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Objectives: Due to inconsistent epidemiological evidence on health effects of air pollution on progression of atherosclerosis, we investigated several air pollutants and their effects on progression of atherosclerosis, using carotid intima media thickness (cIMT), coronary calcification (CAC), and thoracic aortic calcification (TAC)., Methods: We used baseline (2000-2003) and 5-y follow-up (2006-2008) data from the German Heinz Nixdorf Recall cohort study, including 4,814 middle-aged adults. Residence-based long-term air pollution exposure, including particulate matter (PM) with aerodynamic diameter ≤ 2.5 μ m ( PM 2.5 ), ( PM 10 ), and nitrogen dioxide ( NO 2 ) was assessed using chemistry transport and land use regression (LUR) models. cIMT was quantified as side-specific median IMT assessed from standardized ultrasound images. CAC and TAC were quantified by computed tomography using the Agatston score. Development (yes/no) and progression of atherosclerosis (change in cIMT and annual growth rate for CAC/TAC) were analyzed with logistic and linear regression models, adjusting for age, sex, lifestyle variables, socioeconomic status, and traffic noise., Results: While no clear associations were observed in the full study sample (mean age 59.1 ( ± 7.6 ) y; 53% female), most air pollutants were marginally associated with progression of atherosclerosis in participants with no or low baseline atherosclerotic burden. Most consistently for CAC, e.g., a 1.5   μ g / m 3 higher exposure to PM 2.5 (LUR) yielded an estimated odds ratio of 1.19 [95% confidence interval (CI): 1.03, 1.39] for progression of CAC and an increased annual growth rate of 2% (95% CI: 1%, 4%)., Conclusion: Our study suggests that development and progression of subclinical atherosclerosis is associated with long-term air pollution in middle-aged participants with no or minor atherosclerotic burden at baseline, while overall no consistent associations are observed. https://doi.org/10.1289/EHP7077.

Aims: Air pollution and noise are potential risk factors for subclinical atherosclerosis. Longitudinal analyses, especially on the interplay of these environmental factors, are scarce and inconsistent. Hence we investigated long-term traffic-related exposure to air pollution and noise with the development and progression of thoracic aortic calcification, a marker of subclinical atherosclerosis., Methods: We used baseline (2000-2003) and follow-up (2006-2008) data from the German Heinz Nixdorf Recall cohort study, including 4814 middle-aged adults. Residence-based air pollution (PM 2.5 (aerodynamic diameter ≤ 2.5 µm), PM 10 , nitrogen dioxide and particle number), and noise was assessed with dispersion models. Thoracic aortic calcification was quantified from non-contrast enhanced electron beam computed tomography. The presence and extent of thoracic aortic calcification progression were analysed with multiple logistic and linear regression models, respectively, adjusting for age, sex, lifestyle variables, socioeconomic status and respective co-exposure., Results: We observed no association in the full study sample ( n  = 3155, mean age 59.1 (±7.6) years, 52.8% women). While an interquartile range in particle number and night-time noise yielded odds ratios of 1.20 (1.03, 1.40) and 1.21 (1.00, 1.46) for binary thoracic aortic calcification progression, and 0.02 (-0.01, 0.05) and 0.04 (0.00, 0.07) higher growth rates of thoracic aortic calcification in participants with baseline thoracic aortic calcification less than 10, negative findings were observed in those with baseline thoracic aortic calcification of 10 or greater. Results were similar for other pollutants and daytime noise., Conclusion: Our study shows no overall associations. Subgroup analyses suggest independent associations of traffic-related air pollution and noise with the development and progression of subclinical atherosclerosis in participants with no or minor thoracic aortic calcification at baseline, in contrast to negative findings in those with advanced calcification.

