细颗粒物暴露与心血管疾病队列研究进展

细颗粒物(PM2.5)的暴露与心血管疾病具有较强的相关性,是心血管疾病发生和加重过程中可控的危险因素。PM2.5来源广泛,组成成分复杂,可通过多种生物学机制引起心血管疾病的发生、发展。本文主要综述国内外基于人群的队列研究,评价PM2.5对心血管疾病的慢性效应,并总结了PM2.5健康危害的干预研究,并提出了我国探索PM2.5对心血管疾病慢性效应研究的局限性,为心血管疾病防治提供一些参考和依据。     

Low β-carotene concentrations increase the risk of cardiovascular disease mortality among Finnish men with risk factors

Background & aimsHealthy diet rich in fruits and vegetables is an important factor in prevention of cardiovascular diseases (CVD). Some previous epidemiological studies have suggested that dietary and serum carotenoids are associated with decreased CVD mortality, but the results have been inconsistent. We assessed relations between the concentrations of serum carotenoids and CVD mortality among Eastern Finnish men.Methods & resultsThe study population consisted of 1031 Eastern Finnish men aged 46–65 years in the Kuopio Ischaemic Heart Disease Risk Factor (KIHD) cohort. Subjects were classified quartiles according to concentrations of carotenoids and subgroups according to risk factors. Hazard ratios of serum lycopene, α-carotene and β-carotene were estimated by the Cox proportional hazard model after adjusting for potential confounding factors. During the median 15.9-year follow-up, 122 deaths from CVDs, were identified among the cohort subjects. Low serum concentrations of β-carotene were strongly related to an increased CVD mortality risk after adjustment for confounders. For β-carotene, the hazard ratio (95% confidence interval) for the lowest versus highest quartile was 2.23 (1.26–3.93; P = 0.006). However, the strongest risk of CVD mortality was observed among smokers with lowest levels of β-carotene (HR = 3.15, 95%, CI: 1.19–8.33; P = 0.020). Other carotenoids and the sum of carotenoids were not significantly related to increased risk of CVD mortality.ConclusionsLow concentrations of serum β-carotene concentrations may increase the risk for CVD mortality among Eastern Finnish men; thus elevated serum concentrations of β-carotene may have clinical and public health relevance.     

All-cause and cardiovascular mortality risk in U.S. adults with and without type 2 diabetes: Influence of physical activity,pharmacological treatment and glycemic control

AimsThis study determined the joint association between physical activity, pharmacotherapy, and HbA1c control on all-cause and cardiovascular disease (CVD) mortality risk in adults with and without type 2 diabetes (T2D).Methods12,060 adults from NHANES III and NHANES continuous (1999–2002) surveys were used. Cox proportional hazards analyses were included to estimate mortality risk according to physical activity, pharmacotherapy, and glycemic control (HbA1c < 7.0%) status, with physically active, treated and controlled (goal situation) as the referent.ResultsCompared to the referent, adults with T2D who were uncontrolled, or controlled but physically inactive had a higher all-cause mortality risk (p < 0.05). Compared to the referent, only adults with T2D who were physically inactive had a higher CVD mortality risk, regardless of treatment or control status (p < 0.05). Normoglycemic adults had a similar all-cause and CVD mortality risk as the referent (p > 0.05).ConclusionsPhysical activity and glycemic control are both associated with lower all-cause and CVD mortality risk in adults with T2D. Adults with T2D who are physically active, pharmacologically treated, and obtain glycemic control may attain similar mortality risk as normoglycemic adults.     

Differences in cardiovascular mortality in smokers, past-smokers and non-smokers: Findings from the FRENA registry

