Publications by authors named "Raimund Erbel"

684 Publications

Interaction of Alzheimer's Disease-Associated Genetic Risk with Indicators of Socioeconomic Position on Mild Cognitive Impairment in the Heinz Nixdorf Recall Study.

J Alzheimers Dis 2021 Jun 28. Epub 2021 Jun 28.

Institute for Medical Informatics, Biometry and Epidemiology, University of Duisburg-Essen, Essen, Germany.

Background: The apolipoprotein E (APOE) ɛ4 allele is reported to be a strong genetic risk factor for mild cognitive impairment (MCI) and Alzheimer's disease (AD). Additional genetic loci have been detected that influence the risk for late-onset AD. As socioeconomic position (SEP) is also strongly related to cognitive decline, SEP has been suggested to be a possible modifier of the genetic effect on MCI.

Objective: To investigate whether APOEɛ4 and a genetic sum score of AD-associated risk alleles (GRSAD) interact with SEP indicators to affect MCI in a population-based cohort.

Methods: Using data of 3,834 participants of the Heinz Nixdorf Recall Study, APOEɛ4 and GRSAD by SEP interactions were assessed using logistic regression models, as well as SEP-stratified genetic association analysis. Interaction on additive scale was calculated using the relative excess risk due to interaction (RERI). All analysis were additionally stratified by sex.

Results: Indication for interaction on the additive scale was found between APOEɛ4 and low education on MCI (RERI: 0.52 [95% -confidence interval (CI): 0.01; 1.03]). The strongest genetic effects of the APOEɛ4 genotype on MCI were observed in groups of low education (Odds ratio (OR): 1.46 [95% -CI: 0.79; 2.63] for≤10 years of education versus OR: 1.00 [95% -CI: 0.43; 2.14] for≥18 years of education). Sex stratified results showed stronger effects in women. No indication for interaction between the GRSAD and SEP indicators on MCI was observed.

Conclusion: Results indicate that low education may have an impact on APOEɛ4 expression on MCI, especially among women.
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http://dx.doi.org/10.3233/JAD-210244DOI Listing
June 2021

High Depressive Symptoms in Previously Undetected Diabetes - 10-Year Follow-Up Results of the Heinz Nixdorf Recall Study.

Clin Epidemiol 2021 9;13:429-438. Epub 2021 Jun 9.

Institute for Medical Informatics, Biometry and Epidemiology, University Hospital of Essen, Essen, Germany.

Aim: To determine the 10-year cumulative incidence of high depressive symptoms in people with diagnosed and, in particular, previously undetected diabetes compared to those without diabetes in a population-based cohort study in Germany.

Materials And Methods: We included 2813 participants (52.9% men, mean age (SD) 58.9 (7.7) years, 7.1% diagnosed diabetes, 5.6% previously undetected diabetes) from the Heinz Nixdorf Recall study. We calculated the odds ratios (OR) with 95% confidence intervals (CI) using multiple logistic regression analyses for diagnosed and undetected diabetes.

Results: Cumulative 10-year incidences (95%-CI) of high depressive symptoms in participants with diagnosed diabetes, previously undetected diabetes, and without diabetes were 15.4% (10.7-21.2), 10.1% (5.9-15.9), and 12.4% (11.1-13.8), respectively. Age-sex-adjusted ORs were 1.51 (1.01-2.28) in participants with diagnosed diabetes compared to those without, 1.40 (0.92-2.12) after adjustment for BMI, physical activity, education, and smoking, and 1.33 (0.87-2.02) after further adjustment for stroke and myocardial infarction. ORs in participants with previously undetected diabetes were 0.96 (0.56-1.65), 0.85 (0.49-1.47), and 0.85 (0.49-1.48), respectively, and lower in men than in women.

Conclusion: As expected, we found an increased odds of developing high depressive symptoms in participants with diagnosed diabetes. However, the odds ratios decreased when we considered comorbidities and other covariates. Interestingly, in participants with previously undetected diabetes, the odds was not increased, even 10 years after detection of diabetes. These results support the hypothesis that high depressive symptoms develop due to diabetes-related burdens and comorbidities and not due to hyperglycemia or hyperinsulinemia.
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http://dx.doi.org/10.2147/CLEP.S294342DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8203301PMC
June 2021

Family aggregation of sleep characteristics: Results of the Heinz Nixdorf Recall and the Multi-Generation Study.

PLoS One 2021 4;16(6):e0252828. Epub 2021 Jun 4.

Institute for Medical Informatics, Biometry and Epidemiology, Medical Faculty, University Duisburg-Essen, Essen, Germany.

Introduction: Poor sleep is a risk factor for adverse health events. For health prevention, it may be helpful to know whether poor sleep or sleep disorders in individuals are associated with sleep problems in their partners or children.

