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Background: Studies investigating the link between long-term exposure to air pollution and incidence of diabetes are still scarce and results are inconsistent, possibly due to different compositions of the particle mixture. We investigate the long-term effect of traffic-specific and total particulate matter (PM) and road proximity on cumulative incidence of diabetes mellitus (mainly type 2) in a large German cohort. Methods: We followed prospectively 3607 individuals without diabetes at baseline (2000-2003) from the Heinz Nixdorf Recall Study in Germany (mean follow-up time 5.1 years). Mean annual exposures to total as well as traffic-specific PM10 and PM2.5 at residence were estimated using a chemistry transport model (EURAD, 1 km² resolution). Effect estimates for an increase of 1 µg/m³ in PM were obtained with Poisson regression adjusting for sex, age, body mass index, lifestyle factors, area-level and individual-level socio-economic status, and city. Results: 331 incident cases developed. Adjusted RRs for total PM10 and PM2.5 were 1.05 (95 %-CI: 1.00;1.10) and 1.03 (95 %-CI: 0.95;1.12), respectively. Markedly higher point estimates were found for local traffic-specific PM with RRs of 1.36 (95 %-CI: 0.98;1.89) for PM10 and 1.36 (95 %-CI: 0.97;1.89) for PM2.5. Individuals living closer than 100 m to a busy road had a more than 30 % higher risk (1.37;95 %-CI: 1.04;1.81) than those living further than 200 m away. Conclusions: Long-term exposure to total PM increases type two diabetes risk in the general population, as does living close to a major road. Local traffic-specific PM was related to higher risks for type two diabetes than total PM. [ABSTRACT FROM AUTHOR]

There is increasing evidence that sleep disorders are associated with cognitive decline. We, therefore, examined the cross-sectional association of sleep-disordered breathing (SDB), sleep quality, and three types of sleep complaints (difficulties initiating sleep, difficulties maintaining sleep, and early morning awakening) with mild cognitive impairment (MCI) and its subtypes. A group of 1,793 participants (51% men; 63.8 ± 7.5 years) of the population-based Heinz Nixdorf Recall study (total sample n = 4,157) received a screening for SDB and self-report measures of sleep complaints. Group comparisons were used to compare performances among five cognitive subtests. Multivariate logistic regression models were calculated to determine the association of MCI (n = 230) and MCI subtypes (amnestic MCI, n = 120; non-amnestic MCI, n = 110) with SDB severity levels, poor sleep quality, and sleep complaints. Severe SDB (apnea-hypopnea index ≥⃒30/h, n = 143) was not associated with MCI, amnestic MCI, or non-amnestic MCI. Poor sleep quality was associated with MCI (Odds ratio (OR) = 1.40, 95% confidence interval (CI) = 1.02-2.03; fully adjusted) as well as frequently reported difficulties initiating sleep (OR = 1.94, 1.20-3.14), difficulties maintaining sleep (OR = 2.23, 1.27-4.63), and early morning awakening (OR = 2.30, 1.32-4.00). Severe difficulties initiating sleep (OR = 2.23, 1.21-4.13) and early morning awakening (OR = 2.88, 1.45-5.73) were solely associated with the amnestic MCI subtype, whereas, severe difficulties maintaining sleep (OR = 3.84, 1.13-13.08) were associated with non-amnestic MCI. Our results suggest that poor sleep quality, rather than SDB, is associated with MCI. The selective association of difficulties initiating sleep and early morning awakening with amnestic MCI and of difficulties maintaining sleep with non-amnestic MCI might serve as a marker to improve diagnostic accuracy in the earliest stages of cognitive impairment and will be further investigated in our longitudinal examination. [ABSTRACT FROM AUTHOR]