BackgroundThe influence of smoking on outcome in patients with coronary artery disease (CAD) is controversial. Even less is known about its influence in patients with cerebrovascular (CVD), or peripheral artery (PAD) disease.Patients and methodsFRENA is an ongoing, observational registry of consecutive outpatients with symptomatic CAD, CVD, or PAD. We reviewed their cardiovascular mortality according to smoking status.ResultsAs of May 2008, 2501 patients had been enrolled in FRENA. Of these, 439 (18%) were current smokers, 1086 (43%) past-smokers, 976 (39%) had never smoked. Current- and past-smokers were 10 years younger, more often males, and more likely to have chronic lung disease, but had diabetes, hypertension, heart failure, or renal insufficiency less often than non-smokers. Over a mean follow-up of 14 months, 123 patients died (cardiovascular death, 68). On univariate analysis, current smokers had a significantly lower rate of cardiovascular death: 1.1 (95% CI: 0.4–2.4) per 100 patient-years in current smokers; 1.9 (95% CI: 1.2–2.8) in past-smokers; 3.5 (95% CI: 2.5–4.7) in non-smokers, with no differences between patients with CAD, CVD or PAD. Mean age at cardiovascular death was 82 ± 6.4; 70 ± 9.9 and 67 ± 15 years, respectively. On multivariate analysis, smoking status was not independently associated with a lower risk for cardiovascular death.ConclusionsCurrent and past-smokers with CAD, CVD or PAD had a less than half cardiovascular mortality than those who never smoked, but this may be explained by the confounding effect of additional variables. They died over 10 years younger than non-smokers.     

Efficacy of folic acid supplementation in cardiovascular disease prevention: An updated meta-analysis of randomized controlled trials

BackgroundIn observational studies, lower serum homocysteine levels are associated with a lower incidence of cardiovascular disease (CVD). However, individual randomized controlled trials (RCTs) have yielded mixed findings regarding the efficacy of therapeutic homocysteine in lowering cardiovascular risk. Our aim was to perform an updated meta-analysis of relevant RCTs to assess the efficacy of folic acid supplementation in the prevention of CVD, coronary heart disease (CHD), and stroke.MethodsWe performed systematic search to identify RCTs reported at least one of the CVD, CHD, or stroke as outcomes. Relative risk (RR) with 95% confidence interval was used as a measure of the association between folic acid supplementation and risk of CVD, CHD, stroke, and all-cause mortality. The analysis was further stratified by factors that could affect the treatment effects.ResultsThe systematic search identified 26 RCTs enrolling 58,804 participants. Pooling the RRs showed that folic acid supplementation was not associated with any significant change in the risk of CVD (RR 0.98, 0.95 to 1.02; p = 0.36), CHD (RR 1.03, 0.98 to 1.08; p = 0.23), and all-cause mortality (RR 1.00, 0.96 to 1.04; p = 0.92), but was linked to a decreasing trend in stroke risk (RR 0.93, 0.86 to 1.00; p = 0.05). In stratified analyses, the only heterogeneity was found for stroke risk reduction among groups with (RR 1.07, 0.92 to 1.25) vs. without (RR 0.88, 0.81 to 0.96) mandatory grain fortification (P for heterogeneity = 0.03).ConclusionsThis meta-analysis suggests that there might be a potentially modest benefit of folic acid supplementation in stroke prevention.     

Particulate Matter Air Pollution and Atherosclerosis

Particulate matter (PM) air pollution less than 2.5 μm in diameter (PM_2.5), which is now an all-pervading element of modern-day society, is associated with heightened cardiovascular morbidity and mortality. Not only can short-term PM_2.5 exposure trigger acute cardiovascular events, but longer-term exposure over years augments cardiovascular risk to an even greater extent. One biological mechanism capable of explaining this observation is that chronic exposure may promote the progression and vulnerability of atherosclerotic plaques. Indeed, recent epidemiologic studies have demonstrated an association between ambient PM_2.5 exposure and the presence or extent of atherosclerosis in humans. Several animal experiments have provided corroborating evidence that chronic exposures in fact do enhance the progression and perhaps vulnerability of atherosclerotic lesions. Due to the billions of people continually exposed to PM_2.5, the long-term pro-atherosclerotic effects of this ubiquitous air pollutant are likely to be of enormous and growing global public health importance.     