Methods: In the MultiGeneration Study (MGS, conducted from 2013 to 2016), 1237 partners (aged 27 to 90 years) and 1660 adult children (aged 18 to 66 years) of index persons were recruited. Index persons are participants of the Heinz Nixdorf Recall Study, a population-based cohort study in the Ruhr area (study start 1999-2001, 4841 participants aged 45-75 years). We used two analysis populations: one with 1181 index persons whose partners were in MGS, and one with 1083 index persons with at least one adult child in MGS. Sleep characteristics were assessed using questionnaires (including the Pittsburgh Sleep Quality Index). The exposure was the presence of a sleep characteristic of the index subject.

Results: Children showed the investigated sleep characteristics more often if these were also present in their parent (e.g., RR (relative risk) = 1.28 (95% CI: 1.06-1.55) for poor sleep quality). In partners, strong associations were observed for rising times and napping, but only weak associations for snoring, poor sleep quality and sleep disorders. Snoring of the bed partner is a risk factor for poor sleep (e.g., RR = 1.67 (0.91-3.07) for difficulties falling asleep).

Conclusion: Aggregation is observed for many sleep characteristics in people living in partnerships as well as in parents and their adult children.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0252828PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8177478PMC
June 2021

Pharmacogenetic association of diabetes-associated genetic risk score with rapid progression of coronary artery calcification following treatment with HMG-CoA-reductase inhibitors -results of the Heinz Nixdorf Recall Study.

Naunyn Schmiedebergs Arch Pharmacol 2021 Aug 22;394(8):1713-1725. Epub 2021 May 22.

Institute of Pharmacology and Toxicology, Centre for Biomedical Education and Research, Witten/Herdecke University, Witten, Germany.

HMG-CoA-Reductase inhibitors (HMGRIs) are currently the most widely used group of drugs in patients with coronary artery disease (CAD) and are given preemptively to patients with high levels of cholesterol, including those with diabetes mellitus (DM). However, intake of HMGRIs also increases the progression of coronary artery calcification (CAC) and the risk of developing DM. This study aimed to investigate whether HMGRI intake interacts with the diabetes-associated genetic risk score (GRS) to affect CAC progression using data from the population-based Heinz Nixdorf Recall (HNR) study. CAC was measured in 3157 participants using electron-beam computed tomography twice, at baseline (CAC) and 5 years later (CAC). CAC progression was classified as slow, expected, or rapid based on predicted values. Weighted DM GRS was constructed using 100 diabetes mellitus-associated single nucleotide polymorphisms (SNPs). We used log-linear regression to evaluate the interaction of HMGRI intake with diabetes-associated GRS and individual SNPs on CAC progression (rapid vs. expected/slow), adjusting for age, sex, and log(CAC + 1). The prevalence of rapid CAC progression in the HNR study was 19.6%. We did not observe any association of the weighted diabetes mellitus GRS with the rapid progression of CAC (relative risk (RR) [95% confidence interval (95% CI)]: 1.01 [0.94; 1.10]). Furthermore, no indication of an interaction between GRS and HMGRI intake was observed (1.08 [0.83; 1.41]). Our analyses showed no indication that the impact of HMGRIs on CAC progression is significantly more severe in patients with a high genetic risk of developing DM than in those with a low GRS.
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http://dx.doi.org/10.1007/s00210-021-02100-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8298241PMC
August 2021

Vitamin D and white matter hyperintensities: results of the population-based Heinz Nixdorf Recall Study and 1000BRAINS.

Eur J Neurol 2021 Jun 31;28(6):1849-1858. Epub 2021 Mar 31.

Institute for Urban Public Health, University Hospital of University Duisburg-Essen, Essen, Germany.

Background And Purpose: Cross-sectional studies showed an inverse association between serum 25-hydroxyvitamin D (25OHD) and white matter hyperintensities (WMHs) whereas the few longitudinal studies did not. The association between baseline 25OHD and WMHs at 10-year follow-up in the Heinz Nixdorf Recall Study plus 1000BRAINS was investigated.

Methods: Data of 505 participants (49% women, 56.2 ± 6.6 years) with 25OHD at baseline (2000-2003) and WMH volume and grade of WMHs using the Fazekas classification at 10-year follow-up were analysed. The association between deseasonalized 25OHD and the base-10 logarithm of WMH volume was evaluated by multiple linear regression, adjusted for age, sex, education, smoking, alcohol consumption, sports, diabetes mellitus, systolic blood pressure and total cholesterol. β-estimators were transformed back (10 ). Using multiple logistic regression, odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated to evaluate the association between deseasonalized 25OHD and Fazekas grades (0, absence and 1, punctate foci vs. 2, beginning and 3, large confluence).

Results: Mean 25OHD was 17.0 ± 8.2 ng/ml, and mean deseasonalized 25OHD was 16.9 ± 7.5 ng/ml. Mean WMH volume was 16.6 ± 17.4 ml, range 1-132 ml. Most grade 2-3 WMHs were found to be periventricular (39% of the participants), parietal (32%) and frontal (31%) (temporal 6%, occipital 3%). The linear regression showed an inverse association between 25OHD and WMH volume. On average, a 25OHD increase of 1 ng/ml was associated with a reduced WMH volume by a factor of 0.99 (95% CI 0.98; 1.00) (fully adjusted). There was also some indication for an inverse association between 25OHD and extent of periventricular (OR 0.98 [95% CI 0.96; 1.01]), frontal (0.99 [0.97; 1.02]) and parietal (0.98 [0.95; 1.00]) WMHs according to the Fazekas classification.

