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Recent genome-wide association studies have identified several single nucleotide polymorphisms (SNPs) associated with glucose levels. We tested the hypothesis here whether the cumulative effect of glucose raising SNPs, assessed via a score, is associated with glucose levels. A total of 1,434 participants of Greek descent from the THISEAS study and 1,160 participants form the GOMAP study were included in this analysis. We developed a genetic risk score (GRS), based on the known glucose-raising loci, in order to investigate the cumulative effect of known glucose loci on glucose levels. In the THISEAS study, the GRS score was significantly associated with increased glucose levels (mmol/L) (β ± SE: 0.024 ± 0.004, P = 8.27e-07). The effect of the genetic risk score was also significant in the GOMAP study (β ± SE: 0.011 ± 0.005, P = 0.031). In the meta-analysis of the two studies both scores were significantly associated with higher glucose levels GRS: β ± SE: 0.019 ± 0.003, P = 1.41e-09. Also, variants at the SLC30A8, PROX1, MTNR1B, ADRA2A, G6PC2, LPIN3 loci indicated nominal evidence for association with glucose levels (p < 0.05). We replicate associations of the established glucose raising variants in the Greek population and confirm directional consistency of effects (binomial sign test p = 6.96e-05). We also demonstrate that the cumulative effect of the established glucose loci yielded a significant association with increasing glucose levels.

Tumours of the heart are rare, and in the vast majority of cases are myxomas that have a benign profile. According to their location, their clinical manifestations differ but there are cases that are completely asymptomatic [M. Yuce, S. Dagdelen, M. Ergelen, N. Eren, N. Caglar, A huge obstructive myxoma located in the right heart without causing any symptom. Int J Cardiol 2007;114:405–406.], found only post-mortem. Herein we describe the case of a 45-year-old female patient previously asymptomatic who presented with syncope due to a large right atrial myxoma with extracardiac localization as embolic phenomenon in the pulmonary artery tree.

Severe hyperkalaemia is a life threatening electrolyte abnormality that if not treated urgently, might cause electric death. Hyperkalaemia induced electrocardiogram (ECG) alterations vary according to the levels and rate of increase of potassium concentration ([K(+)]) in the extracellular milieu but the paradox is that not all these cases provide ECG changes. We describe the first case in the literature of transient sinus rhythm (SR) recovery despite severe hyperkalaemia in a 57-year-old (yo) male patient with impressive ECG changes considering the heart rhythm and QRS morphology. We also review the literature for the mechanism of ECG alterations induced by hyperkalaemia.

Background There are few data regarding the long-term prognosis of young survivors of acute myocardial infarction (AMI). We explored the long-term outcome in individuals who had sustained a premature ST-segment elevation AMI. Methods We recruited 257 consecutive patients who had survived their first AMI ≤35 years of age. Patients were followed up for up to 18 years. Clinical end points included all major adverse coronary events (MACE): cardiac death, readmission for acute coronary syndrome, arrhythmias, or coronary revascularization due to clinical deterioration. Results The most prevalent risk factor at presentation was smoking (93.7%). Follow-up data were obtained from 237 patients (32.2 ± 3.7 years old). The median follow-up period was 9.1 years. During follow-up, 139 (58.6%) patients reported continuation of smoking. Ninety-one (38.4%) patients had recurrent MACE (13 deaths, 59 acute coronary syndromes, 2 arrhythmias, and 17 revascularizations). Multivariable Cox regression analysis showed that persistence of smoking, left ventricular ejection fraction (LVEF), and reperfusion therapy (fibrinolysis or primary coronary angioplasty) were independent predictors of MACE after adjustment for conventional risk factors. Continuation of smoking remained an independent predictor for MACE after additional adjustments for LVEF (hazard ratio 2.154, 95% CI 1.313-3.535, P = .002) or reperfusion treatment (hazard ratio 2.327, 95% CI 1.423-3.804, P = .001). Harrell c statistic showed that the model with persistent smoking had the best discriminatory power compared with models with LVEF or reperfusion treatment. Conclusions In the era of statins and reperfusion treatment, continuation of smoking is the strongest independent long-term predictor for recurrent MACE in young survivors of premature AMI.

The aim of the present case-control study was to estimate, by density gradient ultracentrifugation, LDL heterogeneity in myocardial infarction, and to evaluate the effect of smoking and β-blocker treatment on LDL subfraction profile. Our results show that patients who survive myocardial infarction have an abundance of small, dense LDL in their plasma, compared with controls. Patients who were on β-blockers and those who smoked showed a more atherogenic LDL subfraction profile than the rest. In patients on β-blocker treatment, the proportion of LDL3 was positively correlated with triglyceride concentration and body mass index. Dense LDL predominates in patients irrespective of smoking or β-blocker treatment. The relative risk, calculated by logistic regression as the odds ratio of high LDL3, was 7·5 (95% confidence interval 2·5-22·1) and was not significantly influenced when smoking, β-blocker treatment, triglycerides or the other parameters of the study were included in the statistical model.

Background: Quantitative coronary angiography has been shown to allow accurate assessment of coronary stenosis. Exercise and dobutamine stress echocardiography both are established methods for assessing the functional importance of coronary stenosis. The relation, however, between exercise and dobutamine stress-induced wall motion abnormalities and the severity and location of stenosis remains controversial. Methods and Results: Thirty patients with single-vessel coronary artery disease with ≥50% minimal luminal reduction and stable angina participated in the study. Severity of coronary artery stenosis was assessed by means of computed angiography. During peak exercise echocardiography 23 patients had wall motion abnormalities and 7 did not. A positive test result was associated with severity of stenosis ≥80% for 65% of stenoses (P < .05 versus severity of stenosis

Objectives To assess the incidence and natural course of paravalvular leaks detected early after aortic valve replacement. Background Although the use of echocardiography has simplified the postoperative assessment of patients with aortic valve replacement, there are no data regarding the natural history of early detected paravalvular aortic leaks. Methods Eighty-four consecutive patients with aortic valve replacement were prospectively followed clinically every 6 months and by echocardiography early (11 ± 7 days), at midterm (27 ± 3 months), and late (63 ± 4 months) after aortic valve replacement. The competence of artificial valves was assessed by Doppler color flow mapping. Results Paraprosthetic leaks were detected in 40 (47.6%) aortic prostheses during the early study; the majority (90%) were small. All leaks remained unchanged during the follow-up period. Left ventricular dimensions and function did not differ between patients with or without paravalvular leak during the follow-up. Left ventricular fractional shortening, however, increased during the intermediate study in both subgroups, indicating improved left ventricular function overall. Three patients had severe paravalvular regurgitation suddenly develop from late infective endocarditis, and 1 patient had a degenerative tissue valve failure 4 years after implantation. Conclusions Paraprosthetic aortic leaks detected early after surgery, in the absence of valve infection, are common, are usually small, and have a benign course. However, the development of new, usually severe, regurgitation should raise the suspicion of prosthetic valve endocarditis or bioprosthetic valve failure. (Am Heart J 1999;138:351-7.)

