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Aims Streptococcus pneumoniaeis the most common cause of community-acquired pneumonia (CAP) and CAP-related mortality in adults. Pneumococcal vaccination (PV) could protect subjects from cardiovascular events by reducing pneumonia severity or even preventing it. We sought to determine the ability of PV to protect from the risk of cardiovascular events.Methods and results A comprehensive search of electronic databases was conducted up to March 2014. Cohort studies that reported relative risk (RR) estimates with 95% confidence intervals (CI) were included. Eleven studies were included (332,267 participants, mean follow-up 20.1 months). The pooled RRs for cardiovascular events and cardiovascular mortality were 0.86 (95% CI: 0.76–0.97) and 0.92 (95% CI: 0.86–0.98; fixed-effects), respectively, for subjects with PV versus without PV. Protective ability was more prominent in high cardiovascular risk populations and with older age. The protective role of PV was attenuated after 1 year (RR: 0.72; 95% CI: 0.59–0.88 vs RR: 1.03; 95% CI: 0.93–1.14; p= 0.002, for follow-up >1 year vs ≤1 year, respectively). It also increased as the presence of cardiovascular and pulmonary disease increased. Regarding myocardial infarction (MI) and cerebrovascular events, the protective role of PV was statistically significant only in the elderly (RR: 0.90; 95% CI: 0.817–0.999; fixed-effects and RR: 0.86; 95% CI: 0.75–0.99, respectively).Conclusion PV is associated with decreased risk of cardiovascular events and mortality. This protective effect increases at older age and in high cardiovascular risk subjects and decreases as the time elapses from PV. PV decreases the risk of MI and cerebrovascular events in the elderly.

Erectile dysfunction (ED) carries an independent risk for cardiovascular (CV) events. We conducted a meta-analysis of all longitudinal studies for determining the ability of ED to predict risk of clinical events and to dissect factors influencing this ability.

Objective: The aim of this work was to investigate the association between consumption of dairy products and levels of various inflammatory markers among adults with no evidence of cardiovascular or other chronic disease.Methods: The ATTICA study is a cross-sectional survey that enrolled 1514 men (18–87 years old) and 1528 women (18–89 years old) from the Attica region in Greece. Fasting blood samples were collected and dietary habits (including consumption of dairy products [i.e., milk, cheese, and yogurt]) were evaluated using a validated food frequency questionnaire.Results: We observed that C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) levels of individuals consuming between 11 and 14 servings of dairy products per week were almost 16%, 5%, and 12% lower, respectively, than in those consuming fewer than 8 servings (p< 0.05), while those consuming more than 14 servings per week had 29%, 9%, and 20% lower levels of CRP, IL-6, and TNF-α, respectively (p< 0.01), even after adjustments were made for age, gender, smoking, physical activity, body mass, dietary habits, and other potential confounders.Conclusion: We identified an inverse association between dairy products consumption and levels of various inflammatory markers among healthy adults. Additional clinical trials are needed to refute or confirm our findings.

Wave reflections are implicated increasingly in clinical research.

One of the most common causes of drug withdrawal from the market is the prolongation of the QT interval associated with polymorphic ventricular tachycardia or torsade de pointes (TdP) that can degenerate into ventricular fibrillation and sudden cardiac death. Cardiac and non-cardiac drugs prolong the QT interval and cause TdP by blocking cardiac K+ channels in general, and selectively blocking the rapidly activating delayed rectifier channel IKr. Co-assembly of HERG (human-ether-a-go-go-related gene) alpha-subunits and MiRP1 (MinK-related peptide 1) beta-subunits recapitulate the behavior of native human IKr, and the majority of mutations of HERG and MiRP1 decrease the repolarizing current, delay ventricular repolarization and prolong the QT. Thus, drug-induced QT prolongation and TdP might represent an iatrogenic reproduction of the congenital long-QT syndrome (LQTS). Current evidence suggests that 5 to 10% of persons in whom TdP develops on exposure to QT-interval prolonging drugs harbor mutations associated with the LQTS and can therefore be viewed as having a subclinical form of the congenital syndrome. This clinical observation is entirely consistent with the concept of reduced repolarization reserve arising from a mutation in an ion-channel gene, which predisposes the carrier to drug-induced TdP. This review centers on the possible molecular mechanisms underlying drug-induced QT prolongation and TdP, the description of specific drugs and risk factors facilitating the development of TdP, and the recommendations for preventing and treating this potentially fatal arrhythmia.

This study investigated in prepubertal obese children (POC), compared with prepubertal lean children (PLC), a possible relation among plasma total homocysteine (tHcy)—an independent risk factor for future atherosclerosis—and MCP-1 and RANTES, two circulating chemokines inducing leukocyte transendothelial migration (TEM), implicated in the initial stages of the inflammatory part of the atherosclerotic process. Seventy-two POC were evaluated for circulating tHcy, MCP-1, and RANTES, and compared with 42 healthy PLC. The mean adjusted (for age, sex as well as log10total insulin, vitB12, folate, total cholesterol, HDL cholesterol, log10triglycerides, and log10glucose levels) differences in tHcy, MCP-1, and RANTES levels between PLC and POC were all significant [1.16 nmol/mL (P= 0.03), 26.6 pg/mL (P= 0.02), and 52.9 pg/mL (P= 0.03), respectively]. In PLC, but not in POC, tHcy levels were negatively associated with both circulating MCP-1 (B = −1.68, P= 0.007) and RANTES (B = −1.16, P= 0.01) after adjusting for age, sex, BMI, as well as log10total insulin, vitB12, folate, total cholesterol, HDL cholesterol, log10triglycerides, and log10glucose levels. In conclusion, in POC there is a lack, in contrast to PLC, of a possibly autoregulatory, negative association of elevated tHcy levels to increased MCP-1 and RANTES levels. This could contribute to future, homocysteine-induced atherosclerosis.