Arterial hypertension promotes atherosclerosis and cardiovascular events. We evaluated how cardiovascular risk and atherosclerosis progression are associated with blood pressure, antihypertensive treatment, and treatment efficacy. In 3555 participants of the population-based Heinz Nixdorf Recall study without previous cardiovascular disease (mean±SD; age, 58.9±7.6 years, 46.9% men), we analyzed associations of baseline antihypertensive treatment efficacy (normotension without antihypertensives, normotension with antihypertensives, hypertension without antihypertensives, hypertension with antihypertensives, based on 140/90 mmHg cutoffs) with incident coronary artery calcification (CAC) and CAC progression during 5-year-follow-up and with incident cardiovascular events during 13.5-year-follow-up. We further evaluated associations of incident arterial hypertension and efficacy of new antihypertensive treatment at the 5-year-follow-up with subsequent cardiovascular events. At baseline, 1706 participants had normotension without antihypertensives, 553 normotension with antihypertensives, 786 hypertension without antihypertensives, and 510 hypertension with antihypertensives. Six hundred forty-seven participants experienced rapid CAC progression. One hundred seven, 132, and 249 had incident stroke, coronary event, and cardiovascular event, respectively. Compared with normotensives without antihypertensives, normotensives with antihypertensives had an elevated stroke (hazard ratio, 2.33 [95% CI, 1.19-4.55]), coronary (2.04 [95% CI, 1.20-3.45]), and cardiovascular (2.23 [95% CI, 1.48-3.36]) risk, and increased baseline CAC, but not increased CAC progression. Participants without hypertension at baseline, who were newly hypertensive but achieved normotension with antihypertensives at the 5-year-follow-up, again exhibited elevated stroke (4.80 [95% CI, 1.38-16.70]) and cardiovascular (2.99 [95% CI, 1.25-7.16]) risk, whereas coronary risk was less elevated (2.24 [95% CI, 0.70-7.18]). Normotensives with antihypertensives have an elevated cardiovascular risk. They are characterized by elevated baseline CAC but show no signs of increased CAC progression.

Aims: Thoracic aortic calcification (TAC) is measured by computed tomography (CT). We investigated the association of TAC-progression with incident cardiovascular (CV) events and all-cause mortality in a population-based cohort and to determine its predictive value for these endpoints., Methods and Results: In 3080 participants (45-74 years, 53.6% women), risk factors and TAC via CT were measured at baseline and at a second examination after 5.1 ± 0.3 years. Hard coronary, hard CV events as well as CV events including revascularization and all-cause mortality were recorded during a follow-up time of 7.8 ± 2.2 years after the second CT scan. Cox regression analysis determined the association of TAC-progression with observed endpoints. The predictive value of TAC-progression was assessed using Harrell's C index. We observed 81 hard coronary, 154 hard CV, 231 CV events including revascularization, and 266 deaths. In the crude analysis, event rates increased continuously with the level of TAC-change over 5 years for all endpoints. After adjustment, the significant association of TAC-progression with hard CV events [hazard ratio (HR) 1.28, 95% confidence interval (CI) 1.05-1.57] and all-cause mortality (HR 1.34, 95% CI 1.14-1.58) persisted, per one standard deviation increase in TAC-progression (log(TAC + 1)). Regarding aortic segments separately, HRs were consistently higher for descending thoracic aorta. When adding TAC (baseline and progression) to the model containing classical risk factors and coronary artery calcification (CAC), Harrell's C indices did not increase for any of the observed endpoints., Conclusion: TAC-progression is associated with incident hard CV events and all-cause mortality but fails to improve event prediction over CAC., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com.)

Background and Aims: As a modifiable lifestyle factor, diet is hypothesized to play an important role in the progression of atherosclerosis. The aim of this study was to explore associations of comprehensive dietary patterns derived by cluster analysis with degree and progression of coronary artery calcification (CAC) over five years of follow-up., Methods and Results: In the population-based Heinz Nixdorf Recall study, 3718 participants (45-75 years; 47.6% men) without coronary heart disease completed a food frequency questionnaire at baseline. Five distinct dietary patterns were identified using cluster analysis: "Health-conscious", "Traditional German/Less alcohol", "Mediterranean-like", "Western" and "Animal fat/Alcohol" (used as reference). CAC was measured using electron-beam computed tomography at baseline and five years later. CAC after five years was predicted based on sex- and age-specific baseline percentiles. After comparing observed and predicted CAC Scores, CAC progression was classified as slow, expected, or rapid. Compared to "Animal fat/Alcohol" diet, a "Mediterranean-like" diet was associated with a relative risk (RR) for a rapid CAC progression in both sexes (men: 0.61; 95%-confidence interval [95%-CI]: 0.41; 0.90; women: 0.59; 95%-CI: 0.45; 0.78). Furthermore, reduced RRs were observed in women with a "Health-conscious" and a "Traditional German/Less alcohol" diet (0.63; 95%-CI: 0.47; 0.84, respectively 0.69; 95%-CI: 0.52; 0.90). No association was observed for a "Western" diet for both sexes. Similar results were revealed for degree of CAC., Conclusion: The study results support the hypothesis that a "Mediterranean-like" diet is associated with a lower CAC-progression and lower degree of CAC in men and women., (Copyright © 2017 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.)