We present a patient with a history of a Sorin tilting disc prosthetic mitral valve implanted 20 years ago who developed acute dyspnoea. Echocardiogram revealed a unique pattern of 'obstruction alternans' of mitral valve prosthesis due to pannus formation. We emphasize the need for urgent surgical treatment of this potentially fatal complication.

Background: Hypotensive response during dobutamine stress echocardiography (DSE) is a common complication, lacking the prognostic significance of hypotension during exercise treadmill test. Hypothesis: The present study aimed to assess the possible mechanisms of hypotensive response during DSE and to compare it with exercise treadmill test. Methods: In all, 91 patients with known coronary artery disease (CAD) underwent both DSE and exercise treadmill test. Dobutamine-induced hypotension was defined as a systolic blood pressure drop ≥20 mmHg from baseline or from the previous level of infusion. Results: Twenty-one (23%) patients, 10 of whom also had bradycardia, developed hypotension during dobutamine infusion. Five (5.5%) patients were severely symptomatic and the infusion was stopped prematurely, while in the remaining 16 the addition of atropine allowed the continuation of the test. Patients prone to hypotension were predominantly female (p = 0.0004). had smaller (p = 0.01) and better functioning left ventricles (p = 0.0004), were unlikely to have rest wall motion abnormalities (p = 0.0008) or multivessel CAD (p = 0.02), and had less ischemia (wall motion score difference) (p = 0.03). Hypotension during exercise treadmill test was observed in only one (1%) patient with left main disease. Conclusions: Hypotension during DSE is unrelated to the anatomical or functional extent of CAD and is frequent in the setting of a well-functioning left ventricle. We suppose that vigorous contraction of a small chamber during dobutamine infusion results in an excessive stimulation of cardiac mechanoreceptors that mediate reflex hypotension and bradycardia.

Aim The present study aimed to assess the incidence and type of lipid disorders in the offspring of young Greek coronary patients. Methods One hundred and ninety-three children and youngsters were divided into two groups. Group A consisted of 104 children whose fathers had sustained a myocardial infarction before the age of 55 years. Eighty-nine young subjects matched for age, gender, dietary and smoking habits without a familial history of coronary artery disease served as controls (group B). Total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol and lipoprotein(a) were measured in the children and the affected fathers. Results Fifty-three percent of the offspring of young coronary patients had elevated total cholesterol or elevated triglycerides or decreased high density lipoprotein cholesterol or a combination, while the 80·4% of the affected fathers had lipid disorders. The distribution of lipid disorders in the children bore a striking resemblance to those seen in their affected fathers and there was a significant correlation between offspring–father total cholesterol, low density lipoprotein cholesterol and lipoprotein(a). When excess lipoprotein(a) was added to the lipid disorders the incidence of dyslipidaemia in the offspring of the affected individuals was increased to 63·5%. Conclusions Dyslipidaemia is very common in the offspring of Greek men with premature coronary artery disease; this occurrence emphasizes the need always to evaluate the lipid profile in these children. The detection of dyslipidaemia necessitates the early institution of preventive measures with the expectation that the incidence of cardiovascular disease will decrease later in life.

We investigated whether visceral adipose tissue (VAT) measured by ultrasonography is better than waist circumference (WC) in predicting the presence of subclinical carotid atherosclerosis. We recruited 100 individuals without a history of cardiovascular disease or diabetes mellitus. VAT volume was measured by ultrasonography and common carotid artery intima-media thickness (CCA-IMT) by B-mode ultrasonography. Both VAT and WC were positively associated with body mass index, triglycerides, uric acid, systolic/diastolic blood pressure and high sensitivity C-reactive protein and inversely correlated with high-density lipoprotein cholesterol. However, only VAT was associated with CCA-IMT (r = 0.309, p = 0.002). Multivariate logistic regression analysis revealed that VAT, but not WC, was an independent predictor of carotid plaques after adjustment for cardiovascular risk factors (odds ratio [OR] = 1.017, 95% confidence interval [CI] = 1.003-1.031, p = 0.017), and this association persisted after additional adjustment for WC (OR = 1.024, 95% CI = 1.003-1.031, p = 0.027). Our data suggest that VAT volume measured by ultrasonography may be a better predictor of subclinical carotid atherosclerosis than waist circumference in healthy individuals.

The right ventricle differs from the left ventricle in many anatomic and physiologic aspects. This disparity renders the right ventricle less vulnerable to ischemia and less susceptible to myocardial injury when right coronary artery occlusion occurs compared with the extent of left ventricular dysfunction during left coronary artery occlusion. Acute right ventricular (RV) myocardial infarction is usually caused by proximal right coronary artery occlusion and therefore is usually associated with inferior myocardial infarction. Conventional echocardiography along with Doppler tissue imaging has played a significant role in early diagnosis of RV myocardial infarction and has a role in prognostic stratification. Stress echocardiography is less validated and more technically demanding in detecting RV reversible dysfunction compared with left ventricular dysfunction. The threshold of RV ischemia during stress echocardiography is higher compared with left ventricular ischemia and usually affects the inferior RV wall. Further studies, particularly with the use of novel echocardiographic techniques such as speckle-tracking and three-dimensional echocardiography, may be required to better elucidate the role of the right ventricle in coronary artery disease.

Cardiovascular risk factors have been identified in the postprandial state, particularly in patients with coronary artery disease (CAD). Tea consumption has been linked to cardiovascular risk reduction, but the beneficial effect of tea has not been investigated under postprandial conditions. The objective was to examine the effect of green tea on postprandial levels of plasma total antioxidant capacity (TAC), serum lipids, C-reactive protein (CRP) and glucose in patients with CAD.In a randomized controlled, parallel design with 2 arms, 43 patients with CAD were assigned to consume breakfast consisting of bread, butter and 330 ml water or tea (4.5 g green tea/330 ml, providing approximately 400 mg catechins). Blood samples were drawn immediately before and 1.5, 3 and 5 h after breakfast. TAC was measured in plasma with the ferric reducing antioxidant power of plasma and oxygen radical absorbance capacity assays. Total cholesterol, high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), triglycerides, glucose, CRP, uric acid and pancreatic lipase levels were measured in serum.Tested biomarkers did not differ between tea and water group at baseline, 1.5, 3 and 5 h (P0.05) postprandially. However, TAC increased 1.5 and 3 h after consumption of breakfast with tea (P0.005), but no change was observed after consumption of breakfast with water. Serum triglycerides levels significantly increased 3 h after breakfast with water (P = 0.031), but not after breakfast with tea. Serum uric acid decreased 1.5 h after breakfast with tea (P = 0.038). Pancreatic lipase, CRP, total cholesterol, HDL-C, LDL-C and glucose levels remained unchanged after breakfast with tea at any time point (P0.05).Tea consumption did not affect selected biomarkers at any postprandial time point in patients with CAD.

