose-induced endothelial dysfunction (as EDD) in patients with newly diagnosed type 2 diabetes mellitus (DM). METHODS: Patients with newly diagnosed DM were recruited and were randomly assigned to receive metformin 850 mg/d or metformin 850 mg/d + atorvastatin 10 mg/d for 6 weeks in a single-blind study. All patients underwent glucose loading (75 g oral glucose after 12 hours of fasting) at baseline and at the end of the treatment period. Blood samples were obtained at baseline before glucose loading and 3 hours after loading to determine serum concentrations of cholesterol, lipoproteins, triglycerides, glucose, and glycosylated hemoglobin. EDD was evaluated at baseline and at 1, 2, and 3 hours after loading. The investigators were blinded to the treatment group assignments, and all analyses were performed in a blinded manner. Adverse events (eg, gastrointestinal disorders, myopathy, liver disorders) were monitored based on reported symptoms or signs (eg, myalgias, muscle cramps), clinical examination, and laboratory parameters (eg, increased liver and muscle enzymes). RESULTS: Thirty-two white patients with newly diagnosed type 2 DM were randomly assigned to receive metformin 850 mg/d (n = 17 [12 men]; mean [SD] age, 53.88 [45] years; body mass index [BMI], 28.7 [4.5] kg/m²) or metformin 850 mg/d + atorvastatin 10 mg/d (n = 15 [6 men]; mean age, 52.53 [37] years; BMI, 28.5 [2.1] kg/m²). At baseline, EDD was reduced 1 and 2 hours after glucose loading in both study groups (P < 0.01). Glucose loading was associated with an elevation of blood glucose concentrations at 1 and 2 hours (P < 0.01 vs resting levels before loading), and concentrations returned to resting levels at 3 hours, in both groups at baseline and after treatment. Metformin alone or in combination with atorvastatin was associated with a significant reduction in resting glucose concentrations after 6 weeks (both, P < 0.05 vs baseline), but only the combination of metformin + atorvastatin partly prevented the glucose-induced elevation of serum glucose at 1 hour after loading and the glucose-induced decrease in EDD (both, P < 0.01 vs baseline). CONCLUSIONS: Glucose loading blunted endothelial function, with a deterioration in EDD, in these patients with newly diagnosed type 2 DM. However, combined treatment with metformin and atorvastatin for 6 weeks partly prevented the glucose-induced impairment of EDD in these patients, with a significant difference compared with monotherapy with metformin.

Genetic polymorphism on type 2 receptor of angiotensin II, modifies cardiovascular risk and systemic inflammation in hypertensive males.

BACKGROUND: Angiotensin type 2 receptor (AT2R), plays a crucial role in blood pressure regulation and atherogenesis. AT2R gene is located on chromosome X and the biological effect of polymorphism A1675G in this gene needs to be further specified. We examined the impact of A1675G on the risk and the severity of coronary artery disease (CAD), and the expression of proatherogenic inflammatory molecules in hypertensive patients. METHODS: The study population consisted of 146 with CAD (102 with hypertension) and 266 age-matched individuals without CAD (114 with hypertension). The presence of A1675G polymorphism on AT2R gene was determined by PCR. Serum levels of C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were measured in all the participants. RESULTS: The G allele was associated with decreased risk of CAD among hypertensives (odds ratio (OR) (95% confidence interval (CI))): 0.4 (0.2-0.9), P = 0.01) and less aggressive angiographic CAD (P < 0.001). The G allele was associated with lower IL-6 (median (25-75th percentile): 1.4 (0.6-3.8)), sVCAM-1 (621 (476-799)), CRP (1.2 (0.6-1.7)), and fibrinogen (369 (320-416)) vs. A allele (IL-6: 2.4 (1.1-4.5) P < 0.01, sVCAM-1: 702 (548-925) P < 0.05, CRP: 3.5 (2.0-6.1) P < 0.001, and fibrinogen: 407 (348-514) P < 0.01). The effect of A1675G on serum IL-6, sVCAM-1, and fibrinogen was driven by its effect among hypertensives (IL-6 3.1 (2.1-5.6 in A vs. 1.2 (0.3-3.4) in G P < 0.001, sVCAM-1: 890 (560-1000) in A vs. 556 (377-788) in G P < 0.01, and fibrinogen: 408 (354-510) in A vs. 369 (324-418) in G P < 0.001) whereas it had no effect among nonhypertensives. CONCLUSIONS: Genetic polymorphism A1675G on AT2R gene affects cardiovascular risk and the severity of atherosclerosis by modifying systemic inflammation, especially in hypertensive males.