Background: Long-term exposures to particulate matter air pollution (PM2.5 and PM10) and high traffic load have been associated with markers of systemic inflammation. Epidemiological investigations have focused primarily on total PM, which represents a mixture of pollutants originating from different sources. Objective: We investigated associations between source-specific PM and high-sensitive C-reactive protein (hs-CRP), an independent predictor of cardiovascular disease. Methods: We used data from the first (2000–2003) and second examination (2006–2008) of the Heinz Nixdorf Recall study, a prospective population-based German cohort of initially 4,814 participants (45–75 years of age). We estimated residential long-term exposure to local trafficand industry-specific fine particulate matter (PM2.5) at participants’ residences using a chemistry transport model. We used a linear mixed model with a random participant intercept to estimate associations of source-specific PM and natural log-transformed hs-CRP, controlling for age, sex, education, body mass index, low- and high-density lipoprotein cholesterol, smoking variables, physical activity, season, humidity, and city (8,204 total observations). Results: A 1-μg/m3 increase in total PM2.5 was associated with a 4.53% increase in hs-CRP concentration (95% CI: 2.76, 6.33%). hs-CRP was 17.89% (95% CI: 7.66, 29.09%) and 7.96% (95% CI: 3.45, 12.67%) higher in association with 1-μg/m3 increases in traffic- and industry-specific PM2.5, respectively. Results for PM10 were similar. Conclusions: Long-term exposure to local traffic-specific PM (PM2.5, PM10) was more strongly associated with systemic inflammation than total PM. Associations of local industry-specific PM were slightly stronger but not significantly different from associations with total PM. [ABSTRACT FROM AUTHOR]

Aims Living close to high traffic has been linked to subclinical atherosclerosis, however it is not clear, whether fine particulate matter (PM) air pollution or noise, two important traffic-related exposures, are responsible for the association. We investigate the independent associations of long-term exposure to fine PM and road traffic noise with thoracic aortic calcification (TAC), a reliable measure of subclinical atherosclerosis. Methods and results We used baseline data (2000–2003) from the German Heinz Nixdorf Recall Study, a population-based cohort of 4814 randomly selected participants. We assessed residential long-term exposure to PM with a chemistry transport model, and to road traffic noise using façade levels from noise models as weighted 24 h mean noise (Lden) and night-time noise (Lnight). Thoracic aortic calcification was quantified from non-contrast enhanced electron beam computed tomography. We used multiple linear regression to estimate associations of environmental exposures with ln(TAC+1), adjusting for each other, individual, and neighbourhood characteristics. In 4238 participants (mean age 60 years, 49.9% male), PM2.5 (aerodynamic diameter ≤2.5 µm) and Lnight are both associated with an increasing TAC-burden of 18.1% (95% CI: 6.6; 30.9%) per 2.4 µg/m3 PM2.5 and 3.9% (95% CI 0.0; 8.0%) per 5dB(A) Lnight, respectively, in the full model and after mutual adjustment. We did not observe effect measure modification of the PM2.5 association by Lnight or vice versa. Conclusion Long-term exposure to fine PM and night-time traffic noise are both independently associated with subclinical atherosclerosis and may both contribute to the association of traffic proximity with atherosclerosis. [ABSTRACT FROM PUBLISHER]

Background: A B-type natriuretic peptide (BNP) threshold of 100 pg/ml is used in practice for identification of heart failure, but data about the 'normal' distribution of BNP in a large population in primary prevention are rare. We aimed to characterize the BNP distribution in a healthy subset of a population-based cohort and to evaluate the association of elevated BNP levels with major events. Methods: In a first step, we determined gender-specific distribution and 90th percentiles of BNP in participants who were at baseline free from known determinants of increased BNP, i.e. cardiovascular disease, hypertension or chronic kidney disease. Consecutively, the association of BNP levels above these 90th percentiles with subsequent cardiovascular and coronary events was assessed in the entire cohort. Results: In the BNP-normal sub-sample ( n = 1,639), we defined gender-specific 90th percentile of BNP (31.3 pg/ml for men, 45.5 pg/ml for women). From overall 3,697 subjects (mean age 59.4, 52.4 % female), 194 subjects developed a major cardiovascular event and 122 myocardial infarction during a mean follow-up period of 8.0 ± 1.5 years. The 90th percentiles derived from the normal subset as threshold showed strong associations with major events in the entire cohort even after adjusting for traditional risk factors: hazard ratio (95 % CI): 1.86 (1.37; 2.53), p < 0.0001 for cardiovascular, and 1.77 (1.19; 2.62), p = 0.005 for coronary events. Conclusion: The gender-specific 90th percentile of BNP (31 pg/ml for males and 45 pg/ml for females) obtained from a BNP-normal sub-sample is associated with incident major cardiovascular and coronary events, suggesting that even BNP values lower than 100 pg/ml could imply prognostic information in the general population. [ABSTRACT FROM AUTHOR]