BackgroundType D personality has been associated with a variety of emotional and social difficulties as well as with poor prognosis in patients with established coronary heart disease (CHD). We examined the psychometric properties and validity of the Type D Scale-14 (DS14) and the prevalence of Type D personality among Greek patients with CHD while taking into account demographic; clinical, such as diabetes mellitus, hypertension, and hypercholesterolemia; as well as psychological variables such as depression, anxiety, and psychological stress.MethodsNinety-six patients with stable coronary heart disease and 80 healthy participants from the general population completed the Greek version of the DS14 and the Hospital Anxiety and Depression Scale (HADS).ResultsCronbach's α coefficient for the negative affectivity (NA) and social inhibition (SI) subscales was 0.83 and 0.72 for the CHD and 0.88 and 0.76 for the control group, respectively. Internal-structural validity was assessed by a factor analysis (two-factor solution), and the factor structure of the original DS14 was replicated. Using the standardized cutoff point of NA ≥10 and SI ≥10, instead of the median scores, in order to have compatible results with the majority of studies, the prevalence of Type D personality was 51% for the CHD patients and 13% for the control group. Higher NA and SI were connected with higher anxiety, depression, and total psychological stress. Finally, more patients with CHD and Type D personality than those without were diagnosed with type 2 diabetes; however, no differences were observed in hypertension or hypercholesterolemia.ConclusionsThese results indicate that the Type D construct is reliable and valid in a Greek population. The prevalence of Type D personality was higher in patients with stable coronary heart disease than in people from the general population. The DS14 subscales were positively correlated with higher anxiety, depression, and total psychological stress. Regarding other CHD risk factors, only diabetes mellitus was found more frequently in CHD patients with Type D personality.Keywords: Coronary heart disease, Type D personality, DS14, Validity, HADS

SummaryTo assess whether plasminogen activator inhibitor 1 (PAI-1) activity is elevated in the progeny of young coronary men, 193 young subjects were recruited and divided into two groups. Group A consisted of 104 children whose fathers had suffered a myocardial infarction before the age of 55 (“cases”). Eighty-nine young subjects matched for age, sex, body mass index (BMI) and smoking habits without familial history of coronary artery disease (CAD) served as controls (group B). Children with a family history of diabetes mellitus or hypertension were excluded from both groups. We measured PAI-1 activity, tissue-type plasminogen activator (t-PA) antigen, a2-antiplasmin, fibrinogen, lipids and apolipoproteins in both groups. PAI-1 activity levels were also determined in the men who suffered a premature myocardial infarction 4 months after their discharge. PAI-1 activity levels were higher in cases compared to controls (3.13 ± 1.9 vs 2.17 ± 1.9 U/ml, p = 0.0014). t-PA antigen and a2-antiplasmin did not differ significantly between the two groups, while fibrinogen, total cholesterol, low-den-sity lipoprotein cholesterol, apolipoprotein B and lipoprotein(a) were significantly higher in group A. PAI-1 was positively correlated with triglycerides (r = 0.22, p = 0.024), apolipoprotein B (r = 0.21, p = 0.039) and fibrinogen (r = 0.22, p = 0.029 ) in cases and with BMI in both cases (r = 0.37, p = 0.0003) and controls (r = 0.23, p = 0.044). In stepwise multiple regression analysis, only apolipoprotein B (p = 0.008) and BMI (p = 0.0014) were significant determinants of PAI-1 activity in cases. There was also a positive correlation between PAI-1 activity levels of the affected fathers and their children (r = 0.30, p = 0.01). The present data support the hypothesis that elevated PAI-1 levels in the offspring of men with premature myocardial infarction impair their fibrinolytic capacity contributing to their familial predisposition to CAD.

We examined whether the levels of fibrinogen are elevated in the offspring of middle-aged coronary patients. One hundred and seventy-six young subjects were divided into two groups. Group A consisted of 100 children and youngsters (mean age 17 +/- 6 years) whose fathers had sustained a myocardial infarction under the age 55 years without associated history of diabetes mellitus or hypertension. Seventy-six healthy young subjects (mean age 18 +/- 5 years) matched for gender, dietary and smoking habits without familial history of coronary artery disease, diabetes mellitus or hypertension served as the control group (group B). Fibrinogen, total cholesterol, triglycerides, high and low density lipoprotein cholesterol, apolipoprotein A-1, apolipoprotein B and lipoprotein (a) were measured. Sons and daughters with a history of premature paternal myocardial infarction had higher levels of fibrinogen compared with control subjects (304.1 +/- 60 vs 274 +/- 53 mg. dl-1, P0.001). This difference was maintained when the above groups were divided into single sex groups. Total cholesterol, low density lipoprotein cholesterol, apolipoprotein B and lipoprotein (a) were also significantly higher in group A. Children of affected individuals who had a good lipid profile also had significantly higher fibrinogen levels compared to control group. The results support the hypothesis that the higher plasma levels of fibrinogen in the offspring of middle-aged coronary men could partially explain their predisposition for coronary artery disease. Since the levels of fibrinogen have a major genetic component, they could be a useful marker in identifying children at high risk for coronary artery disease, especially among those with no lipid abnormalities.

The aim of this study was to examine the prognostic value of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) associated with high-density lipoprotein (HDL) (HDL-Lp-PLA(2)) in patients with stable coronary artery disease (CAD).Lp-PLA(2) is a novel risk factor for cardiovascular disease. It has been postulated that the role of Lp-PLA(2) in atherosclerosis may depend on the type of lipoprotein with which it is associated.Total plasma Lp-PLA(2) and HDL-Lp-PLA(2) mass and activity, lipids, and C-reactive protein were measured in 524 consecutive patients with stable CAD who were followed for a median of 34 months. The primary endpoint was cardiac death, and the secondary endpoint was hospitalization for acute coronary syndromes, myocardial revascularization, arrhythmic event, or stroke.Follow-up data were obtained from 477 patients. One hundred twenty-three patients (25.8%) presented with cardiovascular events (24 cardiac deaths, 47 acute coronary syndromes, 28 revascularizations, 22 arrhythmic events, and 2 strokes). Total plasma Lp-PLA(2) mass and activity were predictors of cardiac death (hazard ratio [HR]: 1.013; 95% confidence interval [CI]: 1.005 to 1.021; p = 0.002; and HR: 1.040; 95% CI: 1.005 to 1.076; p = 0.025, respectively) after adjustment for traditional risk factors for CAD. In contrast, HDL-Lp-PLA(2) mass and activity were associated with lower risk for cardiac death (HR: 0.972; 95% CI: 0.952 to 0.993; p = 0.010; and HR: 0.689; 95% CI: 0.496 to 0.957; p = 0.026, respectively) after adjustment for traditional risk factors for CAD.Total plasma Lp-PLA(2) is a predictor of cardiac death, while HDL-Lp-PLA(2) is associated with lower risk for cardiac death in patients with stable CAD, independently of other traditional cardiovascular risk factors.

To extend understanding of the genetic architecture and molecular basis of type 2 diabetes (T2D), we conducted a meta-analysis of genetic variants on the Metabochip, including 34,840 cases and 114,981 controls, overwhelmingly of European descent. We identified ten previously unreported T2D susceptibility loci, including two showing sex-differentiated association. Genome-wide analyses of these data are consistent with a long tail of additional common variant loci explaining much of the variation in susceptibility to T2D. Exploration of the enlarged set of susceptibility loci implicates several processes, including CREBBP-related transcription, adipocytokine signaling and cell cycle regulation, in diabetes pathogenesis. © 2012 Nature America, Inc. All rights reserved.