Conclusions: Lower 25OHD may be a risk factor for the occurrence of WMHs.
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http://dx.doi.org/10.1111/ene.14810DOI Listing
June 2021

Population impact of different hypertension management guidelines based on the prospective population-based Heinz Nixdorf Recall study.

BMJ Open 2021 02 17;11(2):e039597. Epub 2021 Feb 17.

Department of Neurology, University Hospital Essen, Essen, Germany.

Objective: Hypertension guidelines strongly differ between societies. The current American College of Cardiology/American Heart Association (ACC/AHA) guideline recommends higher proportions of the general population for antihypertensive medication than the previous American and European guidelines. How cardiovascular risk differs between persons with and without antihypertensive medication recommendation has not been examined. Additionally, the population impact of American, European and international guidelines has not been compared systematically within the same study population.

Methods: We compared the prevalence of antihypertensive medication recommendation according to the American (Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure 7 (JNC7), ACC/AHA 2017), European (European Society of Hypertension (ESH)/European Society of Cardiology (ESC) 2013/2018), and international (WHO/International Society of Hypertension (ISH) 2003, ISH 2020) guidelines in 3092 participants of the population-based Heinz Nixdorf Recall study not taking antihypertensive medication at the baseline examination (58.1±7.5 years, 48.7% males). We furthermore compared incident cardiovascular events during the 5-year follow-up between participants with and without antihypertensive medication recommendation.

Results: The ACC/AHA 2017 guideline recommended the highest percentage of participants for antihypertensive medication (45.8%) compared with the JNC7 (37.2%), ESH/ESC 2013 (17.8%), ESC/ESH 2018 (26.7%), WHO/ISH 2003 (20.3%) or ISH 2020 (25.0%) guidelines. Participants with antihypertensive medication recommendation according to the ACC/AHA 2017 guideline had a significantly higher incidence of cardiovascular events during the 5-year follow-up compared with participants without this recommendation (2.5% vs 1.1%, p=0.003).

Conclusions: Our results call for randomised controlled trials to investigate whether applying the stricter ACC/AHA 2017 recommendation leads to a reduction in cardiovascular disease.
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http://dx.doi.org/10.1136/bmjopen-2020-039597DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7893668PMC
February 2021

Effects of Life Events and Social Isolation on Stroke and Coronary Heart Disease.

Stroke 2021 01 15;52(2):735-747. Epub 2021 Jan 15.

Department of Neurology, University Hospital Essen (J.G., E.-E.D., M.J., C.K., D.M.H.), University of Duisburg-Essen, Germany.

The current coronavirus disease 2019 (COVID-19) pandemic represents a severe, life-changing event for people across the world. Life changes may involve job loss, income reduction due to furlough, death of a beloved one, or social stress due to life habit changes. Many people suffer from social isolation due to lockdown or physical distancing, especially those living alone and without family. This article reviews the association of life events and social isolation with cardiovascular disease, assembling the current state of knowledge for stroke and coronary heart disease. Possible mechanisms underlying the links between life events, social isolation, and cardiovascular disease are outlined. Furthermore, groups with increased vulnerability for cardiovascular disease following life events and social isolation are identified, and clinical implications of results are presented.
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http://dx.doi.org/10.1161/STROKEAHA.120.032070DOI Listing
January 2021

Associations Between Systolic Interarm Differences in Blood Pressure and Cardiovascular Disease Outcomes and Mortality: Individual Participant Data Meta-Analysis, Development and Validation of a Prognostic Algorithm: The INTERPRESS-IPD Collaboration.

Hypertension 2021 02 21;77(2):650-661. Epub 2020 Dec 21.

NIHR Exeter Clinical Research Facility, Royal Devon and Exeter Hospital and University of Exeter College of Medicine & Health, England (A.C.S.).