The conjoint detrimental effect of chronic periodontal disease and systemic inflammation on asymmetric dimethyl-arginine in untreated hypertensive subjects.

OBJECTIVE: To investigate the relationship between periodontal disease indexes (PDI) and endothelial dysfunction by means of asymmetric dimethyl-arginine (ADMA) in conditions of both increased and decreased systemic inflammation in the setting of hypertension. METHODS: We studied 108 - aged 52+/-9 years - untreated hypertensive subjects (24 h systolic/diastolic blood pressure [BP] 131+/-11/83+/-9 mmHg) with diverse severity of periodontal disease (i.e. mean clinical loss of attachment, maximum probe depth and gingival index). Subjects underwent office and ambulatory BP measurements, echocardiography, periodontal examination; while from fasting venous blood samples we assessed metabolic profile, and we measured ADMA and high sensitivity C reactive protein (hsCRP) levels. RESULTS: With respect to the median of hsCRP and ADMA (1.79 mg/l and 0.81 micromol/l, respectively) the study population was divided in four groups: low-ADMA/low-hsCRP (n=30), low-ADMA/high-hsCRP (n=27), high-ADMA/low-hsCRP (n=21) and high-ADMA/high-hsCRP (n=30). High-ADMA/high-hsCRP group resulted significantly older compared with both low-ADMA/low-hsCRP and high-ADMA/high-hsCRP groups, while high compared with low-ADMA groups demonstrated increased low-density lipoprotein cholesterol. PDIs were increased in those with high compared with those with low-hsCRP, while the addition of high-ADMA contributed significantly to that comparison. After adjustment for confounders, high-ADMA/high-hsCRP was significantly associated--by means of adjusted z-scores--with mean clinical loss of attachment, maximum probe depth and gingival index by 10.33, 8.84 and 2.74 times more often with respect to the low-ADMA/low-hsCRP pattern. CONCLUSION: PDI are associated in a dose-dependent manner with ADMA in untreated hypertensives and increased systemic inflammation further contributes to that phenomenon.

Inflammatory markers in essential hypertension: potential clinical implications.

There is a growing interest focusing on the inflammatory response caused by essential hypertension. Inflammatory mechanisms play an important role in the pathogenesis and progression of cardiovascular disease. Recent studies have shown that tissue expression and plasma concentrations of several inflammatory markers and mediators are associated with increased risk of hypertension. These molecules include C-reactive protein, adhesion molecules, such as vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and chemokines. The evaluation of these markers may influence the specific pharmacologic responses and the clinical outcome of the patients with essential hypertension. Moreover, therapeutic approaches targeted to lower blood pressure and suppress inflammatory response may have additional clinical benefits. However, further randomized studies are required to determine the potential favorable effects of suppression of inflammation in the management of arterial hypertension.

Obesity and cardiovascular disease: from pathophysiology to risk stratification.

Obesity is associated with numerous co-morbidities such as cardiovascular diseases (CVD), type 2 diabetes, hypertension and others. As obesity is considered to be a major risk factor for atherosclerosis, understanding of the underlying mechanisms leading to obesity and linking obesity with atherogenesis is necessary, for the development of therapeutic strategies against atherosclerosis. The pathophysiology of CVD linked to obesity is an area of intensive research. In this review we examine the role of obesity on CVD, and we focus on specific mechanisms of major importance in atherogenesis, such as the role of adipokines, insulin resistance, endothelial function and cardiac structure with emphasis on the effects of obesity on vascular endothelium and atherosclerosis. We then proceed from the pathophysiology of obesity to clinical practice, and we discuss clinical studies linking obesity with subclinical or overt CVD. We highlight that obesity is an easily assessed cardiovascular risk factor in the clinical setting and strategies to promote optimal body weight should be encouraged.

Role of depression in heart failure--choosing the right antidepressive treatment.