Stroke is the most feared complication of atrial fibrillation (AF). Dronedarone is an antiarrhythmic drug with multichannel-blocking properties. Recently, a post hoc analysis of a large randomized trial has suggested a reduction of stroke risk in patients with paroxysmal or persistent AF receiving dronedarone. We performed a systematic review and meta-analysis on the effect of dronedarone on the occurrence of stroke or transient ischemic attack (TIA) in patients with paroxysmal or persistent AF. We searched PubMed, EMBASE, and ISI Web of Knowledge as well as abstracts of major conferences for randomized trials comparing dronedarone with placebo in patients with paroxysmal or persistent AF. The endpoint was the occurrence of stroke or TIA during follow-up. Fixed effect risk differences (RDs) were calculated with the Mantel-Haenszel method. We also performed random effects analysis with the DerSimonian Laird method. Four trials were included in the analysis; a total of 5967 patients were analyzed, 3183 receiving dronedarone 400 mg twice daily and 2784 receiving placebo. 160 strokes or TIAs were reported in the four trials: 67 in the dronedarone group (2.1%) and 93 in the placebo group (3.3%). In the fixed effect model, patients in the dronedarone group had a significantly lower risk for the occurrence of stroke or TIA during follow-up compared with patients in the placebo group. The RD of the incidence of stroke or TIA in all trials between patients randomized to dronedarone and those randomized to placebo was −0.0094 (95% confidence interval [CI] −0.0178, −0.0011; p = 0.027). The ATHENA trial had by far the highest statistical weight (79.5%). There was no evidence of heterogeneity (χ2 = 2.41, p = 0.300). In the random effects model, the statistical weight of the ATHENA trial was much lower (45.1%) and the RD for stroke or TIA between the dronedarone and the placebo groups did not reach statistical significance (RD −0.0064, 95% CI −0.0144, 0.0016; p = 0.120). First, stroke was not a prespecified outcome measure in the included trials. Second, we did not analyze trials studying patients with permanent AF; very recent data show an adverse outcome in patients with permanent AF receiving dronedarone. The meta-analysis indicates a reduced risk of stroke or TIA in patients with paroxysmal or persistent AF receiving dronedarone. These findings are largely due to the results of the ATHENA trial. Further research on this topic is necessary.

Contains fulltext : 97601.pdf (Publisher’s version ) (Closed access) Abdominal aortic aneurysm (AAA) is a common cause of morbidity and mortality and has a significant heritability. We carried out a genome-wide association discovery study of 1866 patients with AAA and 5435 controls and replication of promising signals (lead SNP with a p value < 1 x 10(-5)) in 2871 additional cases and 32,687 controls and performed further follow-up in 1491 AAA and 11,060 controls. In the discovery study, nine loci demonstrated association with AAA (p < 1 x 10(-5)). In the replication sample, the lead SNP at one of these loci, rs1466535, located within intron 1 of low-density-lipoprotein receptor-related protein 1 (LRP1) demonstrated significant association (p = 0.0042). We confirmed the association of rs1466535 and AAA in our follow-up study (p = 0.035). In a combined analysis (6228 AAA and 49182 controls), rs1466535 had a consistent effect size and direction in all sample sets (combined p = 4.52 x 10(-10), odds ratio 1.15 [1.10-1.21]). No associations were seen for either rs1466535 or the 12q13.3 locus in independent association studies of coronary artery disease, blood pressure, diabetes, or hyperlipidaemia, suggesting that this locus is specific to AAA. Gene-expression studies demonstrated a trend toward increased LRP1 expression for the rs1466535 CC genotype in arterial tissues; there was a significant (p = 0.029) 1.19-fold (1.04-1.36) increase in LRP1 expression in CC homozygotes compared to TT homozygotes in aortic adventitia. Functional studies demonstrated that rs1466535 might alter a SREBP-1 binding site and influence enhancer activity at the locus. In conclusion, this study has identified a biologically plausible genetic variant associated specifically with AAA, and we suggest that this variant has a possible functional role in LRP1 expression. 9 p.

The beneficial effects of statin pretreatment as well as of staccato reperfusion (SR) on myocardium have been demonstrated in patients undergoing cardiac interventions. In this study, we compared the effects of the acute statin administration prior to percutaneous coronary intervention (PCI) with the effects of staccato or abrupt reperfusion on coronary microcirculation in patients with myocardial infarction (MI).We randomly assigned 47 patients who had ST-elevation or non-ST-elevation MI 48 h prior to PCI, into three groups: staccato reperfusion (consisting of 6 periods of 10-s balloon inflation/deflation) plus statin therapy (SRSG), statin therapy plus abrupt reperfusion (SG), and abrupt reperfusion alone (ARG). Myocardial contrast echocardiography (MCE) was performed to assess the blood volume (A), velocity (β) and flow (A × β) of the segments associated with the PCI-treated artery the day following intervention and 30 days after. LV end-diastolic (EDV) and systolic volumes (ESVs), wall motion score index (WMSI) were evaluated.Compared to ARG, SRSG and SG resulted in a greater improvement in A, β and A × β (F = 20.6, p0.001 for A, F = 3.5, p = 0.03 for β and F = 11.3, p0.001 for A × β for the overall effect of intervention) as well as a greater decrease of WMSI, EDV and ESV (p0.01) one month post-PCI. The changes of all echocardiography markers were greater in SRSG than SG (p0.01). The % changes in ESV correlated with the corresponding % changes in MCE indices in SRSG and SG (p0.05).The acute statin administration prior to reperfusion either alone or in synergy with staccato reperfusion ameliorates coronary microcirculatory dysfunction in patients with myocardial infarction.

Recently, the concept that high density lipoprotein (HDL) quality is an important parameter for atheroprotection is gaining ground, though little data exists so far to support it. In an attempt to identify measurable qualitative parameters of HDL associated with increased risk for premature myocardial infarction (MI), we studied the structural characteristics of HDL from patients who survived an MI at a young age (≤35 years).We studied 20 MI patients and 20 healthy control subjects. HDL of patients had reduced apolipoprotein A-I (apoA-I), apolipoprotein M, and paraoxonase 1 levels and significantly elevated apolipoprotein C-III (apoCIII) levels (all p0.05). Specifically, the HDL apoA-I/apoC-III ratio was 0.24±0.01 in patients versus 4.88±0.90 in controls (p0.001). These structural alterations correlated with increased oxidation potential of HDL of the MI group compared to controls (2.5-fold, p=0.026). Electron microscopy showed no significant difference in average HDL particle diameter between the two groups though a significant difference existed in HDL diameter distribution, suggesting the presence of different HDL subpopulations in MI and control subjects. Indeed, non-denaturing two-dimensional electrophoresis revealed that MI patients had reduced pre-β1(α), pre-β1(b) and α(2), and elevated α(1), α(3), and pre-α(4) HDL.Reduction in the HDL apoA-I/apoC-III ratio, changes in the HDL subpopulation distribution and an increase in HDL oxidation potential correlated with the development of MI in young patients. The possibility that such changes may serve as markers for the early identification of young individuals at high risk for an acute coronary event should be further explored.