A cross sectional study comparing traditional risk factors with N-terminal pro-BNP in high risk groups for cardiovascular disease in Trinidad,West Indies

ObjectiveCardiovascular disease is a leading cause of morbidity and mortality worldwide and traditional risk factors for cardiovascular disease have been well-elaborated. In recent years, the use of biomarkers has emerged for identifying individuals at high risk with the aim of earlier identification and risk mitigation. Among the most promising non-traditional markers are BNP and NT-proBNP. This study aims to compare whether serum NT-proBNP co-segregates with traditional cardiovascular risk factors in elderly type 2 diabetic and non diabetic in a population with high prevalence of CVD.MethodsThis study utilized a cross sectional design. Blood samples collected were analyzed for hs-CRP, total serum cholesterol, triglyceride, LDL cholesterol, HDL cholesterol, fasting glucose, insulin, and NT-proBNP.ResultsMean serum NT-proBNP levels were significantly elevated in diabetics (X = 125.5 ± 49.7) compared to non diabetics (X = 64.3 ± 34.6). In diabetics, NT-proBNP demonstrated statistically significant spearman's coefficients with respect to systolic blood pressure, triglyceride, hs-CRP, fasting glucose and insulin. Among non diabetics there was no relationship between NT-proBNP, blood pressure and insulin. Multivariate logistic regression revealed relation between diabetics; elevated NT-proBNP, blood pressure, triglyceride, CRP, fasting glucose and plasma insulin compared with non diabetics where NT-proBNP showed significant relation only to diastolic blood pressure. Diabetics showed significant correlation with elevated NT-proBNP and traditional risk factors (hypertension, diabetes, dyslipidemia and elevated hs-CRP) as compared with non diabetics.ConclusionsNT-proBNP co-segregates with traditional risk factors for CVD among elderly diabetics and may be a useful additional screening test for those at risk for CVD.     

Pollution atmosphérique et troubles du rythme cardiaque : une étude rétrospective

IntroductionAccording to many studies, exposure to air pollution increases cardiovascular morbidity and mortality. It has also been shown that the frequency of heart rhythm disorders in Region wallonne is very high.ObjectivesThe objective of this study is to test the hypothesis of a link between rhythm disorders measured by cardiac holters and data from devices measuring the concentration of air pollutants present in ambient air.MethodologyThe health data were obtained via the Erasme hospital's cardiology center. This is a retrospective data collection over the last 2 to 5 years. The environmental data are: PM2.5, PM10, NO2, O3 and temperature. The statistical models were based on “cross-case” analyses.ResultsAn association between PM10 and the number of ESAs was observed. An increase of 10 μg/m³ of PM10 increases the number of ESAs by 20% (P = 0.040). The number of ESAs increases with age (63% more ESAs when age increases by 10 years). A history of intervention also decreases the number of ESAs (−35%), the same phenomenon is observed for pacemaker wearers (−66%). The strongest association observed between NO2 and ESA with an OR of 1.37 (P = 0.027) in the final model. No significant association was observed between the effects of air pollution and VPCs.ConclusionOur analyses resume the effects of the different pollutants on rhythm disorders, the effects adjusted for treatment and co-morbidities. They open the door to other more refined studies based on individual measurements.     

Interleukin-18 and the risk of future cardiovascular disease among initially healthy women

ObjectiveElevated levels of interleukin (IL)-18 have been implicated in the development of atherosclerosis in animals. Data in humans are less clear, and data in women are particularly scarce.Methods and resultsIn a prospective nested case–control study of initially healthy women, we measured baseline plasma IL-18 levels in 253 participants who subsequently developed cardiovascular disease (CVD) and in 253 healthy age- and smoking-matched controls. IL-18 levels were higher at baseline among those who developed CVD (274.1 pg/mL versus 233.8 pg/mL, P < 0.001), and were associated with future CVD (relative risk (RR) for highest versus lowest quartile 2.53; 95% CI, 1.47–4.35, P < 0.001). While that risk was attenuated after adjustment for traditional cardiovascular risk factors (RR 1.60; 95% CI, 0.77–3.34, P = 0.13), those with IL-18 levels at or above a threshold of the 90th percentile (442 pg/mL) remained at elevated risk after adjustment (RR 2.40; 95% CI, 1.05–5.56, P = 0.04). Levels of IL-18 above this threshold modify the fully adjusted risk of future CVD conferred by elevated levels of total cholesterol (P_interaction = 0.02).ConclusionsIn this population of apparently healthy women, IL-18 levels associate with increased risk of cardiovascular disease, but that risk is attenuated in models adjusting for traditional cardiovascular risk factors. Very high levels of IL-18 interact with hypercholesterolemia to alter CVD risk.     