Background: Long-term exposure to particulate matter (PM) has been associated with increased cardiovascular morbidity and mortality but little is known about the role of the chemical composition of PM. This study examined the association of residential long-term exposure to PM components with incident coronary events., Methods: Eleven cohorts from Finland, Sweden, Denmark, Germany, and Italy participated in this analysis. 5,157 incident coronary events were identified within 100,166 persons followed on average for 11.5 years. Long-term residential concentrations of PM < 10 μm (PM10), PM < 2.5 μm (PM2.5), and a priori selected constituents (copper, iron, nickel, potassium, silicon, sulfur, vanadium, and zinc) were estimated with land-use regression models. We used Cox proportional hazard models adjusted for a common set of confounders to estimate cohort-specific component effects with and without including PM mass, and random effects meta-analyses to pool cohort-specific results., Results: A 100 ng/m³ increase in PM10 K and a 50 ng/m³ increase in PM2.5 K were associated with a 6% (hazard ratio and 95% confidence interval: 1.06 [1.01, 1.12]) and 18% (1.18 [1.06, 1.32]) increase in coronary events. Estimates for PM10 Si and PM2.5 Fe were also elevated. All other PM constituents indicated a positive association with coronary events. When additionally adjusting for PM mass, the estimates decreased except for K., Conclusions: This multicenter study of 11 European cohorts pointed to an association between long-term exposure to PM constituents and coronary events, especially for indicators of road dust.

Background: Studies have shown that air pollution is associated with cardiopulmonary mortality, but there has been less research of the possible effect of air pollution on stroke and non-fatal coronary events. The Heinz Nixdorf Recall (HNR) study addressed the question of the effect of long-term air pollution on stroke and coronary events. Ambient acoustic noise was also considered as a risk factor., Methods: The HNR study, initiated in 2000, is a prospective, population-based cohort study in the Ruhr region of Germany. Long-term exposure to fine-particle dust (PM10, PM2.5 and PM(2.5abs) [carbon black content]) and traffic noise at the subjects' home addresses were determined using land-use regression and dispersion models, respectively. Strokes and coronary events were ascertained from patient records by an independent end-point committee on the basis of predefined study criteria. The adjusted hazard ratio (HR) was calculated using Cox regression analysis for an increase in concentration from the 5th to the 95th percentile for each exposure., Results: Data from 4433 subjects were evaluated. The incidence of stroke was 2.03 per 1000 person-years (PY), and that of coronary events was 3.87 per 1000 PY. The highest hazard ratios for stroke were seen for PM10 (HR 2.61, 95% confidence interval [CI] 1.13-6.00) and PM2.5 (HR 3.20, 95% CI 1.26-8.09). The highest hazard ratios for coronary events were found for PM10 (HR 1.07, 95% CI 0.56-2.04) and for PM(2.5abs) (HR 1.37, 95% CI 0.80-2.36)., Conclusion: Long-term exposure to fine-particle dust is associated with a higher risk of stroke, regardless of the subject's exposure to noise at his or her home address. The results for coronary events are less clear, but still suggest increased risk.