We aimed to investigate the proportion of very high-risk patients with coronary heart disease (CHD) who achieve the optional low-density lipoprotein cholesterol (LDL-C) target of70 mg/dl (1.8 mmol/liter), the factors that influence the success rate and the impact on their prognosis.We enrolled 1337 consecutive patients with stable CHD. Fasting lipids were determined and all cardiovascular events were recorded during a median follow-up of 33 months.The majority (86.5%) of patients were taking lipid-lowering medication (95.5% statins), but only 50.6% had LDL-C levels of100 mg/dl (2.6 mmol/liter). In total, 941 (70.4%) patients were considered very high risk and only 15.1% of them had LDL-C levels of70 mg/dl. Τhe use of intensive lipid-lowering medication was associated with 12-fold (95% CI 6.98-20.76; p0.001) higher possibility in achieving LDL-C levels of70 mg/dl. Attainment of LDL-C levels of70 mg/dl by patients at very high risk were independent predictors of all cardiovascular events (HR=0.34, 95% CI 0.17-0.70; p=0.003).The vast majority of very high-risk patients do not achieve the optional LDL-C goal; this is mainly due to the suboptimal uptitration of statin dose and is translated into loss of clinical benefits.

We describe a 45-year-old woman with peripheral embolism in whom echocardiography revealed mobile masses in the aortic arch that were characterized as atherothrombi. The masses were resected surgically 2 months later, since treatment with antiplatelets, anticoagulants and statins failed to resolve them.

Depression is common in patients with coronary artery disease (CAD) and is associated with higher risk of cardiovascular adverse events. We aimed to explore the prognostic role of mild depression on cardiovascular mortality and compare its prognostic value with C-reactive protein (CRP) levels in patients with stable CAD.We initially recruited 523 consecutive patients with stable CAD. Glucose, lipids and CRP levels were measured and an echocardiographic study was performed. In addition, depressive symptomatology was assessed with the Zung Depression Rating Scale (ZDRS, range 20-80). Patients on antidepressant treatment or with ZDRS score ≥60 were excluded. Patients were followed up at 6 month intervals (median 33 months, interquartile range 24-40 months) by telephone interview.Follow-up data were obtained from 485 patients (92.7%). Nineteen patients with baseline CRP levels10 mg/L and eight with non-cardiovascular death were excluded from analysis. Of the remaining 458 patients 113 (24.7%) presented cardiac events. Of them 21 died (4.6%), 42 developed acute coronary syndrome (9.2%), 27 (5.9%) had a revascularization procedure due clinical deterioration, two had a stroke (0.44%) and 21 (4.6%) an arrhythmic event. Multivariate Cox regression analysis showed that ZDRS score was independent predictor of cardiovascular death (hazard ratio [HR]: 1.104 with 95% confidence interval [CI]: 1.039-1.172, p = 0.001) after adjustment for conventional risk factors and CRP. The Wald test statistic of CRP was 2.59, whereas the Wald test statistic of ZDRS score was 3.23, indicating better predictability of ZDRS score. ZDRS score was also independent predictor of both cardiovascular death and arrhythmic event (HR: 1.102 with 95% CI: 1.051-1.156, p0.001) after adjustment for conventional risk factors and CRP levels. The main limitations of our study were the evaluation of depression at one point in time and the assessment of inflammatory burden by measuring only CRP levels.Mild depression is associated with increased cardiovascular mortality and is a better predictor than CRP levels in patients with stable CAD.

We read with great interest the American College of Cardiology/American Heart Association (ACC/AHA) new guidelines on the treatment of blood cholesterol [(1)][1]. The guidelines are based on a thorough evaluation of randomized controlled trials (RCTs), systemic reviews, and meta-analyses of RCTs

There are limited and controversial data regarding the impact of 4G/5G polymorphism of the plasminogen activator inhibitor-1 (PAI-1) gene in the pathogenesis of premature myocardial infarction (MI). We explored whether 4G/5G polymorphism of the PAI-1 gene is associated with the development of MIor= 35 years of age. We recruited 201 consecutive patients who had survived their first acute MIor= 35 years of age (mean age = 32.2 +/- 3.4 years). The control group consisted of 140 healthy individuals matched with cases for age and sex, without a family history of premature coronary heart disease. 4G/5G polymorphism of PAI-1 was tested with polymerase chain reaction and reverse hybridization. 4G allele carriers (4G/4G and 4G/5G genotypes) of PAI-1 were less frequent in patients than in controls (69.6 vs. 83.6%, P = 0.007). 4G carriership of the polymorphism of PAI-1 was associated with lower risk for acute MI (odds ratio 0.45, 95% confidence interval 0.23-0.88, P = 0.02) after adjusting for major cardiovascular risk factors. Patients possessing the 4G allele had higher PAI-1 plasma levels (32.2 +/- 25 vs. 22.2 +/- 11.3 ng/ml, P = 0.006) but lower lipoprotein(a) levels (10.1 [2.1-29.9] vs. 15.3 [8.2-57.1] mg/dl, P = 0.03) compared to 5G/5G homozygotes. Our data indicate that the 4G allele of the PAI-1 4G/5G polymorphism is less frequent among survivors of MI at very young age compared with matched controls.

SummaryCatheter ablation provides curative treatment for atrial fibrillation (AF). Data on anticoagulation after the procedure are sparse. We investigated real-life antithrombotic treatment after AF ablation and examined its adherence to current recommendations. Eight hundred forty-four patients (age 58 ±10 years) underwent AF ablation. Most patients had a CHADS2 score of 0 (46%) or 1 (45%). Seven-day Holter was performed at three, six and 12 months after ablation. Decision on anticoagulation treatment was made by general practitioners and referring cardiologists in consultation with the patients. At discharge, anticoagulants were prescribed for the vast majority (94–96%) of patients. This percentage remained high at three and six months (80–90%) without differences between stroke risk groups. At 12 months, the use of anticoagulants was mainly influenced by the detection of recurrence; usage exceeded 90% in all stroke risk groups in patients with recurrences. In patients without recurrences, differences between risk groups were significant but small, ranging from 42% (CHADS2=0) to 62% (CHADS2≥2) (p=0.033). In multivariate analysis, the only factor independently associated with oral anticoagulation at 12 months was the detection of recurrences (odds ratio=16.2, p

BACKGROUND: Metabolic disorders associated with atherosclerosis and cardiovascular disease have been described in "HIV-infected" individuals. We investigated (i) whether normotensive "HIV-infected" individuals and hypertensive patients have similarities regarding their arterial elastic properties and (ii) the effect of highly active antiretroviral therapy (HAART) and metabolic factors on arterial stiffness. METHODS: In a case-control study, we compared measurements of pulse wave velocity (PWV), arterial blood pressure, and markers of metabolic profile in 56 normotensive, "HIV-infected" patients (mean age 40 +/- 13 years) to 28 age- and sex-matched newly diagnosed untreated patients with hypertension and 28 healthy individuals. RESULTS: "HIV-infected" patients had higher PWV than healthy controls but lower PWV than hypertensives (8.1 +/- 1.4 m/s vs. 6.7 +/- 1.1 m/s vs. 9.0 +/- 1.0 m/s, P = 0.003 and 0.01, respectively). However, patients on HAART had similar PWV with hypertensives (8.4 +/- 1.4 vs. 9.0 +/- 1.0 m/s P = 0.25). Patients on HAART had higher PWV than patients without (8.4 +/- 1.4 m/s vs. 7.5 +/- 1.3 m/s, P = 0.03). Patients on HAART had higher total cholesterol, triglycerides, and diastolic blood pressure than patients naive to HAART (P < 0.05). In multivariate analysis, the independent determinants of increased PWV were HAART duration (unstandardized coefficient b v = 0.007, P = 0.04), serum cholesterol (b = 0.007, P = 0.04), mean or diastolic blood pressure (b = 0.049 and b = 0.060, P < 0.01). CONCLUSIONS: "HIV-infected" individuals have increased arterial stiffness compared to healthy controls. Patients on antiretroviral therapy have similarities regarding their arterial elastic properties with patients with untreated hypertension. There is an independent association between duration of antiretroviral therapy, cholesterol levels, and blood pressure with increased arterial stiffness in "HIV-infected" patients.

