Moderate alcohol consumption by apparently healthy people or patients with cardiovascular disease is associated with lower vascular and all-cause mortality. These findings were extended by two new meta-analyses aimed at assessing the relationship of alcohol drinking with vascular and total mortality in a large series of patients, including not only patients with a history of CVD but also diabetic and hypertensive patients. Two meta-analyses were performed: the first one considered 17 studies reporting secondary risk of vascular mortality; the second one included 14 studies reporting total mortality. The meta-analysis on vascular mortality and alcohol intake showed as an ‘L-shaped’ curve, indicating a protective effect (average 38%) that was maximal at about 40 and remained still significant up to 60 grams/day. J-shaped pooled curves were observed in the meta-analysis on mortality from any cause and in subgroups defined according to different types of patients or characteristics of the studies. While confirming the hazards of excess drinking, our findings indicate that in patients at high cardiovascular risk, low to moderate alcohol consumption is significantly associated with a reduced incidence of secondary non-fatal and/or fatal vascular events and all-cause mortality.
Abstract Background Depression has been associated with increased hospitalization and mortality risk, especially for cardiovascular causes. We previously found a composite circulating inflammation score (INFLA-score) to explain part of this link, although the role of its component and of depressive symptoms domains in this relationship is unexplored. Methods In an Italian population cohort (N = 13,191; age≥35 years; 51.7 % women; 4,856 hospitalizations and 471 deaths, median follow-up 7.28/8.24 years), we estimated the proportion of association explained by C-reactive protein levels (CRP), platelet count, granulocyte-to-lymphocyte ratio (GLR) and white blood cell counts (WBC), in multivariable Cox regressions modelling first hospitalization/mortality for all and cardiovascular (CVD), ischemic heart (IHD) and cerebrovascular disease (CeVD) causes vs depression severity based on an alternative validated version of PHQ-9. We also estimated the proportion of association explained by INFLA-score in the associations of polychoric factors tagging somatic and cognitive depressive symptoms with clinical risks. Results In models adjusted for age, sex and education, significant proportions of the positive influence of depression on clinical risks were explained by CRP (4.8% on IHD hospitalizations), GLR (11% on all-cause mortality) and WBC (24% on IHD/CeVD hospitalizations). Stable associations of somatic but not of cognitive depressive symptoms were observed with increased hospitalization risk (+16% for all causes, +14% for CVD causes), with INFLA-score again explaining small but significant proportions of these associations (2.5% for all causes, 8.6% for IHD causes). Conclusions These findings suggest a prominent explanatory role of leukocytes in the link between depression and clinical (especially CVD) risks, and highlight the importance of inflammation in the influence of somatic depressive symptoms. Therefore, acting on these factors may reduce clinical risks associated with depression. Key messages
The potential benefit of the aspirin/warfarin association as an antithrombotic treatment has been matter of debate in view of the major haemorrhagic effect reported with this drug combination. We have tested the effect of such association in a model of venous thrombosis already shown to be prevented by a fully anticoagulant schedule of warfarin. CD-COBS male rats were treated for three days with either warfarin (0.1 mg/kg i.v. once a day) or salicylate (175 mg/kg i.p. twice a day) or their combination (W+S). Systemic anticoagulation (thrombotest), template bleeaing time and occurrence of experimental venous thrombosis (ligature of inferior vena cava) were followed. Treatment with W or S alone did not affect template bleeding time, whereas the association (W+S) did (320+35 sec versus 120± 10 sec in the control group, p<0.01). Thrombotest was only slightly prolonged by single drug treatment (W= 43%, S=48% versus 90% of controls) but strongly prolonged in the association group (S+W=5%; p<0.001). The mechanism of this combined effect may be multifaceted; competition of both drugs for protein binding and the anticoagulant effect of salicylate itself could contribute. In any case, neither the incidence nor the weight of the thrombus were reduced by any drug treatment. Thus, W+S, in contrast to W alone (<5% thrombotest), was unable to prevent or reduce venous thrombosis, while prolonging bleeding time. Bleeding complications reported in clinical trials by the association of W and aspirin might not be solely due to the antiplatelet effect of aspirin.
The effect(s) of caffeine Intake on cardiovascular functions are still a matter of debate. We have considered here the level of the prothrombin complex activity as a parameter of blood coagulability following caffeine Intake. The activity of the four vitamin K-dependent clotting factors (II, VII, IX and X) was tested after acute and chronic administration of high doses of caffeine. With a single administration of 50 mg/kg caffeine a statistically significant increase in the activity of factors VII, IX and X was observed. The increase lasted for 4, 3 and 2 days respectively. Factor II was not affected by caffeine administration. The same effect was observed during chronic administration (50 mg/kg/day). With a lower dose of caffeine during chronic administration (5 mg/kg/day) only factor X showed a significant increase. A single dose of caffeine (50 mg/kg) given to animals 24h before-a dose of warfarin (0.4 mg/kg i.v.) markedly reduced the anticoagulant effect of warfarin, as measured by the thrombotest. During the latter experiment we measured also the rate of synthesis (Rsyn) of the prothrombin complex activity. Rsyn, during warfarin treatment, was significantly higher in the rats pretreated with caffeine than In controls. γ-Carboxylase activity in rat liver mlcrosomes was measured after administration of 50 mg/kg of caffeine as a single dose. The Incorporation of 14CO2 in the endogenous precursor was higher in the rats pretreated with caffeine than In controls (84,905 cpm/mg of protein versus 59,826 cpm/mg of proteins); this difference, however, was not statistically significant. In conclusion, caffeine jntake may affect the clotting system mainly by stimulating the synthesis of factors of the prothrombin complex and, as a consequence, their response to coumarin anticoagulation.