Gender differences in cardiovascular risk factors among adolescents in Aseer Region,southwestern Saudi Arabia

ObjectiveThe objective of this study was to explore gender differences in the prevalence of silent and clinical apparent cardiovascular risk factors among adolescents in Aseer Region, southwestern Saudi Arabia.Materials and methodsA cross-sectional study on a stratified sample of 1869 adolescents was carried out. They were interviewed and examined for weight and height, systolic and diastolic blood pressure using standardized techniques.ResultsThe study revealed high prevalence of some potential behavioral and biological cardiovascular diseases (CVD) risk factors among adolescent males and females in the study area. Behavioral risk factors included inadequate low consumption of fruits and vegetables, physical inactivity, and smoking. Physical inactivity was significantly more prevalent among females than males (42.9% and 25.7%, respectively). Smoking was significantly more among females than males (11.8% and 1.3%, respectively). Biological risk factors found were family history of CVD, obesity and high blood pressure. Obesity was significantly prevalent among females (29.4%) compared to males (20.6%). Males had significantly more high blood pressure than females. In logistic regression analysis, being male (aOR = 2.992, 95% CI = 1.933–4.742) and obesity (aOR = 2.995, 95% CI = 2.342–3.991) were found to be significant risk factors in developing high blood pressure among adolescents in the region.ConclusionsPresence of cardiovascular risk factors among adolescents is a public health problem in the region. There is a need for a national program in the country to prevent and control cardiovascular risk factors among adolescents.     

Common polymorphism in the cannabinoid type 1 receptor gene (CNR1) is associated with microvascular complications in type 2 diabetes

Endocannabinoids exert their biological effects via interaction with G-protein coupled cannabinoid receptors CB1 and CB2. Polymorphisms in the CNR1 gene (encoding CB1 receptor) were previously found to be associated with dyslipidemia and cardiovascular diseases. We investigated a role of the polymorphism in CNR1 gene in type 2 diabetes and its complications. The study involved 667 T2DM patients and 450 healthy individuals. All subjects were genotyped for G1359A polymorphism by PCR-RFLP procedure. Genotype frequencies did not differ significantly between patients and controls. The statistically significant differences were seen between T2DM patients with diabetic nephropathy (DN) and those without it (OR for risk allele 2.84, 95% CI 2.04–3.94, p < 0.0001). There were also differences between patients with diabetic retinopathy (DR) and those without DR (OR for risk allele 1.81, 95% CI 1.30–2.53, p = 0.0005). No differences were observed in diabetic neuropathy. The A allele was more frequent in patients with coexisting cardiovascular disease (CVD) compared to patients without CVD (p = 0.0044). The novel finding of our study is the association of the G1359A polymorphism with diabetic nephropathy and diabetic retinopathy in patients with T2DM. This polymorphism was also associated with cardiovascular disease in the patient group.     

Changes in body mass index following newly diagnosed type 2 diabetes and risk of cardiovascular mortality: A cohort study of 8486 primary-care patients

AimsElevated body mass index (BMI) is associated with an increased risk of type 2 diabetes and cardiovascular disease (CVD). This study explored the association between BMI changes in the first 18 months of newly diagnosed type 2 diabetes and the risk of long-term CVD mortality.MethodsA total of 8486 patients with newly diagnosed type 2 diabetes and no previous history of CVD or cancer were identified from 84 primary-care centres in Sweden. During the first year after diagnosis, patients were grouped according to BMI change: ‘Increase’, or ≥ +1 BMI unit; ‘unchanged’, or between +1 and–1 BMI unit; and ‘decrease’, or ≤ –1 BMI unit. Associations between BMI change and CVD mortality, defined as death from stroke, myocardial infarction or sudden death, were estimated using adjusted Cox proportional hazards models (NCT 01121315).ResultsBaseline mean age was 60.0 years and mean BMI was 30.2 kg/m². Patients were followed for up to 9 years (median: 4.6 years). During the first 18 months, 53.4% had no change in their BMI, while 32.2% decreased and 14.4% increased. Compared with patients with unchanged BMI, those with an increased BMI had higher risks of CVD mortality (hazard ratio: 1.63, 95% CI: 1.11–2.39) and all-cause mortality (1.33, 1.01–1.76). BMI decreases had no association with these risks compared with unchanged BMI: 1.06 (0.76–1.48) and 1.06 (0.85–1.33), respectively.ConclusionIncreased BMI within the first 18 months of type 2 diabetes diagnosis was associated with an increased long-term risk of CVD mortality. However, BMI decrease did not lower the long-term risk of mortality.     