Background: Abdominal obesity (AO) is associated with increased risk of cardiovascular disease and type 2 diabetes, whereas the Mediterranean diet exerts a cardioprotective effect. Objective: We examined whether a close adherence to a Mediterranean-style diet improves endothelial function in individuals with AO. Design: We recruited 90 subjects with AO without cardiovascular disease or type 2 diabetes. Participants were randomly assigned to the intervention or control group. Both groups were instructed to follow a Mediterranean-style diet for 2 mo. Subjects in the intervention group additionally had to follow a specific relevant daily and weekly food plan with close supervision by a dietitian and provision of basic foods. Flow-mediated dilatation (FMD), lipids, C-reactive protein (CRP), and insulin resistance with the homeostasis model assessment (HOMA-IR) were measured. Results: After 2 mo, subjects in the intervention group increased their intake of total fat due to higher consumption of monounsaturated fatty acids as well as intakes of dietary fiber, vitamin C, and alcohol compared with the control group (all P , 0.05). The intervention group also increased FMD (2.05%; 95% CI: 0.97, 3.13%), whereas no effect was found in the control group (20.32%; 95% CI: 21.31, 0.67%). Changes in lipids and CRP concentrations did not differ between the 2 groups, whereas diastolic blood pressure decreased in the intervention group (26.44 mm Hg; 95% CI: 28.57, 24.31 mm Hg) compared with the control group (20.76 mm Hg; 95% CI: 22.83, 1.31 mm Hg). Finally, there was a trend for a reduction in HOMA-IR in the intervention group compared with the control group (P = 0.072). Conclusion: Close adherence to a Mediterranean-style diet achieved by close dietetic supervision improves endothelial function in subjects with AO. Am J Clin Nutr 2009;90:263‐8.

Introduction: Catheter ablation is potentially curative treatment for atrial fibrillation (AF). However, complications are more frequent and more severe compared with other ablation procedures. We investigated the complication rate in 1,000 AF ablation procedures in a high-volume center and examined possible risk factors. Methods and Results: One thousand consecutive circumferential pulmonary vein radiofrequency ablations were performed for symptomatic, drug-refractory AF. Major complications were defined as the ones that were life threatening, caused permanent harm, and required intervention or prolonged hospitalization. Thirty-nine (3.9%) major periprocedural complications were observed. There was no death immediately associated with the procedure. However, there were 2 deaths (0.2%) of unclear cause, 14 days and 4 weeks after ablation. The most common complications were tamponade (1.3%), treated mainly by percutaneous drainage, and vascular complications (1.1%). There were also 4 thromboembolic events (0.4%): 3 nonfatal strokes and one transient ischemic attack. Importantly, 2 cases (0.2%) of atrial-esophageal fistula and 2 cases (0.2%) of endocarditis were observed. Factors associated with an increased complication risk were age ≥75 years (hazard ratio 3.977, P = 0.022) and congestive heart failure (hazard ratio 5.174, P = 0.001). Conclusion: AF ablation still has a considerable number of major complications that may be life threatening or may lead to severe residues. Atrial-esophageal fistula is still observed despite continuous systematic methods to prevent it. Stroke, tamponade, and vascular complications are the most frequent major complications. However, in most patients treatment can be conservative and results in complete recovery. Advanced age and congestive heart failure seem to be associated with an increased risk of complications.

A 48-year-old man with a medical history of hypertension was admitted with acute dyspnea and pyrexia. Echocardiographic examination revealed a dilated and volume-overloaded left ventricle and severe mitral regurgitation due to ruptured chordae tendinae resulting in posterior leaflet prolapse. Blood cultures were negative. The patient was treated with antibiotics considering that he had a chest infection based on the admission chest x-ray, diuretics, and angiotensin converting enzyme inhibitors, and his clinical condition improved. Subsequently, he was referred for cardiac surgery. Coronary angiography demonstrated normal coronary anatomy, and he had mitral valve repair with placement of a 27-mm Duran …

Introduction Nonrandomized studies suggest a survival benefit for patients with atrial fibrillation (AF) undergoing catheter ablation compared with antiarrhythmic drug (AAD) therapy. Data from randomized trials are lacking. We performed a meta-analysis on mortality in randomized controlled trials comparing AF ablation with AADs. Methods Pubmed, the Cochrane Central Register of Controlled Trials, and abstracts of major conferences were searched for randomized trials comparing AF catheter ablation with AADs. Eight trials with a total of 930 patients were analyzed. Trial quality was assessed by a modified Jadad scale. Follow-up was 1 year in most trials. We assessed fixed effect risk differences (RDs) with the Mantel-Haenzel method, heterogeneity with I 2 statistic, and publication bias with Begg's funnel plot and with Egger's test. Results A total of 7 deaths were reported: 3 in the ablation and 4 in the AAD arm. There was no difference in mortality between AF ablation and AAD therapy. The RD of mortality in all trials between patients randomized to ablation and those randomized to AADs was −0.003 (95% CI −0.018 to 0.013, P = .74) without evidence for heterogeneity ( I 2 = 0%, P = .907). No potential publication bias was found. There was also no difference in rates of stroke or transient ischemic attack between ablation and antiarrhythmic therapy for AF (RD = 0.004, 95% CI −0.010 to 0.018, P = .54). Conclusion This meta-analysis of randomized controlled trials showed similar survival of patients undergoing catheter ablation for AF compared with patients treated with AADs after 12 months of follow-up. There was also no difference in the rates of stroke or transient ischemic attack. These findings can be probably explained by the low-risk young populations who were included in the trials and the relatively short 12-month follow-up.

We report the case of a patient with hepatocellular carcinoma who was admitted to our hospital with fatigue and edema of lower extremities. Transthoracic echocardiographic examination revealed a mobile echogenic cavoatrial mass that infiltrated the inferior vena cava and extended along the vessel protruding into the right cardiac cavities. The differential diagnosis included a tumor mass originating from the liver and subsequently infiltrating the inferior vena cava and extending into the right cardiac cavities or a large thrombus formed on the tumor mass that infiltrated the inferior vena cava.