Major depression is a common feature of heart failure patients and possibly stems from their common biochemical background. Depression and heart failure co-morbidity has several clinical implications on the prognosis of these patients. Furthermore antidepressive drugs have known cardiovascular side effects, while their safety and efficacy in heart failure has not been fully elucidated yet. The right choice of antidepressive treatment in heart failure constitutes an issue of high importance as it can affect the clinical outcome of these patients. In this article we highlight the role of major depression in heart failure and demonstrate their common biochemical background. Moreover we review the acquired so far knowledge on the use of the various categories of antidepressants in heart failure by reference to the existing clinical studies on antidepressants efficacy and safety in heart failure. Even though certain conclusions cannot be drawn yet, evidence suggests that the use of selective serotonin reuptake inhibitors may have a beneficial effect on clinical outcome of heart failure patients.

Rosuvastatin but not ezetimibe improves endothelial function in patients with heart failure, by mechanisms independent of lipid lowering.

INTRODUCTION: Congestive heart failure (HF) is characterised by increased proinflammatory stimulation and impaired endothelial function. Statin treatment exerts a beneficial effect on endothelial function and inflammatory process in patients with atherosclerosis. However, its effect in patients with HF is not well studied. Therefore, in the present study we compared the effect of short-term treatment with rosuvastatin or ezetimibe on endothelial function in patients with HF. METHODS: In this double-blind, placebo controlled, cross-over trial, 22 patients with HF were randomised to receive ezetimibe 20 mg/d or rosuvastatin 10 mg/d for 4 weeks, with 4 weeks wash-out period between the two interventions. Endothelial function was evaluated by flow mediated dilation (FMD) in the brachial artery at the beginning and at the end of each treatment period. RESULTS: There was no change in the baseline brachial diameter after treatment with either ezetimibe (p=NS) or rosuvastatin (p=NS). However, there was a significant improvement of FMD in the rosuvastatin group (p<0.05) but not in the ezetimibe group (p=NS). The changes in lipid levels were similar between groups (p=NS). The change in FMD was not significantly correlated with the decrease of serum LDL in either the ezetimibe or rosuvastatin treated groups. CONCLUSIONS: Rosuvastatin improves endothelial function in patients with congestive heart failure, by mechanisms independent of lipid-lowering. On the contrary, lipid-lowering treatment achieved by ezetimibe is unable to affect endothelial function in these patients. These findings indicate a direct beneficial effect of statins in patients with congestive heart failure, further to lipid-lowering.

Acute effects of different types of oil consumption on endothelial function, oxidative stress status and vascular inflammation in healthy volunteers.

Consumption of different types of oil may have different effects on cardiovascular risk. The exact role of maize oil, cod liver oil, soya oil and extra virgin olive oil on endothelial function, oxidative stress and inflammation is unknown. We evaluated the effect of acute consumption of these types of oil on endothelial function, oxidative stress and inflammation in healthy adults. Thirty-seven healthy volunteers were randomised to receive an oral amount of each type of oil or water. Endothelial function was evaluated by gauge-strain plethysmography at baseline and 1, 2 and 3 h after consumption. Oxidative stress status was determined by total lipid peroxides (PEROX), while inflammatory process was estimated by measuring the soluble form of vascular adhesion molecule 1. Serum levels of the two previous markers were measured at baseline and 3 h after oil consumption. Reactive hyperaemia (RH) was significantly decreased after maize oil consumption compared with controls (P < 0.05). However, the consumption of cod liver oil and soya oil induced a significant improvement of RH after 1 h, compared with controls (P < 0.05). There was no significant effect of any type of oil consumption on endothelium-independent dilatation, total lipid PEROX and vascular adhesion molecule 1 serum levels. Consumption of maize oil leads to impaired endothelial function, while soya oil and cod liver oil slightly improve endothelial function. However, all types of oils did not affect inflammatory process and systemic oxidative stress, suggesting that their effect on endothelial function may not be mediated by free radicals bioavailability.

Leontio Lyceum ALbuminuria (3L Study) epidemiological study: aims, design and preliminary findings.