Objective.The aim of this study is to evaluate the effect of recent depressive episodes on coronary risk, taking into account the presence of several cardiovascular risk factors and various lifestyles, and social conditions that aggregate in the Greek population.Methods and results.CARDIO2000 is a matched case–control study consisting of 750 patients with a first event of acute coronary syndrome and 778 cardiovascular disease-free hospitalized subjects, randomly and stratified selected from several Greek regions. Assessment of depressive symptoms, during the past month, was based on the CES-D Scale (Radloff S, 1977). 158 (21%) coronary patients and 74 (9%) controls had short-term depressive symptoms (P < 0.001). A recent depressive episode increases coronary risk by 12%, after adjusting for several confounders, while the previous outcome seems to differ significantly between sexes (OR-men = 1.09 vs. OR-women = 1.19, P < 0.01). The effect of the interaction between depression and various components of social class (education, occupation, income) increases the coronary risk from 55% to 132%, while the interaction with marital status increases the previous risk by 167%, in divorced/widowed men, and by 123%, in women. Also, significant additive effects were observed between depression and smoking (25% increased coronary risk per pack-year), alcohol consumption (+97%), physical inactivity (+137%) and obesity (+127%).Conclusion.This study showed the moderate effect of recent depression on the risk of developing non-fatal acute coronary syndromes in the investigated population.Also, sex differences and the additional effect of the interactions between short-term depressive episodes and several emerging or established cardiovascular risk factors occurred.

Retrograde nontransseptal balloon mitral valvuloplasty (RNBMV) is a transarterial technique of mitral valvuloplasty, developed with the aim to avoid complications associated with transseptal catheterization. Between April 1988 and December 1999, RNBMV has been attempted in 393 patients with symptomatic mitral stenosis (aged 44 ± 11 years, 322 women, mean echocardiographic score 7.7 ± 1.9) at the University of Athens, Greece. The procedure was completed in 392 cases. Technical success (gain in mitral valve area ≥ 50% with final mitral valve area ≥ 1.5 cm2, and absence of postprocedural mitral regurgitation grade > 2+) was achieved in 344 (87.5%) patients. Unfavorable predictors for immediate outcome included the echocardiographic score (P < 0.001). male gender (P = 0.005), and preprocedural mitral regurgitation (P = 0.003). Complications included death (0.3%), severe mitral regurgitation (3.1%), and femoral artery injury (0.8%). No cases of cardiac peqoration or tamponade have occurred with RNBMV. Patients with a successful immediate outcome were followed clinically for 4.8 ± 2.8 years (maximum 12 years). Event‐free (freedom from cardiac death, mitral valve replacement, redo valvuloplasty, and recurrence of NYHA Class > II) survival rates at 1, 2, 5, and 12 years post‐RNBMV were 99.7 ± 0.3%, 96.1 ± 1.1%, 84.7 ± 2.2%. and 67.6 ± 4.8%, respectively. The echocardiographic score (P < 0.001) and the postprocedural mitral valve area (P < 0.001) were significant independent predictors of long‐term outcome following RNBMV. Experience with RNBMV has fulfilled expectations regarding lowering of the risk of occurrence of specific cardiac complications encountered during mitral valvuloplasty, and reveals this approach as a safe and efficient alternative to the more commonly used antegrade technique.

Objectives. Our aim was to present the immediate and intermediate long-term results of the application of retrograde nontransseptal balloon mitral valvuloplasty (RNBMV) in four cooperating centers from Greece and India.

Objective: It is known that the outer layers of the thoracic aorta receive substantial blood flow through vasa vasorum. This study was undertaken to test the hypothesis that removal of vasa vasorum flow will alter the elastic properties of the ascending aorta. Methods: Distensibility of the ascending aorta was determined before and 30 min after careful removal of the periaortic fat network which contains the vasa vasorum in 10 acutely instrumented dogs (experimental group) and the results were compared with those obtained from six weight matched sham operated control dogs. Aortic distensibility was measured using the formula: distensibility=2 pulsatile changes in aortic diameter÷(diastolic aortic diameterpulse pressure). Aortic pressures were measured directly from the ascending aorta by a pressure gauge. Aortic diameters were simultaneously determined by an elastic air filled ring connected to a transducer. The efficacy of the technique for the interruption of vasa vasorum blood supply to the aortic wall was proved in six additional animals by histology of transverse blocks of aortic wall from the area of interest. Histology was performed before vasa vasorum removal in two animals, 30 min after vasa vasorum removal in another two, and 15 d after vasa vasorum removal in the remainder. Results: At baseline, there was no difference in the measured variables between the two groups. Aortic distensibility decreased significantly in the experimental group after vasa vasorum removal by 0.90(SEM 0.17) 10–6·cm2·dyn–1 (p<0.001), while it remained unchanged in the control group during the experiment. Complete removal of vasa vasorum of the ascending aorta was found in experimental group animals which were killed 30 min after operation, while ischaemic medial necrosis was observed in those killed 15 d after operation. Conclusions: Vasa vasorum removal led to an acute decrease in the distensibility of the ascending aorta. Lack of blood supply to the outer part of the aortic wall is most likely to have accounted for these findings. Cardiovascular Research 1993;27:951-956