Systolic interarm differences in blood pressure have been associated with all-cause mortality and cardiovascular disease. We undertook individual participant data meta-analyses to (1) quantify independent associations of systolic interarm difference with mortality and cardiovascular events; (2) develop and validate prognostic models incorporating interarm difference, and (3) determine whether interarm difference remains associated with risk after adjustment for common cardiovascular risk scores. We searched for studies recording bilateral blood pressure and outcomes, established agreements with collaborating authors, and created a single international dataset: the Inter-arm Blood Pressure Difference - Individual Participant Data (INTERPRESS-IPD) Collaboration. Data were merged from 24 studies (53 827 participants). Systolic interarm difference was associated with all-cause and cardiovascular mortality: continuous hazard ratios 1.05 (95% CI, 1.02-1.08) and 1.06 (95% CI, 1.02-1.11), respectively, per 5 mm Hg systolic interarm difference. Hazard ratios for all-cause mortality increased with interarm difference magnitude from a ≥5 mm Hg threshold (hazard ratio, 1.07 [95% CI, 1.01-1.14]). Systolic interarm differences per 5 mm Hg were associated with cardiovascular events in people without preexisting disease, after adjustment for Atherosclerotic Cardiovascular Disease (hazard ratio, 1.04 [95% CI, 1.00-1.08]), Framingham (hazard ratio, 1.04 [95% CI, 1.01-1.08]), or QRISK cardiovascular disease risk algorithm version 2 (QRISK2) (hazard ratio, 1.12 [95% CI, 1.06-1.18]) cardiovascular risk scores. Our findings confirm that systolic interarm difference is associated with increased all-cause mortality, cardiovascular mortality, and cardiovascular events. Blood pressure should be measured in both arms during cardiovascular assessment. A systolic interarm difference of 10 mm Hg is proposed as the upper limit of normal. Registration: URL: https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42015031227.
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http://dx.doi.org/10.1161/HYPERTENSIONAHA.120.15997DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7803446PMC
February 2021

[Aortic stenosis-which diagnostic algorithms and which treatment?]

Authors:
Raimund Erbel

Herz 2020 Nov;45(7):703-714

Institut für Medizinische Informatik, Biometrie und Epidemiologie (IMIBE), Universitätsklinikum Essen (AöR), Hufelandstraße 55, 45147, Essen, Deutschland.

The progress in cardiology during the last 50 years can best be studied by looking at the diagnostics and treatment of patients with aortic valve stenosis. Previously, the clinical examination, electrocardiography (ECG) and chest X‑ray were used before heart catheterization, which included a transseptal puncture to complete the indications for surgery in young patients. Nowadays, echocardiography, often combined with a dobutamine stress test, is the primary diagnostic tool to which computed tomography for quantification of valve calcification and cardiac magnetic resonance imaging can be of additive value. The treatment of severe aortic valve stenosis is no longer only treated by aortic valve replacement but transluminal aortic valve implantation also represents a new therapeutic option. The change in the age groups of treated patients is also noteworthy. Surgery is recommended for patients under 75 years old but for older patients, especially those with a high risk, interventional catheter-assisted treatment is preferred.
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http://dx.doi.org/10.1007/s00059-020-04980-6DOI Listing
November 2020

Air Pollution and Progression of Atherosclerosis in Different Vessel Beds-Results from a Prospective Cohort Study in the Ruhr Area, Germany.

Environ Health Perspect 2020 10 5;128(10):107003. Epub 2020 Oct 5.

Institute of Occupational, Social and Environmental Medicine, Center for Health and Society, Medical Faculty, Heinrich-Heine University Düsseldorf, Düsseldorf, Germany.

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 (), (), and nitrogen dioxide () 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 () 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 higher exposure to (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.
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http://dx.doi.org/10.1289/EHP7077DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7535085PMC
October 2020

Prevention of sudden death: the role of coronary artery calcification imaging in preventive cardiology.

Authors:
Raimund Erbel

Eur Heart J Cardiovasc Imaging 2020 10;21(11):1225-1226

Institute of Medical Informatics, Biometry and Epidemiology, University Hospital Essen, University Duisburg-Essen, Hufelandstr 55, D-45147 Essen, Germany.

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http://dx.doi.org/10.1093/ehjci/jeaa215DOI Listing
October 2020

Risk prediction for coronary heart disease by a genetic risk score - results from the Heinz Nixdorf Recall study.

BMC Med Genet 2020 09 10;21(1):178. Epub 2020 Sep 10.

Institute for Medical Informatics, Biometry and Epidemiology, University Hospital of Essen, University Duisburg-Essen, Essen, Germany.

Background: A Genetic risk score for coronary artery disease (CAD) improves the ability of predicting coronary heart disease (CHD). It is unclear whether i) the use of a CAD genetic risk score is superior to the measurement of coronary artery calcification (CAC) for CHD risk assessment and ii) the CHD risk assessment using a CAD genetic risk score differs between men and women.

Methods: We included 4041 participants (age-range: 45-76 years, 1919 men) of the Heinz Nixdorf Recall study without CHD or stroke at baseline. A standardized weighted CAD genetic risk score was constructed using 70 known genetic variants. The risk score was divided into quintiles (Q1-Q5). We specified low (Q1), intermediate (Q2-Q4) and high (Q5) genetic risk groups. Incident CHD was defined as fatal and non-fatal myocardial infarction, stroke and coronary death. The association between the genetic risk score and genetic risk groups with incident CHD was assessed using Cox models to estimate hazard ratios (HR) and 95%-confidence intervals (CI). The models were adjusted by age and sex (Model1), as well as by established CHD risk factors (RF) and CAC (Model2). The analyses were further stratified by sex and controlled for multiple testing.