Summary T-wave axis deviation (TDev) may help identifying subjects at risk for major cardiac events and mortality, but the pathogenesis of TDev is not well established; in particular, the possible association between TDev and inflammation is unexplored and unknown. We aimed at investigating the association between low-grade inflammation and TDev abnormalities by conducting a cross-sectional analysis on 17,507 subjects apparently free from coronary heart and haematological diseases enrolled in the MOLI-SANI study. TDev was measured from a standard 12-lead resting electrocardiogram. High sensitivity (Hs) C-reactive protein (CRP), leukocyte (WBC) and platelet counts, neutrophil or granulocyte to lymphocyte ratios were used as markers of inflammation. In multivariable model subjects reporting high CRP levels had higher odds of having borderline and abnormal TDev (OR=1.70; 95 %CI: 1.53–1.90 and OR=1.72; 95 %CI: 1.23–2.41, respectively); the association was still significant, although reduced, after controlling for body mass index (OR=1.17; 95 %CI: 1.05–1.32, for borderline and OR=1.46; 95 %CI: 1.03–2.08, for abnormal). Similarly, higher neutrophil or granulocyte to lymphocyte ratios were associated with increased odds of having abnormal TDev. Neither platelet nor leukocyte counts were associated with abnormal TDev. The relationship between CRP with TDev abnormalities was significantly stronger in men, in non- obese or normotensive individuals, and in those without metabolic syndrome. In conclusion, C-reactive protein and some cellular biomarkers of inflammation such as granulocyte or neutrophil to lymphocyte ratios were independently associated with abnormal TDev, especially in subjects at low CVD risk. These results suggest that a low-grade inflammation likely contributes to the pathogenesis of T- wave axis deviation.
Underweight, overweight, and obesity in childhood and adolescence are associated with adverse health consequences throughout the life-course. Our aim was to estimate worldwide trends in mean body-mass index (BMI) and a comprehensive set of BMI categories that cover underweight to obesity in children and adolescents, and to compare trends with those of adults.We pooled 2416 population-based studies with measurements of height and weight on 128·9 million participants aged 5 years and older, including 31·5 million aged 5-19 years. We used a Bayesian hierarchical model to estimate trends from 1975 to 2016 in 200 countries for mean BMI and for prevalence of BMI in the following categories for children and adolescents aged 5-19 years: more than 2 SD below the median of the WHO growth reference for children and adolescents (referred to as moderate and severe underweight hereafter), 2 SD to more than 1 SD below the median (mild underweight), 1 SD below the median to 1 SD above the median (healthy weight), more than 1 SD to 2 SD above the median (overweight but not obese), and more than 2 SD above the median (obesity).Regional change in age-standardised mean BMI in girls from 1975 to 2016 ranged from virtually no change (-0·01 kg/m2 per decade; 95% credible interval -0·42 to 0·39, posterior probability [PP] of the observed decrease being a true decrease=0·5098) in eastern Europe to an increase of 1·00 kg/m2 per decade (0·69-1·35, PP>0·9999) in central Latin America and an increase of 0·95 kg/m2 per decade (0·64-1·25, PP>0·9999) in Polynesia and Micronesia. The range for boys was from a non-significant increase of 0·09 kg/m2 per decade (-0·33 to 0·49, PP=0·6926) in eastern Europe to an increase of 0·77 kg/m2 per decade (0·50-1·06, PP>0·9999) in Polynesia and Micronesia. Trends in mean BMI have recently flattened in northwestern Europe and the high-income English-speaking and Asia-Pacific regions for both sexes, southwestern Europe for boys, and central and Andean Latin America for girls. By contrast, the rise in BMI has accelerated in east and south Asia for both sexes, and southeast Asia for boys. Global age-standardised prevalence of obesity increased from 0·7% (0·4-1·2) in 1975 to 5·6% (4·8-6·5) in 2016 in girls, and from 0·9% (0·5-1·3) in 1975 to 7·8% (6·7-9·1) in 2016 in boys; the prevalence of moderate and severe underweight decreased from 9·2% (6·0-12·9) in 1975 to 8·4% (6·8-10·1) in 2016 in girls and from 14·8% (10·4-19·5) in 1975 to 12·4% (10·3-14·5) in 2016 in boys. Prevalence of moderate and severe underweight was highest in India, at 22·7% (16·7-29·6) among girls and 30·7% (23·5-38·0) among boys. Prevalence of obesity was more than 30% in girls in Nauru, the Cook Islands, and Palau; and boys in the Cook Islands, Nauru, Palau, Niue, and American Samoa in 2016. Prevalence of obesity was about 20% or more in several countries in Polynesia and Micronesia, the Middle East and north Africa, the Caribbean, and the USA. In 2016, 75 (44-117) million girls and 117 (70-178) million boys worldwide were moderately or severely underweight. In the same year, 50 (24-89) million girls and 74 (39-125) million boys worldwide were obese.The rising trends in children's and adolescents' BMI have plateaued in many high-income countries, albeit at high levels, but have accelerated in parts of Asia, with trends no longer correlated with those of adults.Wellcome Trust, AstraZeneca Young Health Programme.
D-dimer is a high molecular weight fibrinogen derivative resulting from the cleavage of cross-linked fibrin that reflects both thrombin production and/or activation of fibrinolysis.[1][1] Elevated D-dimer levels have been reportedly associated with increased risk of coronary artery disease[2][2],[3
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