Background: B-type natriuretic peptide (BNP) as well as N-terminal-proBNP (NT-proBNP) are associated with cardiac events in the general population. Yet, data from the general population comparing both peptides for their prognostic value is lacking., Methods: Participants from the population-based Heinz-Nixdorf-Recall-study without cardiovascular diseases were included. Associations of BNP and NT-proBNP with incident cardiovascular events (incident myocardial infarction, stroke, or cardiovascular death) were assessed using Cox regression; prognostic value was addressed using Harrell's c statistic., Results: From overall 3589 subjects (mean age: 59.3 ± 7.7 yrs, 52.5% female), 235 subjects developed a cardiovascular event during 8.9 ± 2.2 yrs of follow-up. In regression analysis both natriuretic peptides were associated with incident cardiovascular events, independent of traditional risk factors (hazard ratio (HR) per unit increase on log-scale (95% CI): NT-proBNP: 1.60 (1.39; 1.84); BNP: 1.37 (1.19; 1.58), p<0.0001 respectively). Specifically looking at subjects <60 yrs only NT-proBNP, was linked with events (HR (95% CI): 1.59 (1.19; 2.13) for NT-proBNP, p=0.0019; HR: 1.25 (0.94; 1.65) for BNP, p=0.12, after adjustment for age and gender). Similar results were observed for females (HR (95% CI) 1.65 (1.28; 2.12), p=0.0001 for NT-proBNP, and 1.24 (0.96; 1.61), p=0.10 for BNP after adjustment for age). Adding NT-proBNP/BNP to traditional risk factors increased the prognostic value, with effects being stronger for NT-proBNP (Harrell's c, 0.724 to 0.741, p=0.034) as compared to BNP (0.724 to 0.732, p=0.20)., Conclusion: Both, NT-proBNP and BNP are associated with future cardiovascular events in the general population. However, when both are available, NT-proBNP seems to be superior due to its higher prognostic value, especially in younger subjects and females., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Objectives: The European HeartScore has traditionally differentiated between low and high-risk countries. Until 2012 Germany and Denmark were considered to be high-risk countries but have now been defined as low-risk countries. In this survey we aim to address the consequences of this downgrading., Methods: A screening of 3932 randomly selected (mean age 56 years, 46% male) individuals from Germany and Denmark free of cardiovascular disease was performed. Traditional risk factors were determined, and the HeartScore was measured using both the low-risk and the high-risk country models. A non-contrast Cardiac-CT scan was performed to detect coronary artery calcification (CAC)., Results: Agreement of HeartScore risk groups with CAC groups was poor, but higher when applying the algorithm for the low-risk compared to the high-risk country model (agreement rate: 77% versus 63%, and weighted Kappa: 0.22 versus 0.15). However, the number of subjects with severe coronary calcification (CAC score ≥400) increased in the low and intermediate HeartScore risk group from 78 to 147 participants (from 2.7 % to 4.2 %, p = 0.001), when estimating the risk based on the algorithm for low-risk countries., Conclusion: As a consequence of the reclassification of Germany and Denmark as low-risk countries more people with severe atherosclerosis will be classified as having a low or intermediate risk of fatal cardiovascular disease., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Objective: The C825T polymorphism of the gene encoding the human G protein beta-3 subunit (GNB3) is associated with hypertension and obesity. Moreover, genotypes of the GNB3 polymorphism have been associated with development of coronary artery disease, and the 825T allele is thought to influence the process of atherosclerosis. However, the potential of the C825T polymorphism to predict coronary events has been poorly explored in a longitudinal setting at the population level., Methods: In 4159 Caucasian subjects from the Heinz Nixdorf Recall study cohort (age: 45-75 years, 48% male), genotypes of the GNB3 C825T polymorphism (rs5443) were determined and associated with fatal and non-fatal myocardial infarction (hard coronary events). Established cardiovascular risk factors were used to adjust for confounders., Results: The median follow-up time was 9.9 years (1st/3rd quartiles 9.5/10.2). 