Results: During a median follow-up time of 11.6 ± 3.7 years, 343 participants experienced CHD events (219 men). Per-standard deviation (SD) increase in the genetic risk score was associated with 18% increased risk for incident CHD (Model1: p = 0.002) which did not change after full adjustment (Model2: HR = 1.18 per-SD (p = 0.003)). In Model2 we observed a 60% increased CHD risk in the high (p = 0.009) compared to the low genetic risk group. Stratifying by sex, only men showed statistically significantly higher risk for CHD (Model2: HR = 1.23 per-SD (p = 0.004); intermediate: HR = 1.52 (p = 0.04) and high: HR = 1.88 (p = 0.008)) with no statistically significant risk observed in women.

Conclusion: Our results suggest that the CAD genetic risk score could be useful for CHD risk prediction, at least in men belonging to the higher genetic risk group, but it does not outbalance the value of CT-based quantification of CAC which works independently on both men and women and allows better risk stratification in both the genders.
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http://dx.doi.org/10.1186/s12881-020-01113-yDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7487988PMC
September 2020

Genetic variations in G-protein signal pathways influence progression of coronary artery calcification: Results from the Heinz Nixdorf Recall study.

Atherosclerosis 2020 10 5;310:102-108. Epub 2020 Jul 5.

Klinik für Anästhesiologie & Intensivmedizin, Universität Duisburg-Essen und Universitätsklinikum Essen, Essen, Germany.

Background And Aims: Coronary artery calcification (CAC) is one of the most sensitive and specific markers of coronary atherosclerosis and believed to be heritable. We hypothesized that functionally relevant single-nucleotide polymorphisms (SNPs) in the G-protein signal pathway, which have been previously related to coronary artery disease, are associated with CAC progression.

Methods: 3108 participants from the Heinz Nixdorf Recall study with CAC measurements at both baseline (CACb) and 5-year follow-up (CAC5y) were included. We genotyped SNPs rs1042714 (ADRB2), rs6026584 and rs12481583 (GNAS), and rs5443 (GNB3) and defined a priori risk alleles derived from literature data. Regression analyses were applied to measures of 5-year CAC progression, unadjusted, adjusted for age, sex, and adjusted for age, sex, log(CACb+1) as well as for cardiovascular risk factors.

Results: The presence of one or more risk alleles was associated with a 26.9% (95% CI 5.5-52.4) increase in 5-year CAC progression (p = 0.011) and a 29.2% (95% CI 5.9-57.6) accelerated increase of CAC over the 5-year period compared to what was expected with respect to the baseline CAC percentile value (p = 0.012). Each of those risk alleles increased the 5-year CAC progression by 4.4% (95% CI 1.3-7.6, p = 0.006) and resulted in a 4.9% accelerated increase of CAC over the 5-year period (95% CI 1.6-8.4, p = 0.004). These unadjusted data did not change after adjustment.

Conclusions: Genetic variations in the G-protein signal pathway are associated with CAC progression in a cumulative fashion, indicating the importance of the pathway for genetic heritability in CAC progression and coronary artery disease.
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http://dx.doi.org/10.1016/j.atherosclerosis.2020.06.020DOI Listing
October 2020

Blood pressure and cognitive decline - the impact of hypertension over one decade.

Neuropsychol Dev Cogn B Aging Neuropsychol Cogn 2021 07 16;28(4):528-542. Epub 2020 Jul 16.

Department of Neurology, University Hospital of Essen, University of Duisburg-Essen , Germany.

Background: Midlife hypertension is a risk factor for cognitive decline in late-life but little is known about the impact of long-term hypertension on cognitive change over time.

Methods: We examined blood pressure and cognitive function in 2777 participants (baseline: 2000-2003, 45-75 years, 48.4% men) from the Heinz Nixdorf Recall study. Blood pressure was assessed at three study visits and cognitive function was assessed at both follow-ups (mean follow-up: 5.1 years). Z-score differences in five neuropsychological tests, defining cognitive decline, were derived from linear regression models including age and education. The association of cognitive decline over 5 years and blood pressure over 10 years (classified as: normal blood pressure (>10 years, reference), prevalent hypertension (>10 years), incident hypertension t1 (>5 years), incident hypertension t2 (<5 years), temporary hypertension (at least one hypertensive reading)) was calculated using linear regression models resulting in coefficient b and 95% confidence interval. We calculated interactions with age (linear and with a cutoff at 65 years).

Results: Participants with prevalent hypertension showed a greater cognitive decline in both verbal memory tests. Incident hypertension t1 was associated with a greater decline in the visuospatial organization test. There was no interaction with age.

Conclusion: This study showed that prevalent high blood pressure over 10 years is related to cognitive decline. Prevalent hypertension with longer exposure time may be more detrimental than temporary hypertension for cognitive function.
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http://dx.doi.org/10.1080/13825585.2020.1792403DOI Listing
July 2021

Associations between shift work and risk of colorectal cancer in two German cohort studies.

Chronobiol Int 2020 08 13;37(8):1235-1243. Epub 2020 Jul 13.

Institute for Prevention and Occupational Medicine of the German Social Accident Insurance (IPA), Institute of the Ruhr University Bochum , Germany.