Introduction There are limited and controversial data regarding the impact of G-455A polymorphism of β-fibrinogen gene in the pathogenesis of premature myocardial infarction (MI). We examined whether the G-455A polymorphism of β-fibrinogen gene is associated with the development of MI ≤ 35 years of age. Methods We recruited 181 consecutive patients who had survived their first acute MI ≤ 35 years of age (mean age = 32.2 ± 3.4 years). The control group consisted of 129 healthy individuals matched with cases for age and sex, without a family history of premature coronary heart disease. G-455A polymorphism of β-fibrinogen was tested with polymerase chain reaction and reverse hybridization. Results There was a higher prevalence of carriers of the A allele (GA+AA genotype) in controls than in patients (odds ratio [OR] 0.57, 95% confidence interval [CI] 0.36 to 0.91, p = 0.02). G-455A polymorphism of β-fibrinogen gene was associated with lower risk for acute MI (OR 0.46, 95% CI 0.25 to 0.83, p = 0.01) after adjusting for major cardiovascular risk factors. Fibrinogen levels were higher in patients compared to controls [332 (292-385) vs. 311 (262-373) mg/dL, p = 0.01], but the adjusted for classical risk factors fibrinogen levels did not differ (OR 1.003, 95% CI 0.99 to 1.01, p = 0.37). Patients possessing the A allele did not differ in their fibrinogen and lipid levels compared to patients with the -455GG genotype. Conclusions Our data indicate that the presence of the G-455A polymorphism of β-fibrinogen gene has a “protective effect” against the development of non-fatal acute MI ≤ 35 years of age in Greece.

Background There are few and conflicting data regarding the prognostic role of continued smoking in very young survivors of acute myocardial infraction (AMI) after the event. Design We conducted a prospective study to evaluate the impact of smoking habits on long-term outcome in individuals who sustained AMI at the age of ≤ 35 years. Methods We recruited 147 consecutive patients who had survived their first AMI at the age of ≤ 35 years. Patients were followed up for up to 10 years. Clinical end points were: readmission for acute coronary syndrome, cardiac death or coronary revascularization because of clinical deterioration. Results The most prevalent risk factor at presentation was smoking (94.8%). Follow-up data were obtained by 135 patients (32 ± 3 yeas old, 115 men). During follow-up 75 (55.6%) patients reported continuation of smoking. Forty-four (32.6%) patients presented cardiac events (three cardiac deaths, 30 acute coronary syndromes, and 11 revascularizations). Multivariate data analysis showed that persistence of smoking (relative risk = 2.35, 95% confidence interval 1.5–5.25, P = 0.03) and ejection fraction at presentation (relative risk = 0.95, 95% confidence interval 0.91–0.98, P= 0.008) were the only significant predictors of cardiac events after adjusting for various confounding factors. In addition, continuation of smoking was the most significant predictor of cardiac events during follow-up in our sample (i.e. had the lowest log-likelihood ratio as compared with ejection fraction or other covariates). Conclusion Persistence of smoking is the most powerful predictor for the recurrence of cardiac events in patients with premature AMI.

Introduction – The levels of circulating proinflammatory cytokines may express the extent of the inflammatory response and their participation in plaque progression and rupture needs to be evaluated. We aimed to investigate differences in circulating levels of proinflammatory cytokines and in plaque infiltration by macrophages between patients undergoing carotid endarterectomy for symptomatic and asymptomatic carotid atherosclerotic disease. Methods – One hundred nineteen patients (91 men and 28 women; mean age 66 ± 8 years; range 42–83 years) who underwent carotid endarterectomy for significant (>70%) carotid bifurcation stenosis were enrolled in this study. Patients were characterized as symptomatic (n = 62) or asymptomatic (n = 57) after neurological examination. Serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), IL-1β, serum amyloid A (SAA), and high-sensitivity C-reactive protein (hs-CRP) were evaluated. Macrophage infiltration of the plaque was assessed quantitatively from endarterectomy specimens using the monoclonal antibody CD68. Results – Serum IL-6 levels were significantly higher in patients with symptomatic compared with those with asymptomatic carotid disease (3.3 [2.0–6.5] pg/ml vs 2.5 [1.9–4.1] pg/ml, P = 0.02). TNF-α, IL-1β, SAA, and hs-CRP levels did not differ significantly between the two groups. Symptomatic patients had also more intense macrophage accumulation in the carotid plaque compared with asymptomatic patients (0.6 ± 0.1% vs 0.4 ± 0.1%, P

There is increasing evidence that cellular adhesion molecules (CAMs) play an important role in the pathophysiology of acute ischaemic stroke. We examined the prognostic value of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) on in-hospital mortality in patients with ischaemic stroke.We recruited 241 consecutive patientsor=65 years of age who were admitted with acute ischaemic stroke. Serum levels of sICAM-1 and sVCAM-1 were determined within 12 h from admission. Seventy-six subjects without evidence of cardiovascular disease, matched for age and sex, served as controls.Patients with acute ischaemic stroke had higher sICAM levels compared to controls [267 (220-325) versus 200 (179-225) ng/ml, p0.001]. Sixteen (6.6%) patients died during hospitalization. sICAM-1 and sVCAM-1 levels were significantly higher in patients who died compared to those who survived [370 (324-453) versus 260 (219-313) ng/ml, p0.001 and 790 (495-985) versus 576 (494-671) ng/ml, p=0.01, respectively] but only sICAM-1 levels were independently associated with early death, after adjusting for various confounding factors. For 10 ng/ml increase in sICAM-1 levels there was a 9% higher risk of dying. Cut-off point analysis revealed that sICAM-1 levels322 ng/ml were the optimal points that discriminated those who died from the rest of the patients.High sICAM-1 levels on admission are associated with early death in ischaemic middle-aged stroke patients suggesting a pathogenetic role of inflammation in the evolution of ischaemic stroke.

The selection of cases and controls in case–control studies is of crucial importance. In assembling a group of cases consideration must be given to the diagnostic criteria for definition of the disease, and to the source of the cases [1]. Moreover, it is preferable that the cases should be limited to those that were newly diagnosed as having the investigated disease [1]. Regarding the details about the selection of cases in our study [2] we would like to say that we enrolled 100 consecutive patients who had survived their first episode of myocardial infarction (MI) before the age of 36 years and admitted to the Coronary Care Unit of General Hospitals of Nikea and “Attikon”, between January 1996 and December 2004. All admitted patients agreed to participate in the study. Only one patient could not be interviewed due to the severity of his clinical condition and was excluded. This patient was presented with acute dyspnoea and died within 48 h from admission due to the development of cardiogenic shock. This loss was the only in-hospital death of all admitted patients with premature acute MI and is consistent with the low mortality rate that has been previously reported in this age group [3]. We did not collect information regarding the number of patients who suffered a sudden cardiac death prior to admission and originated from the catchment areas of the two hospitals. This actually limits our findings to those who admitted alive at the Cardiology clinic. Regarding the admission pattern of the two hospitals the vast

To assess the effect of simvastatin on serum levels of monocyte chemoattractant protein-1 (MCP-1), interleukin-6, tumor necrosis factor-alpha, macrophage colony stimulating factor, C-reactive protein and serum amyloid A in hypercholesterolaemic patients without coronary heart disease.Sixty consecutive hypercholesterolaemic patients were randomly assigned in a 2:1 process to 40 mg of simvastatin daily (n=40) and to hypolipidaemic only diet (n=20) for 3 months. Blood was taken at baseline and at the end of the study and analysed for lipids and inflammatory markers.From the inflammatory markers only MCP-1 was decreased significantly (217.4+/-48 versus 177+/-75 pg/ml, p0.001) after treatment with simvastatin and this reduction was independent of lipid changes.Simvastatin significantly decreases only MCP-1 levels in hypercholesterolaemic patients suggesting that this molecule is probably a sensitive marker to detect the anti-inflammatory effect of simvastatin in blood.