148 subjects (3.6%) experienced a hard coronary event. The 10-year event-free survival rate was CC, 96.1%; CT 96.9%, TT, 93.7% (p = 0.018). Multivariable analysis showed that the TT genotype is a significant risk factor for hard coronary events (hazard ratio (HR) = 1.9 (95% confidence interval (CI) 1.2-2.9); p = 0.008) after adjustment for age, sex, diabetes, systolic blood pressure, body mass index, high-density lipoprotein, and coronary artery calcification as determined by electron beam computed tomography at baseline. While prognosis in females was independent of GNB3 genotypes, analysis in males even elevated the HR for TT versus C-allele to 2.6 (95% CI 1.6-4.2; p < 0.001)., Conclusion: The GNB3 825 TT genotype is a significant and independent risk factor for hard coronary events independent of other established cardiovascular risk factors at a population level in males., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Aim: Coronary artery calcification (CAC), as a sign of atherosclerosis, can be detected and progression quantified using computed tomography (CT). We develop a tool for predicting CAC progression., Methods and Results: In 3481 participants (45-74 years, 53.1% women) CAC percentiles at baseline (CACb) and after five years (CAC₅y) were evaluated, demonstrating progression along gender-specific percentiles, which showed exponentially shaped age-dependence. Using quantile regression on the log-scale (log(CACb+1)) we developed a tool to individually predict CAC₅y, and compared to observed CAC₅y. The difference between observed and predicted CAC₅y (log-scale, mean±SD) was 0.08±1.11 and 0.06±1.29 in men and women. Agreement reached a kappa-value of 0.746 (95% confidence interval: 0.732-0.760) and concordance correlation (log-scale) of 0.886 (0.879-0.893). Explained variance of observed by predicted log(CAC₅y+1) was 80.1% and 72.0% in men and women, and 81.0 and 73.6% including baseline risk factors. Evaluating the tool in 1940 individuals with CACb>0 and CACb<400 at baseline, of whom 242 (12.5%) developed CAC₅y>400, yielded a sensitivity of 59.5%, specificity 96.1%, (+) and (-) predictive values of 68.3% and 94.3%. A pre-defined acceptance range around predicted CAC₅y contained 68.1% of observed CAC₅y; only 20% were expected by chance. Age, blood pressure, lipid-lowering medication, diabetes, and smoking contributed to progression above the acceptance range in men and, excepting age, in women., Conclusion: CAC nearly inevitably progresses with limited influence of cardiovascular risk factors. This allowed the development of a mathematical tool for prediction of individual CAC progression, enabling anticipation of the age when CAC thresholds of high risk are reached., (© The Author 2014. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Background: Aortic valve calcification (AVC) is considered a manifestation of atherosclerosis. In this study, we investigated whether AVC adds to cardiovascular risk prediction beyond Framingham risk factors and coronary artery calcification (CAC)., Methods: A total of 3944 subjects from the population based Heinz Nixdorf Recall Study (59.3±7.7 years; 53% females) were evaluated for coronary events, stroke, and cardiovascular disease (CVD) events (including all plus CV death) over 9.1±1.9 years. CT scans were performed to quantify AVC. Cox proportional hazards regressions and Harrell's C were used to examine AVC as event predictor in addition to risk factors and CAC., Results: During follow-up, 138 (3.5%) subjects experienced coronary events, 101 (2.6%) had a stroke, and 257 (6.5%) experienced CVD events. In subjects with AVC>0 versus AVC=0 the incidence of coronary events was 8.0% versus 3.0% (p<0.001) and the incidence of CVD events was 13.0% versus 5.7% (p<0.001). The frequency of events increased significantly with increasing AVC scores (p<0.001). After adjustment for Framingham risk factors, high AVC scores (3rd tertile) remained independently associated with coronary events (HR 2.21, 95% CI 1.28 to 3.81) and CVD events (HR 1.67, 95% CI 1.08 to 2.58). After further adjustment for CAC score, HRs were attenuated (coronary events 1.55, 95% CI 0.89 to 2.69; CVD events 1.29, 95% CI 0.83 to 2.00). When adding AVC to the model containing traditional risk factors and CAC, Harrell's C indices did not increase for coronary events (from 0.744 to 0.744) or CVD events (from 0.759 to 0.759)., Conclusions: AVC is associated with incident coronary and CVD events independent of Framingham risk factors. However, AVC fails to improve cardiovascular event prediction over Framingham risk factors and CAC., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