The association between shift work and the risk of colorectal cancer (CRC) is still unclear. Therefore, we studied the associations between exposure to shift or night work and incident CRC in two German population-based cohort studies, the Heinz Nixdorf Recall Study (HNR) and the Study of Health in Pomerania (SHIP). Including up to 6,903 participants, we analyzed the cohorts pooled and individually. We estimated incidence rate ratios (IRRs) with adjusted log-linear Poisson regression models with the natural logarithm of person-years as offset and performed subgroup analyses by sex and tumor localization in HNR. The pooled analysis revealed no increased risks for men working in night shifts (IRR: 1.03, 95% CI: 0.62; 1.71). In male HNR participants, we found an increased risk estimate for cancer of the distal colon in shift workers (IRR: 1.60, 95% CI: 0.53; 4.87) and in shift workers who did not perform night work (IRR: 3.93, 95% CI: 0.98; 15.70), but not in night workers. In SHIP, we observed elevated CRC risk estimates for rotating shift work including night work (IRR: 1.45, 95% CI: 0.72; 2.92) and for long-term exposure (IRR: 1.79, 95% CI: 0.81; 3.92) for men. In conclusion, night-shift work was not associated with CRC, although an increased risk was suggested for rotating shift work including nights in SHIP. The heterogeneity of shift-work jobs and schedules and associated lifestyle factors should be taken into account to disentangle a possible relationship between shift work and the risk for CRC in future investigations.
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http://dx.doi.org/10.1080/07420528.2020.1782930DOI Listing
August 2020

Is the Obesity Paradox in Type 2 Diabetes Due to Artefacts of Biases? An Analysis of Pooled Cohort Data from the Heinz Nixdorf Recall Study and the Study of Health in Pomerania.

Diabetes Metab Syndr Obes 2020 16;13:1989-2000. Epub 2020 Jun 16.

Department of Study of Health in Pomerania/Clinical-Epidemiological Research, Institute for Community Medicine, University Medicine Greifswald, Greifswald, Germany.

Aims/hypothesis: There is controversy on whether an obesity paradox exists in type 2 diabetes, ie, that mortality is lowest in overweight or obesity. We examined the role of potential biases in the obesity paradox.

Methods: From two regional population-based German cohort studies - the Heinz Nixdorf Recall Study and the Study of Health in Pomerania (baseline examinations 2000-2003/1997-2001) - 1187 persons with diabetes at baseline were included (mean age 62.6 years, 60.9% males). Diabetes was ascertained by self-report of physician's diagnosis, antidiabetic medication, fasting/random glucose or haemoglobin A1c. Mortality data were assessed for up to 17.7 years. We used restricted cubic splines and Cox regression models to assess associations between body mass index (BMI) and mortality. Sensitivity analyses addressed, inter alia, exclusion of early death cases, of persons with cancer, kidney disease or with history of cardiovascular diseases, and of ever smokers. Furthermore, we examined the role of treatment bias and collider bias for the obesity paradox.

Results: In spline models, mortality risk was lowest for BMI at about 31 kg/m. Sensitivity analyses carried out one after another had hardly any impact on this result. In our cohort, persons with diabetes and BMI ≥30 kg/m did not have better treatment than non-obese patients, and we found that collider bias played only a minor role in the obesity paradox.

Conclusion: In a cohort of 1187 persons with diabetes, mortality risk was lowest in persons with moderate obesity. We cannot explain this result by a variety of sensitivity analyses.
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http://dx.doi.org/10.2147/DMSO.S242553DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7305936PMC
June 2020

Long-term exposure to ambient source-specific particulate matter and its components and incidence of cardiovascular events - The Heinz Nixdorf Recall study.

Environ Int 2020 09 24;142:105854. Epub 2020 Jun 24.

Environmental Epidemiology Group, Institute of Occupational, Social and Environmental Medicine, Medical Faculty, Medical Research School Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.

Background: Few studies have examined the risk of long-term exposure to source-specific airborne pollutants on incidence of cerebrovascular and cardiovascular events.

Objectives: We aimed to estimate the effect of long-term exposure to source-specific air pollution and particulate matter (PM) components on incidence of stroke, coronary heart disease (CHD), and total cardiovascular events (CVE) in the population-based Heinz Nixdorf Recall study (HNR).

Methods: We used baseline (2000-2003) and 14-year follow-up data of the HNR Study, an ongoing population-based prospective cohort study in Western Germany. Participants' residential mean exposures to NO and total and source-specific PM, PM, accumulation mode particle number concentration (PN), and PM components were modelled using a dispersion and chemical transport model. We used Cox regression to evaluate the effect of pollutants (per 1 μg/m increase and per interquartile range - IQR) on risk of stroke and CHD, adjusting for socio-demographic characteristics, lifestyle risk factors and nighttime traffic noise exposure.