We determined the prognostic value of transient increases in high-sensitive serum troponin I (hsTnI) during a marathon and its association with traditional cardiovascular risk factors and imaging-based risk markers for incident coronary events and all-cause mortality in recreational marathon runners. Baseline data of 108 marathon runners, 864 age-matched controls and 216 age- and risk factor-matched controls from the general population were recorded and their coronary event rates and all-cause mortality after 6 ± 1 years determined. hsTnI was measured in 74 marathon finishers before and after the race. Other potential predictors for coronary events, i.e., Framingham Risk Score (FRS), coronary artery calcium (CAC) and presence of myocardial fibrosis as measured by magnetic resonance imaging-based late gadolinium enhancement (LGE), were also assessed. An increase beyond the 99 % hsTnI-threshold, i.e., 0.04 μg/L, was observed in 36.5 % of runners. FRS, CAC, or prevalent LGE did not predict hsTnI values above or increases in hsTnI beyond the median after the race, nor did they predict future events. However, runners with versus without LGE had higher hsTnI values after the race (median (Q1/Q3), 0.08 μg/L (0.04/0.09) versus 0.03 μg/L (0.02/0.06), p = 0.039), and higher increases in hsTnI values during the race (median (Q1/Q3), 0.05 μg/L (0.03/0.08) versus 0.02 μg/L (0.01/0.05), p = 0.0496). Runners had a similar cumulative event rate as age-matched or age- and risk factor-matched controls, i.e., 6.5 versus 5.0 % or 4.6 %, respectively. Event rates in runners with CAC scores <100, 100-399, and ≥400 were 1.5, 12.0, and 21.4 % ( p = 0.002 for trend) and not different from either control group. Runners with coronary events had a higher prevalence of LGE than runners without events (57 versus 8 %, p = 0.003). All-cause mortality was similar in marathon runners (3/108, 2.8 %) and controls (26/864, 3.0 % or 5/216, 2.4 %, respectively). Recreational marathon runners with prevalent myocardial fibrosis develop higher hsTnI values during the race than those without. Increasing coronary artery calcium scores and prevalent myocardial fibrosis, but not increases in hsTnI are associated with higher coronary event rates. All-cause mortality in marathon runners is similar to that in risk factor-matched controls. [ABSTRACT FROM AUTHOR]

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A parental history of premature coronary heart disease (CHD) is an established risk factor for CHD events in descendants. The study aim was to investigate whether subclinical coronary artery calcification (CAC) differs between asymptomatic individuals (a) without a parental CHD history, (b) with a parental history and (c) without knowledge of parental CHD history. The inclusion of individuals without knowledge of parental CHD history is a new approach. We also differentiated between CHD of mother and father to gain insight into their individual contributions. Data was obtained for 4,301 subjects aged 45-75 years free of overt CHD from the baseline screening of the population-based Heinz Nixdorf Recall study. CAC, measured by electron-beam computed tomography, was modeled conducting logistic regressions. Model 1 included family history, Model 2 was adjusted for age (and gender) and Model 3 added common CHD risk factors. The CAC score was dichotomized using the age and sex-specific 75th percentile. The odds ratio (OR) for CAC ≥ age and sex-specific 75th percentile was 1.33 among individuals with parental premature CHD history (95 % confidence interval [95 %CI]: 1.08, 1.63), which did not change after full adjustment (OR 1.40, 95 %CI: 1.13, 1.74). Individuals with an unknown biological father or mother had a high chance of elevated CAC scores (fully adjusted; father: OR 1.38, 95 %CI: 1.01, 1.90, mother: OR 1.86, 95 %CI: 0.90, 3.84) compared to the reference group. The current study showed an association between parental CHD history and CAC independent of common CHD risk factors. This association affirms the use of parental CHD history in cardiovascular risk assessment among asymptomatic adults in routine practice. The observation that individuals who did not know their mother or father are prone to increased CAC scores needs further confirmation in large scale studies. [ABSTRACT FROM AUTHOR]