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/m(3) 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.

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.

Background: On the basis of the Heinz Nixdorf RECALL Study (HNR) we estimated the impact of classical atherosclerotic risk factors on different ankle-brachial-index (ABI) criteria., Patients and Methods: In a subgroup of participants (n = 2586) who had normal ABI at baseline ABI measurement was repeated at a 5 years follow-up and 3 different ABIs were defined: "ABI-high" calculated from the higher pressure, "ABI-low" from the lower pressure of both foot arteries of each leg. "Pure-ABI-low" was defined by exclusion of participants with ABI-high from those with ABI-low. Mönckebergs mediacalcinosis (MC) was accepted in case of ABI-high > 1.4 in one leg., Results: According to ABI-high 2 %, to ABI-low 7.8 % and pure-ABI-low 5.8 % of the participants developed peripheral arterial disease (PAD) (ABI < 0.9) and 3.6 % developed MC within the 5 years. Age did not play any role whereas female gender, diabetes mellitus and smoking were associated with an increased relative risk of pathologic ABI-high and ABI-low. Looking at the pure-ABI-low group only, female gender and smoking showed significant associations. None of the analysed risk factors except gender had an impact on the development of MC., Conclusions: Classical risk factors have different impact on incidence of PAD as defined by different ABI criteria.

Study Objectives: Several studies have assessed the association between midday nap and cardiovascular outcomes and reported heterogenous results. Concern exists that confounding might have distorted these results and contributed to discrepancies among them. This study prospectively examines the association between midday nap habits and the occurrence of coronary artery disease in a non-Mediterranean population., Participants: The baseline examination of 4,123 participants aged 45-75 years., Measurements: Measurements included interviews, physical examinations, laboratory tests, and electron beam computed tomography. We studied the influence of midday nap habits on risk of coronary artery disease. We adjusted for several potential confounders including measures of subclinical atherosclerosis-such as coronary calcium score and ankle brachial index-at baseline. Cardiac events during a median follow-up of 8.1 years were defined as nonfatal myocardial infarction and sudden cardiac death., Results: Overall, 135 of 4,123 subjects (3.3%) either suffered from acute myocardial infarction (81 subjects) or died due to a sudden cardiac death (54 subjects) during follow-up. After adjustment for several confounders including measures of subclinical atherosclerosis, regular long (> 60 min) midday nap was associated with an increased hazard ratio of cardiac events (hazard ratio 2.12, 95% confidence interval 1.11-4.05)., Conclusions: As our detailed confounder analyses showed, confounding is not the sole explanation for this finding. Future research on midday naps should focus on biological mechanisms that may be responsible for increasing the risk of coronary artery disease among subjects taking regular long midday naps.

The Heinz Nixdorf Recall Study is a population-based study that aims to improve the prediction of cardiovascular events by integrating new imaging and non-imaging modalities in risk assessment. One focus of the study is the evaluation of the quantification of subclinical coronary artery calcifications (coronary artery calcification, CAC) as a prognostic factor in predicting cardiac events. Primary endpoints are myocardial infarction and sudden cardiac death. The study was initiated in the late 1990s and enrolled a total of 4,814 participants aged 45-75 years between December 2000 and August 2003. A 5-year follow-up examination took place between 2006 and 2008. Currently, the 10-year follow-up is under way and is estimated to be finished in July 2013. Extending the original aims of the study, serial CAC measurements will allow the characterization of the natural history of CAC dynamics, the identification of its determinants and an understanding of the impact of CAC progression on the primary endpoints. The Heinz Nixdorf Recall Study will significantly extend our knowledge about new modalities in the prediction of cardiac events.

Balloon aortic valvuloplasty (BAV), introduced since almost 20 years, has experienced a revival for its use in the treatment of elderly patients with severe calcified aortic stenosis that are associated with high operative risk and co-morbidities. This is due to the introduction of new balloon catheters and techniques. This study reports about 75 such cases performed within the past 28 months. The mean age of our patient group was 78 +/- 7 years (median = 80 years). Risk calculation with the EuroSCORE demonstrated an average value of 24.4 +/- 19.5%. BAV was performed along with burst pacing to reduce transvalvular blood flow for stabilization of the balloon catheter until blood pressure dropped to less than 50 mmHg. BAV was performed in 72 patients with a procedural success rate of 73%. There was a decrease of 31 mmHg peak-to-peak gradient across the aortic valve from 63 +/- 35 to 32 +/- 22 mmHg (P < 0.0001). Mean gradient was reduced from 51 +/- 24 to 27 +/- 15 mmHg (P < 0.0001). Aortic valve area increased by 49% from 0.84 +/- 0.33 to 1.25 +/- 0.45 cm(2) (P < 0.0001). Serious adverse events (SAE) occurred in 17% of the 75 BAV procedures. Follow-up revealed a significant improvement in 6-month and 1-year survival. The improved technology of BAV makes this technique attractive for elderly patients who are at high operative risk or in cases where valve replacement was refused for any reason.