The objective of this study was to determine the effect of alpha-linolenic acid (ALA) supplementation on blood lipids and inflammatory markers, in relation to apolipoprotein (apo) E genotype. The diets of 50 dyslipidemic male patients were supplemented with 15 mL of flaxseed oil per day for 12 weeks. Retrospectively, 3 apo E genotype variants were found (epsilon2/epsilon3, n=7; epsilon3/epsilon3, n=33; epsilon3/epsilon4, n=10). No significant differences were found among apo E genotypes in any variables at baseline. ALA supplementation produced a small but significant decrease in high-density lipoprotein cholesterol (from 1.12 to 1.08 mmol/L, 43 to 42 mg/dL; p=0.008) and apo A-I levels (from 1.28 to 1.24 g/L, p=0.036) in the epsilon3/epsilon3 homozygotes. In addition, ALA supplementation resulted in a significant decrease in the serum concentration of serum amyloid A (SAA) (p=0.014), C-reactive protein (CRP) (p=0.013), macrophage colony-stimulating factor (MCSF) (p0.001), and interleukin (IL)-6 (p=0.028). Serum SAA and MCSF were also significantly decreased in the epsilon3/epsilon4 group (p=0.005 and p=0.017, respectively). In contrast, ALA produced no effects on any of the inflammatory markers in the epsilon2/epsilon3 group. ALA may have beneficial effects on inflammation in dyslipidemic carriers of the apo epsilon3/epsilon3 and epsilon3/epsilon4 genotypes, but not in carriers of the epsilon2 allele.

Depression has been reported to be an independent risk factor for coronary heart disease (CHD). We investigated the association of depressive symptoms with lipids and coagulation factors in young individuals free of CHD.We recruited 1073 young healthy individuals candidates for military academies (mean age=18.4+/-0.8 years, males 762) in whom the presence of depressive symptoms was assessed by using the depression scale of Minnesota Multiphasic Personality Inventory test. Total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, lipoprotein (a), fibrinogen, factors VII, VIII and X were measured.The depression score ranged from 22 to 90. The participants were divided into quartiles according to the depression score. Three hundred twenty-two subjects were classified in the upper quartile (score48) and 269 in the lower quartile (score37) of the depression score. Factor VII (102.95+/-24 versus 98.5+/-20%) and X levels (92+/-11 versus 89.7+/-10%) were significantly higher in individuals in the upper quartile compared to the lower quartile of the depression score. In a logistic regression model with factor VII as dependent variable (upper versus lower quartile) and depression score, age, gender, body mass index, exercise and smoking as predictor variables, depression was an independent predictor of factor VII levels with an adjusted odds ratio for high levels of factor VII of 1.05 (95% confidence interval 1.008-1.09, p=0.01). Factor VII levels were associated with triglycerides (r=0.21, p=0.001) while factor X with triglycerides (r=0.22, p0.001) and cholesterol levels (r=0.12, p0.001).Depressed mood is associated with a hypercoagulant profile as it is expressed by the higher levels of coagulation factors VII and X. This might partially explain the higher propensity for CHD of people with depressive symptoms.

Background: Several studies have shown that non-high density lipoprotein (HDL) cholesterol is a strong and independent predictor of cardiovascular events. We investigated whether non-HDL cholesterol can discriminate young individuals with myocardial infarction (MI) from age- and sex-matched controls. Methods: We conducted a case–control study which included 100 consecutive patients who had survived their first MI before the age of 36 years and 100 age- and sex-matched healthy controls without a history of cardiovascular disease. Cardiovascular risk factors were reported and fasting lipids and apolipoproteins were measured. Results: Patients with premature MI had significantly higher levels of total cholesterol, low density lipoprotein cholesterol, triglycerides, apolipoprotein B, lipoprotein (a) and non-HDL cholesterol and significantly lower levels of HDL cholesterol and apolipoprotein A. Multivariate logistic regression analysis showed that for every 10mg/dl increase in non-HDL cholesterol levels, the odds of having a MI were increased by 34% after controlling for age, sex, body mass index, presence of hypertension, diabetes and smoking habits. Moreover, participants in the highest tertile of non-HDL cholesterol levels had 28-fold higher odds for having a MI (95% confidence interval, 7.5–104.1), compared to those in the lowest tertile. Finally, discriminant analysis showed that non-HDL cholesterol ( λ -Wilks=0.68) was the strongest discriminator for MI among all studied risk factors while smoking ( λ -Wilks=0.80) was the strongest discriminator for MI among the non-lipid risk factors. Conclusions: Our study suggests that among conventional lipid and non-lipid risk factors non-HDL cholesterol is the best discriminator to predict the presence of MI in individuals under the age of 36 years.

Background Despite the detrimental effects of smoking on the cardiovascular system, a significant number of patients with coronary heart disease continue to smoke. We aimed to record compliance to medication and attitude towards recommended lifestyle changes in patients who suffered from myocardial infarction (MI) and continued to smoke after the coronary event. Methods A total of 1011 consecutive patients ( 6 months) were recruited during the period 2000–2003 from the outpatient cardiology clinic of a district general hospital. All patients were interviewed and blood was taken for lipid measurements. Glycosylated haemoglobin (HbA 1 c ) was also measured in all diabetics. Results Three hundred and twenty-nine (32.5%) patients reported smoking at interview, while 338 (33.5%) were ex-smokers of whom 278 (45.8% of all smokers) had quit smoking after MI and 344 (34%) had never smoked. Persistent smokers had significantly lower high-density lipoprotein cholesterol levels than nonsmokers (1.03±0.28 vs. 1.09±0.29 mmol/l, p =0.001). Persistent smokers with diabetes had poorer glycaemic control than nonsmoker diabetic patients as indicated by HbA 1c levels (8±1.7% vs. 7.2±1.3%, p =0.001). Fewer persistent smokers were taking hypolipidaemic drugs than nonsmokers (31% vs. 40.3%, p =0.005). Finally, persistent smokers were less frequently performing regular exercise than nonsmokers (42% vs. 51%, p =0.008). Conclusions Patients who remain smokers after MI have a more negative attitude towards health aspects, are less compliant with their medications, and therefore constitute a high-risk subgroup, which requires special attention and should be professionally encouraged and supported to stop smoking.

To assess the in-hospital prognostic value of cellular adhesion molecules (CAMs), the levels of soluble CAMs were measured at admission in 114 patients with severe unstable angina. Patients with an eventful in-hospital course (death, nonfatal acute myocardial infarction, and recurrence of angina) had higher levels of soluble vascular cell adhesion molecule-1 than those without events (p = 0.01); this association was independent of classic risk factors and C-reactive protein.