Background: Atherosclerosis is the primary cause of coronary heart disease (CHD), preceding the onset of cardiovascular disease by decades in most cases. Here we examine the association between single nucleotide polymorphisms (SNPs) integrated on Metabochip and coronary artery calcification (CAC), a valid risk factor for CHD, in an unselected, population-based German cohort. Methods: The Metabochip is a custom iSELECT array containing >195,000 SNPs that was designed to support large-scale follow-up of putative associations for metabolic and cardiovascular-associated traits. We used generalized linear regression models to explore the impact of Metabochip SNPs on quantitative CAC in 4,329 participants. Results: The 9p21 variant, rs1537373, was most strongly associated (Beta = 0.30; 95% confidence interval (CI) = 0.21-0.39; p = 4.05x10-11) with quantitative CAC. The second strongest association with CAC was with rs9349379 in the phosphatase and actin regulator 1 gene, PHACTR1, (Beta = 0.30; 95% CI = 0.22-0.40; p = 4.67x10-11). Both SNPs remained nominally significant in dichotomized analyses for the presence of any CAC (odds ratiors1537373 (OR) = 1.19; 95% CI = 1.07-1.31; p = 0.001 and ORrs9349379 = 1.26; 95% CI = 1.14-1.40); p = 1.5×10-5). Fine mapping of the 9p21 and PHACTR1 gene region revealed several other SNPs that were strongly associated with CAC. Conclusion: We demonstrate that SNPs near 9p21 and in PHACTR1 that have previously been shown to be associated with CHD are strongly associated with CAC in the Heinz Nixdorf Recall Study cohort. Our findings suggest that the 9p21 and 6q24 loci might be involved in cardiac outcome via promoting development of atherosclerosis in the coronary arteries. [ABSTRACT FROM AUTHOR]

Thoracic aortic calcification (TAC) and coronary artery calcium (CAC) have been proposed for risk assessment of coronary artery and cardiovascular disease events. The aim of this analysis is to assess the prevalence of TAC and to determine its relationship with cardiovascular risk factors and CAC in a general unselected population. TAC was measured from electron beam computed tomography scans and quantified by Agatston-Score in 4,025 participants aged 45-75 years (mean age 59.4 ± 7.8 years, 53 % female) from the Heinz Nixdorf Recall Study. Multivariable generalized linear regression was used to evaluate relationships between TAC and cardiovascular risk factors and CAC. Overall 2,538/4,025 (63.1 %) participants revealed TAC. Prevalence of TAC was greater in men than in women (65.2 vs. 61.7 %, p = 0.009). TAC was most strongly associated with age, systolic blood pressure, smoking and high levels of LDL-cholesterol. Prevalence of CAC was significantly higher in participants with TAC than without (74.0 vs. 57.6 %, p < 0.0001) demonstrating an increased risk of having CAC in the presence of TAC (prevalence ratio (PR) 1.29 [95 % CI: 1.22-1.35], p < 0.0001, PR adjusted for risk factors 1.14 [1.09-1.20], p < 0.0001). In general population, TAC has high prevalence and largely shares cardiovascular risk factors with CAD while being independently associated with present CAC. [ABSTRACT FROM AUTHOR]

Background: Patients with diabetes mellitus (DM) have an increased risk for periprocedural complications and adverse cardiac events after percutaneous coronary intervention. We addressed the potential for coronary microvascular obstruction and restenosis in patients with and without DM undergoing stenting for saphenous vein bypass graft (SVG) stenosis under protection with a distal occlusion/aspiration device. Methods: SVG plaque volume and composition were analyzed using intravascular ultrasound before stent implantation. Percent diameter stenosis was determined from quantitative coronary angiography before, immediately after and 6 months after stent implantation. Coronary aspirate was retrieved during stent implantation and divided into particulate debris and plasma. Total calcium, several vasoconstrictors, and tumor necrosis factor (TNF)α in particulate debris and coronary aspirate plasma were determined. Results: Patients with and without DM had similar plaque volume, but larger necrotic core and greater particulate debris release in patients with than without DM (20.3±2.7 vs. 12.7±2.6% and 143.9±19.3 vs. 75.1±10.4 mg, P<0.05). The TNFα concentration in particulate debris and coronary aspirate plasma was higher in patients with than without DM (15.9±6.6 vs. 5.1±2.4 pmol/mg and 2.2±0.7 vs. 1.1±0.2 pmol/L, P<0.05), whereas total calcium and vasoconstrictors were not different. Patients with DM had a greater percent diameter stenosis 6 months after stent implantation than those without DM (22.17±5.22 vs. 6.34±1.11%, P<0.05). The increase in TNFα immediately after stent implantation correlated with restenosis 6 months later (r=0.69, P<0.05). Conclusion: In diabetics, particulate debris and coronary aspirate plasma contained more TNFα, which might reflect the activity of the underlying atherosclerotic process. [ABSTRACT FROM AUTHOR]