Results: In 4,105 included participants (aged 45-76 at baseline, 52.5% women), we observed 118 cases of first stroke and 373 cases of first CHD during 46,748 person-years under risk. The median survival time within the cohort was 13.3 years. No effect of exposure to ambient air pollution on risk of CHD was observed, but distinct effects were observed for stroke. Ambient traffic-specific PM showed a stronger effect on stroke than industry-specific PM: hazard ratios (95% confidence interval) for total, traffic-specific, and industry-specific PM were 1.16 (1.02-1.34), 2.53 (1.07-5.97), and 1.27 (1.03-1.56) per 1 μg/m increase, respectively. PM components showed no substantially different effects from those of total PM per IQR, but higher associations were observed for NH and SO per 1 μg/m. However, the exposure contrast of ammonium and sulfate components was very low.

Conclusion: Traffic-specific PM exhibited stronger effects than total and industry-specific PM on risk of stroke. Among components, NH and SO showed higher effects. No effect was observed for PM and CHD.
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http://dx.doi.org/10.1016/j.envint.2020.105854DOI Listing
September 2020

Associations between haemoglobin A and mortality rate in the KORA S4 and the Heinz Nixdorf Recall population-based cohort studies.

Diabetes Metab Res Rev 2021 Feb 24;37(2):e3369. Epub 2020 Jul 24.

German Center for Diabetes Research, Düsseldorf, Germany.

Background: There is limited knowledge about mortality risk in persons with increased haemoglobin A (HbA ) levels below the diabetes threshold. Moreover, little is known about how associations between increased HbA and mortality depend on the length of follow-up. Therefore, we studied associations between HbA and mortality over long-term follow-up in persons with and without known diabetes.

Methods: We used data from two German population-based cohort studies: KORA S4 Study (Southern Germany, n = 1458, baseline visits in 1999 to 2001, baseline age 55 to 74 years, mortality follow-up 16.8 years) and Heinz Nixdorf Recall (HNR) Study (Ruhr area, n = 4613, baseline visits in 2000 to 2003, baseline age 45 to 75 years, mortality follow-up 17.8 years). Adjusted log-linear models were fitted to estimate relative risks (RRs) with 95% confidence intervals (CI).

Results: In both cohorts, participants with HbA 39 to 41 mmol/mol (5.7%-5.9%) and HbA 42 to 46 mmol/mol (6.0% to 6.4%) did not have a larger overall mortality risk than participants with HbA  < 39 mmol/mol (5.7%): the corresponding adjusted RRs were 1.00 (95% CI: 0.83-1.21) and 1.01 (0.80-1.27) in KORA and 0.99 (0.82-1.21) and 0.83 (0.65-1.07) in the HNR Study. For the pooled cohorts, the RR for HbA 39 to 46 mmol/mol (5.7%-6.4%) was 0.96 (0.85-1.07). Associations between newly detected diabetes (HbA  ≥ 6.5%) and mortality were weak after 4 and 8 years of follow-up, but were stronger after 12 years of follow-up, whereas associations between previously known diabetes (baseline) and mortality decreased.

Conclusions: HbA -defined pre-diabetes is not associated with overall mortality. For newly detected and previously known diabetes, mortality risks vary with length of follow-up.
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http://dx.doi.org/10.1002/dmrr.3369DOI Listing
February 2021

Genetic risk scores for coronary artery disease and its traditional risk factors: Their role in the progression of coronary artery calcification-Results of the Heinz Nixdorf Recall study.

PLoS One 2020 7;15(5):e0232735. Epub 2020 May 7.

Institute of Pharmacology and Toxicology, Centre for Biomedical Education and Research, Witten/Herdecke University, Witten, Germany.

Background: Atherosclerosis is the primary cause of coronary artery disease (CAD). Several observational studies have examined the association of traditional CAD risk factors with the progression of coronary artery calcification (CAC). In our study we investigated the effect of 11 different genetic risk scores associated with CAD and CAD risk factors on the progression of CAC.

Methods And Results: We included 3097 participants from the Heinz Nixdorf Recall study who had available CAC measurements at baseline (CACb) and at the 5-year follow-up (CAC5y). A weighted genetic risk score for CAD and each of the CAD-associated risk factors was constructed. Multiple regression analyses were applied to i) the difference between the observed log(CAC5y+1) (log(obs)) and expected log(CAC5y+1) (log(exp)) at the 5-year follow-up following the individual's log(CACb+1) percentile for the time between scans (log(obs)-log(exp)) and ii) the 5-year CAC progression, defined as 5*(log(CAC5y+1)-log(CACb+1))/time between the scans, adjusted for age, sex, and log(CACb+1) as well as for risk factors. The median percent deviation from the expected (CAC5y+1) and the 5-year progression of (CAC+1) in our study were 0 (first quartile: Q1; third quartile: Q3: -0.32; 0.48) and 45.4% (0%; 171.0%) respectively. In the age-, sex- and log(CACb+1)-adjusted model, the per-standard deviation (SD) increase in CAD genetic risk score was associated with the percent deviation from the expected (CAC5y+1) (9.7% (95% confidence interval: 5.2%; 14.5%), p = 1.6x10-5) and the 5-year progression of CAC (7.1% (3.0%; 11.4%), p = 0.0005). The CAD genetic risk score explains an additional 0.6% of the observed phenotypic variance for "log(obs)-log(exp)" and 0.4% for 5-year progression of CAC. Additionally, the per-SD increase in the CAC genetic risk score was associated with the percent deviation from the expected (CAC5y+1) (6.2% (1.9%; 10.8%, p = 0.005)) explaining an additional 0.2% of the observed phenotypic variance. However, the per-SD increase in the CAC genetic risk score was not associated with the 5-year progression of CAC (4.4% (0.4%; 8.5%), p = 0.03) after multiple testing. Adjusting for risk factors did not change the results. None of the other genetic risk scores showed an association with the percent deviation from the expected (CAC5y+1) or with the 5-year progression of CAC.