The association between estimated glomerular filtration rate,albuminuria, and risk of cardiovascular hospitalizations and all-cause mortality among patients with type 2 diabetes

Aims

We evaluated the simultaneous effects of all clinically recognized categories of albuminuria and estimated glomerular filtration rate (eGFR) on cardiovascular disease (CVD) and mortality

Effect of cigarette smoking on insulin resistance risk

ObjectivesSmoking is one of the main risk factors for cardiovascular disease (CVD). The mechanism(s) of the effects of smoking on CVD are not clearly understood; however, a number of atherogenic characteristics, such as insulin resistance have been reported. We aim to investigate the effects of cigarette smoking on insulin resistance and to determine the correlation between this parameter with smoking status characteristics.Study designThis study was conducted on 138 non-smokers and 162 smokers aged respectively 35.6 ± 16.0 and 38.5 ± 21.9 years. All subjects are not diabetic.MethodsFasting glucose was determined by enzymatic methods and insulin by chemiluminescence method. Insulin resistance (IR) was estimated using the Homeostasis Model of Assessment equation: HOMA-IR = [fasting insulin (mU/L) × fasting glucose (mmol/L)]/22.5. IR was defined as the upper quartile of HOMA-IR. Values above 2.5 were taken as abnormal and reflect insulin resistance.ResultsCompared to non-smokers, smokers had significantly higher levels of fasting glucose, fasting insulin and HOMA-IR index. These associations remained significant after adjustment for confounding factors (age, gender, BMI and alcohol consumption). A statistically significant association was noted between the smoking status parameters, including both the number of cigarettes smoked/day and the duration of smoking, and fasting insulin levels as well for HOMA-IR index. Among smokers, we noted a positive correlation between HOMA-IR index and both plasma thiocyanates and urinary cotinine.ConclusionOur results show that smokers have a high risk to developing an insulin resistance and hyperinsulinemia, compared with a matched group of non-smokers, and may help to explain the high risk of cardiovascular diseases in smokers.     

Normal weight obese (NWO) women: an evaluation of a candidate new syndrome

Background and aimsObesity, an independent risk factor for cardiovascular disease (CVD), has been associated with the early development of coronary atherosclerosis in adolescents and young men. A subset of metabolically obese but normal weight individuals was identified, with potentially increased risks for development of the metabolic syndrome despite their normal body mass index. We determined the relationship among body fat distribution and selected CVD risk factors to distinguish normal weight obese from controls with normal metabolic profiles.Methods and resultsWe analysed anthropometric variables, body composition by DXA, RMR by indirect calorimetry and bioumoral variables of 74 clinically healthy Caucasian Italian women. Significant differences were observed in the biochemical HDL-chol values between NWO and controls and pre-obese-obese. Significant correlations were found among cardiovascular risk indexes, LEAN of the right part of the trunk and TC/HDL (R = −0.69, p < 0.001) and LDL/HDL (R = −0.72, p < 0.001), and LEAN and RMR (R = 0.44, p = 0.022) of NWO women.ConclusionsIn normal weight obese women the cardiovascular risk indexes are related to metabolic variables and to body fat mass distribution. NWO individuals showed a relationship between the decrease in LEAN of the left leg and an increase in CVD risk factors. We suggest that LEAN distribution seems to be a potential predictor of CVD.     