INTRODUCTION: The significance of microalbuminuria (MA) in paediatric essential hypertension has yet to be established. The Leontio Lyceum ALbuminuria Study (3L Study) was designed to determine the prevalence of MA among Greek schoolchildren and to evaluate these rates in relation to the children's anthropometric and lifestyle characteristics, and dietary habits. METHODS: During April 2009, 498 students from the Leontio Lyceum, aged 12-17 years (7th-12th grade), were asked to participate in the 3L Study. For each child a questionnaire was completed that was developed for the purposes of the study to retrieve information on socio-demographic and lifestyle characteristics, as well as dietary habits (through a semi-quantitative Food Frequency Questionnaire), and physical activity status. Overweight and obesity were defined using the international body mass index cut-off points established for children and young people. Office blood pressure (BP) was measured on two different occasions and those students who had BP >95th percentile for gender, age and height on both occasions were considered as hypertensives. Microalbuminuria was determined as albumin to creatinine ratio >or=22 mg/g in boys and >or=31 mg/g in girls in a morning spot urine sample using a quantitative assay (DCA 2000). RESULTS: The prevalence of MA was found to be 12.9% and that of childhood hypertension 5.2%. The prevalence of overweight status was 25.8% and 5.8% of the students were classified as obese. Low physical activity was reported by 7% of boys and girls, while 46.5% of the students reported participation in vigorous physical activities during a normal week. Based on the KIDMED score of each student, only 6% of them were classified as high adherers to a Mediterranean diet and 41.9% were classified as having very low diet quality. CONCLUSIONS: In this paper we present the aims, design and preliminary results of an epidemiological study on MA, hypertension, increased body size and lifestyle characteristics among Greek schoolchildren.

The role of inflammation in atrial fibrillation: a myth or a fact?

Atrial fibrillation (AF) is the most common sustained rhythm disturbance resulting in substantial morbidity and mortality as well as increased medical costs in general population. The possible association between AF and inflammation is suggested by several studies that are based on the identification of inflammatory serum biomarkers that are elevated in patients with AF. In this population, the successfulness of maintenance of sinus rhythm after cardioversion and the risk of cardioembolic stroke are related to the inflammatory burden. Furthermore, the positive effect of the antiinflammatory agents on the prevention and modulation of AF further supports this hypothesis.

Left ventricular hypertrophy versus chronic kidney disease as predictors of cardiovascular events in hypertension: a Greek 6-year-follow-up study.

OBJECTIVES: We assessed the comparative prognostic role of left ventricular hypertrophy (LVH) and chronic kidney disease (CKD) for major cardiovascular events in a prospective observational study in Greek essential hypertensive patients. METHODS: We followed up 1652 hypertensive patients (mean age 54.3 years, 696 male patients, office blood pressure 147/93 mmHg) free of cardiovascular disease for a mean period of 6 years. CKD and echocardiographically detected LVH were evaluated at baseline along with five major traditional risk factors [age > 65 years, sex, current smoking, diabetes mellitus and dyslipidemia (low density lipoprotein > 160 mg/dl)]. End points of interest were the incidence of coronary artery disease, stroke, all-cause mortality and their composite. RESULTS: At the end of follow-up, coronary artery disease was the most prevalent (5.2%), followed by stroke (5%) and total mortality (3.1%). The presence of both LVH and CKD is associated with a 2.5-fold increase in coronary artery disease (P = 0.034), four-fold in stroke (P = 0.002) and 3.2-fold in the composite (P < 0.001), whereas the presence of LVH alone was associated with a 2.5-fold higher risk for stroke (P = 0.009) and 1.7-fold for the composite (P = 0.018). By multivariate Cox regression analysis, LVH (hazard ratio = 1.53, P = 0.036) and CKD (hazard ratio = 1.66, P = 0.039) turned out to be independent prognosticators of the composite end point, whereas age more than 65 years (hazard ratio = 4.59, P < 0.001) and the presence of LVH (hazard ratio = 2.01, P = 0.043) were the only predictors of stroke. CONCLUSIONS: In hypertensive patients free of cardiovascular disease, CKD and LVH are both independent prognosticators of the composite end point of all-cause death and cardiovascular morbidity, whereas LVH but not CKD is a major predictor for stroke.

Association of inflammatory markers with angiographic severity and extent of coronary artery disease.

Inflammatory processes play a pivotal role in the pathogenesis of atherosclerosis and mediate many of the stages of atheroma development, from initial leukocyte recruitment to eventual rupture of the unstable atherosclerotic plaque. Several systemic inflammatory markers reflect different degrees of inflammation and have been indicated as independent risk factors in cardiovascular disease, especially in unstable coronary syndromes. However, whether elevated levels of circulating inflammatory markers play a role in the extent and severity of atherosclerosis remains controversial. The present review summarizes our current understanding of the relationship between inflammatory markers and the presence and extent of coronary atherosclerosis, in order to assess the potential utility of these markers in identifying patients with higher levels of atherosclerotic burden.