The Heinz Nixdorf Recall Study, which was inaugurated in 2000, is an ongoing population-based study to evaluate the prediction of cardiovascular events by integrating new imaging and nonimaging modalities in risk assessment. A focus is the additional prognostic value of coronary artery calcification (CAC). Currently used risk stratification algorithms often describe the individuals' risk based on few established risk factors only inaccurately. Using noninvasive quantification of CAC progression, the natural history of atherosclerosis with its repetitive, frequently subclinical plaque ruptures, may detect an unstable course of the disease long before the disease irreversibly manifests in sudden death or myocardial infarction. While the independent additional prognostic value of CAC quantification has been shown in asymptomatic patients at intermediate risk, only few studies provided evidence for an independent prognostic value of serial CAC measurements. In the Heinz Nixdorf Recall Study, the impact of established and new risk factors, e.g., the metabolic syndrome, psychosocial and environmental risk factors, or genetic variables, can be assessed. Further, the association of CAC progression with the incidence of other cardiovascular diseases such as heart failure or aortic or aortic valve calcification can be described. Since April 2006, the participants of the study return to the study center 5 years after baseline recruitment to assess health status and to determine the risk factor profile. Based on recently published data, serial CAC measurements have been granted allowing for (1) characterization of the natural history of CAC progression, and (2) identification of its determinants. The rationale of serial CAC quantification is discussed in this article.The Heinz Nixdorf Recall Study will contribute to the appraisal of new imaging modalities in risk stratification.

The German Socio-Economic Panel (SOEP) serves a global research community by providing representative annual longitudinal data of respondents living in private households in Germany. The dataset offers a valuable life course panorama, encompassing living conditions, socioeconomic status, familial connections, personality traits, values, preferences, health, and well-being. To amplify research opportunities further, we have extended the SOEP Innovation Sample (SOEP-IS) by collecting genetic data from 2,598 participants, yielding the first genotyped dataset for Germany based on a representative population sample (SOEP-G). The sample includes 107 full-sibling pairs, 501 parent-offspring pairs, and 152 triads, which overlap with the parent-offspring pairs. Leveraging the results from well-powered genome-wide association studies, we created a repository comprising 66 polygenic indices (PGIs) in the SOEP-G sample. We show that the PGIs for height, BMI, and educational attainment capture 22∼24%, 12∼13%, and 9% of the variance in the respective phenotypes. Using the PGIs for height and BMI, we demonstrate that the considerable increase in average height and the decrease in average BMI in more recent birth cohorts cannot be attributed to genetic shifts within the German population or to age effects alone. These findings suggest an important role of improved environmental conditions in driving these changes. Furthermore, we show that higher values in the PGIs for educational attainment and the highest math class are associated with better self-rated health, illustrating complex relationships between genetics, cognition, behavior, socio-economic status, and health. In summary, the SOEP-G data and the PGI repository we created provide a valuable resource for studying individual differences, inequalities, life-course development, health, and interactions between genetic predispositions and the environment. [ABSTRACT FROM AUTHOR]