The relationship between resting heart rate and incidence and progression of coronary artery calcification: The multi-ethnic study of atherosclerosis (MESA)

ObjectiveElevated resting heart rate has been independently associated with cardiovascular and all-cause mortality. The pathophysiological mechanisms by which this increased risk occurs are unclear. We hypothesized that elevated resting heart rate will be associated with increased development of atherosclerosis, as assessed by the incidence and progression of coronary artery calcium (CAC).MethodsThe Multi-Ethnic Study of Atherosclerosis is a prospective cohort study of participants free of clinical cardiovascular disease at entry. Among persons without CAC at baseline, the association between increasing clinical categories of heart rate (<60, 61–70, 71–80, >80 bpm) and CAC incidence was assessed by relative risk regression after adjusting for covariates. Among those with detectable CAC at baseline, progression of CAC was assessed using multivariable robust linear regression.ResultsOur study population consisted of 6004 individuals (62 ± 10 years, 48% males). Among 3079 individuals with no detectable CAC at baseline, 20% (n = 620) developed CAC. After adjusting for CVD risk factors, participants with a baseline resting heart rate >80 bpm had an increased risk of incident CAC as compared to those with a resting heart rate <60 (relative risk = 1.65, 95% CI = 1.02, 2.66). Among persons with CAC present at baseline, participants with a baseline resting heart rate >80 bpm had greater CAC score progression than those with a resting heart rate <60 (β = 17.10; 95% CI = 4.29, 29.85).ConclusionElevated resting heart rate, a well-described predictor of cardiovascular mortality with unclear mechanism, is associated with increased incidence and progression of coronary atherosclerosis among individuals free of CVD at baseline.     

Subclinical coronary atherosclerosis and resting ECG abnormalities in an unselected general population

ObjectivesExposure to cardiovascular (CV) risk factors may result in coronary atherosclerosis and myocardial disease, which is reflected in the extent of coronary artery calcification (CAC) and resting ECG abnormalities, respectively. We studied the association of CAC with ECG abnormalities in a general population without myocardial infarction or revascularization.MethodsThe total cohort of 4814 subjects (45–75 years) were randomly selected from the general population for the Heinz Nixdorf Recall Study, an ongoing study designed to assess the prognostic value of modern risk stratification methods. In addition to measuring standard risk factors, digitized resting ECGs and the EBT-based Agatston score were obtained. Subjects were separated into those without (n = 1929) and with CV disease (CVD) or treated risk factors (tRF) (n = 2558).ResultsIn both groups, a positive CAC-score was more frequent and CAC-scores were higher in men and women with ECG abnormalities as compared to those with normal ECGs (p < 0.05 each). In persons without CVD/tRF, a CAC ≥75th percentile was more frequent in those with LVH (42.4%) and QTc >440 ms (34.2%) as compared to normal ECGs (23.0%, p < 0.01 for both). In persons with CVD/tRF, a CAC-score ≥75th percentile was found in subjects with A-Fib (46.3%), borderline-LVH (39.1%), ECG signs of MI (40.5%) and major ECG abnormalities (40.3%) versus 31.2% in those with normal ECGs (p < 0.03 for all). In multivariate analysis, LVH (p = 0.025) and major ECG abnormalities (p = 0.04) remained independently associated with CAC in subjects without and with CVD/tRF, respectively.ConclusionsECG-based evidence of myocardial disease is often associated with an elevated CAC burden, suggesting a link between epicardial and myocardial manifestations of risk factor exposure. The association of CAC burden with different ECG abnormalities in different clinical groups may have implications for the interpretation of the resting ECG and CAC burden in risk stratification.     

Risk reductions for cardiovascular disease with pravastatin treatment by dyslipidemia phenotype: A post hoc analysis of the MEGA Study