Context and Aim: The link between headaches and exposure to loud noise in occupational settings has been established. However, the effect of less intense but chronic residential traffic noise exposure on headache occurrence is less clear.Settings and Design: We included 3,025 participants from the Heinz Nixdorf Recall study in Germany for this cross-sectional analysis.Methods and Material: Residential road traffic noise exposure at the 2006-2008 address was modelled in A-weighted decibels (dB(A)) according to the European Noise Directive (2002/49/EC) for 24-hour (Lden) and night-time noise (22-6 h, Lnight). Indoor traffic noise exposure was obtained by modifying Lden and Lnight based on residence orientation, window type, and personal window opening habits. Traffic noise exposure below 55, 45 dB(A), 35 and 25 dB(A) were set as the reference for Lden, Lnight, Lden,indoor and Lnight,indoor, respectively. Average number of days with headache per month over the past three months was ascertained during the follow-up (2011-2015) medical interview.Statistical Analysis Used: Prevalence Odds Ratios (POR) of having eight or more headaches per month per 5 dB(A) increase in traffic noise exposure were calculated using logistic regression, adjusting for age, sex, sport, number of chronic conditions, years of education and smoking status.Results: The mean age of participants was 58.3. Mean Lden was 54 dB(A). Median monthly headache days was one. No association was seen between traffic noise exposure and having ≥8 headaches/month for all the examined traffic noise indicators. However, traffic noise was positively associated with traffic noise-annoyance and insomnia; and night-time traffic noise-annoyance and insomnia were positively associated with headache.Conclusion: In conclusion, our data did not provide any evidence for an association between chronic traffic noise exposure and prevalence of headaches at this population's exposure levels. This should be explored in different populations given that this is the first study of its type and that noise exposure was generally low in our population. [ABSTRACT FROM AUTHOR]

New approaches in urban development are required to transform cities into sustainable places. This demands a higher degree of urban density, which is hardly conceivable without an increase in sound - mostly in the form of noise. To achieve a high level of acceptance for densification, high-quality and acoustically pleasant urban spaces are essential. Noise reduction measures are necessary, but not sufficient. What is needed is a broadening of the perspective of noise. For urban public health we propose the soundscape approach from two different scientific disciplines. Here, sounds are qualities that can be designed in urban spaces and are an important resource for a healthy city. Linking knowledge about the acoustic environment with human perception will significantly improve our understanding of the relationships between urban acoustic environments, urban spatial contexts, and their effects on human health, both qualitatively and quantitatively. However, a systematic application of these approaches to urban soundscapes is still missing, as is the joint implementation of soundscape approaches in noise impact and urban public health research. This paper aims to introduce the terms sound and noise as well as two soundscape approaches. Subsequently, the aims and methods of the acoustic quality and health in urban environments (SALVE) pilot project are presented. The paper provides early insight into the new field of urban sound quality and soundscapes in the context of urban public health.

Background: Until now, insomnia has not been much of interest in epidemiological neighbourhood studies, although literature provides evidence enough for insomnia-related mechanisms being potentially dependent on neighbourhood contexts. Besides, studies have shown differences in sleep along individual social characteristics that might render residents more vulnerable to neighbourhood contextual exposures. Given the role of exposure duration and changes in the relationship between neighbourhoods and health, we studied associations of neighbourhood unemployment and months under residential turnover with insomnia by covering ten years of residential history of nearly 3,000 urban residents in the Ruhr Area, Germany. Methods: Individual data were retrieved from the Heinz Nixdorf Recall Study, a population-based study of randomly chosen participants from adjacent cities, which contains self-rated insomnia symptoms and individual social characteristics. Participants' residential addresses were retrospectively assessed using public registries. We built individually derived exposure measures informing about mean neighbourhood unemployment rates and months under high residential turnover. These measures were major predictors in multivariate logistic regressions modelling the association between social neighbourhood characteristics and insomnia in the whole sample and subgroups defined by low income, low education, social isolation, and change of residence. Traffic-related noise, age, gender, economic activity, and education were considered as covariates. Results: Nearly 12 per cent of the participants complained about insomnia. Associations of neighbourhood unemployment with insomnia were more consistent than those of residential turnover in the whole sample (adjusted OR 1.42, 95% CI 1.00-2.03 for neighbourhood unemployment and OR 1.33, 95% CI 0.78-2.25 for residential turnover in the highest exposure categories). In low-income and socially isolated participants, neighbourhood unemployment odds of reporting insomnia were particularly elevated (adjusted OR 2.90, 95% CI 1.39-6.02 and OR 3.32, 95% CI 1.11-9.96, respectively). Less educated participants displayed relatively high odds of reporting insomnia throughout all upper neighbourhood unemployment exposure categories. Change of residence weakened associations, whereas undisrupted exposure sharpened them by trend. Conclusions: Our findings hint at multiple stressors being effective in both the neighbourhood context and individual resident, possibly reflecting precarious life situations undermining residents' sleep and health chances. Moreover, our results suggest a temporal dependency in the association between neighbourhood and insomnia. [ABSTRACT FROM AUTHOR]