BackgroundThe beneficial effect of statins for cardiovascular disease (CVD) prevention has been well established. However, the effectiveness among different phenotypes of dyslipidemia has not been confirmed.ObjectiveWe evaluated the effect of pravastatin on the incidence of CVD in relation to the phenotype of dyslipidemia.MethodsThe MEGA Study evaluated the effect of low-dose pravastatin on primary prevention of CVD in 7832 Japanese patients, who were randomized to diet alone or diet plus pravastatin and followed for more than 5 years. These patients were classified into phenotype IIa (n = 5589) and IIb (n = 2041) based on the electrophoretic pattern for this post hoc analysis.ResultsIn the diet group there was no significant difference in the incidence of coronary heart disease (CHD), stroke, CVD, and total mortality between the two phenotypes. Phenotype IIb patients, compared to phenotype IIa, had lower levels of high-density lipoprotein cholesterol (HDL-C) and a significantly higher incidence of CVD in relation to a low HDL-C level (<47.5 mg/dL; p = 0.02). Furthermore, pravastatin decreased the relative risk for each major endpoint in both type IIa and type IIb dyslipidemia. Significant risk reductions were observed for CHD by 38% (p = 0.04) and CVD by 31% (p = 0.02) in type IIa dyslipidemia but not in phenotype IIb.ConclusionPravastatin therapy provided significant risk reductions for CHD and CVD in patients with phenotype IIa dyslipidemia, but not in those with phenotype IIb dyslipidemia.     

Knowledge of cardiovascular risk factors and awareness of non-pharmacological approach for risk prevention in young survivors of acute myocardial infarction. The cardiovascular risk prevention project "Help Your Heart Stay Young"

Background and aimsKnowledge of cardiovascular disease (CVD) risk factors in young patients who experienced myocardial infarction (MI) is poorly described.Methods and resultsKnowledge of traditional CVD risk factors, non-fatal cardiovascular events and of non-pharmacological factors able to reduce CVD risk and education level were evaluated by questionnaires in subjects who visited their family doctors. Sixty-one participants with history of MI in age <50 years (MI+) were compared with 3749 subjects with age <50 years, from the same population source, but without history of MI (MI−). MI+ were more frequently men (p < 0.01), did not have significantly higher prevalences of family history of CVD, diabetes and hypertension. MI+ individuals reported previous non-fatal stroke (13% vs. 0.5%, p < 0.001), overweight, diabetes, and hypercholesterolemia (all p < 0.001) more frequently than controls, whereas prevalence of arterial hypertension, smoking habit and physical inactivity did not differ between the two groups; MI+ and MI− individuals did not differ in terms of the proportion of those who were unaware of being hypertensive, diabetic or hypercholesterolemic. MI+ participants reported more frequently lower education level than controls (p < 0.05). Knowledge of non-pharmacological approach for CVD risk reduction was similar in MI+ and MI−. In a logistic multivariate analysis, male gender (adjusted odds ratio = 5.8) and high cholesterol level (adjusted odds ratio 2.8, both p < 0.01) were independent correlates of MI+. CVD risk factors distribution was similar between participants with juvenile MI+ and MI in age ≥50 years (n = 167) extracted from the same population source; however, stroke was reported more frequently in juvenile MI+ than in those who had MI at age ≥50 years/old (13% vs. 4%, p < 0.01).ConclusionsJuvenile non-fatal MI was associated with metabolic CVD risk factors, with higher cerebrovascular co-morbidity and lower education level.     

Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress

Air pollution is associated with significant adverse health effects, including increased cardiovascular morbidity and mortality. Exposure to particulate matter with an aerodynamic diameter of <2.5 microm (PM(2.5)) increases ischemic cardiovascular events and promotes atherosclerosis. Moreover, there is increasing evidence that the smallest pollutant particles pose the greatest danger because of their high content of organic chemicals and prooxidative potential. To test this hypothesis, we compared the proatherogenic effects of ambient particles of <0.18 microm (ultrafine particles) with particles of <2.5 microm in genetically susceptible (apolipoprotein E-deficient) mice. These animals were exposed to concentrated ultrafine particles, concentrated particles of <2.5 microm, or filtered air in a mobile animal facility close to a Los Angeles freeway. Ultrafine particle-exposed mice exhibited significantly larger early atherosclerotic lesions than mice exposed to PM(2.5) or filtered air. Exposure to ultrafine particles also resulted in an inhibition of the antiinflammatory capacity of plasma high-density lipoprotein and greater systemic oxidative stress as evidenced by a significant increase in hepatic malondialdehyde levels and upregulation of Nrf2-regulated antioxidant genes. We conclude that ultrafine particles concentrate the proatherogenic effects of ambient PM and may constitute a significant cardiovascular risk factor.