Conclusions: The association of the CAC genetic risk score and the CAD genetic risk score provides evidence that genetic determinants for CAC and CAD influence the progression of CAC.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0232735PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7205301PMC
August 2020

Associations between self-reported sleep characteristics and incident mild cognitive impairment: The Heinz Nixdorf Recall Cohort Study.

Sci Rep 2020 04 16;10(1):6542. Epub 2020 Apr 16.

Department of Neurology, University Hospital of Essen, University of Duisburg-Essen, Essen, Germany.

Associations of sleep characteristics with mild cognitive impairment (MCI) have been examined in cross-sectional, but rarely in longitudinal studies. Incident MCI and sleep characteristics were assessed in 1,890 participants of the first and second follow-up of the Heinz Nixdorf Recall study, a population-based cohort study in Germany (age at first follow-up 50-80 years, mean follow-up 5.2 years). MCI was assessed with extensive cognitive tests. Sleep questionnaires including PSQI (Pittsburgh Sleep Quality Index) were used to assess sleep quality, sleep disturbances, time asleep, and time in bed. Relative risks (RR) of developing MCI when exposed to sleep characteristics were assessed in regression models adjusted for sociodemographic and cardiovascular risk factors. Poor sleep quality (PSQI > 5) (RR = 1.43, 95% CI: 1.12-1.82, fully adjusted, reference: PSQI ≤ 5) and difficulties initiating sleep (almost nightly versus never) (RR = 1.40, 0.94-2.08) were associated with incident MCI. For time in bed, the risk of MCI was increased for ≤ 5 hours (RR = 2.86, 1.24─6.60, reference:7 to <8 hours). In this longitudinal study with older participants, MCI risk was increased in persons with poor sleep quality, difficulties initiating sleep, and short time in bed.
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http://dx.doi.org/10.1038/s41598-020-63511-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7162850PMC
April 2020

Association between lipoprotein(a) (Lp(a)) levels and Lp(a) genetic variants with coronary artery calcification.

BMC Med Genet 2020 03 27;21(1):62. Epub 2020 Mar 27.

Institute for Medical Informatics, Biometry and Epidemiology, University Hospital of Essen, University Duisburg-Essen, Essen, Germany.

Background: To examine the association between lipoprotein(a) (Lp(a)) levels, LPA (rs10455872 and rs3798220) and IL1F9 (rs13415097) single nucleotide polymorphisms (SNPs) with coronary artery calcification (CAC), an important predictor for coronary artery disease (CAD).

Methods: We used data from 3799 (mean age ± SD: 59.0 ± 7.7 years, 47.1% men) Heinz Nixdorf Recall study participants. We applied linear regression models to explore the relation between the log-transformed Lp(a) levels and LPA and IL1F9 SNPs with log (CAC + 1). The association between the SNPs and log-transformed Lp(a) levels was further assessed using linear regression. The models were adjusted for age and sex (Model 1) and additionally for Lp(a) levels (Model 2).

Results: We observed a statistically significant association between log-transformed Lp(a) levels and CAC (Model 1: beta per log-unit increase in Lp(a) levels = 0.11; 95% confidence interval [95% CI] [0.04; 0.18], p = 0.002). Furthermore, the LPA SNP rs10455872 showed a statistically significant association with CAC (Model 1: beta per allele = 0.37 [0.14; 0.61], p = 0.002). The association between rs10455872 and CAC was attenuated after adjustment for Lp(a) levels (Model 2: beta per allele = 0.26 [- 0.01; 0.53], p = 0.06). Both LPA SNPs also showed a statistically significant association with Lp(a) levels (Model 1: beta per allele: 1.56 [1.46; 1.65], p < 0.0001 and beta per allele: 1.51 [1.33; 1.69], p < 0.0001)). The Mendelian randomization analysis showed that Lp(a) is a causal risk factor for CAC (estimate per log-unit increase in Lp(a) levels (95% CI), p: 0.27 [0.11; 0.44], p = 0.001). The IL1F9 SNP did not show any statistically significant association with Lp(a) levels or with CAC.

Conclusions: We provide evidence for the association of LPA rs10455872 with higher levels of Lp(a) and CAC in our study. The results of our study suggest that rs10455872, mediated by Lp(a) levels, might play a role in promoting the development of atherosclerosis leading to cardiovascular disease events.
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http://dx.doi.org/10.1186/s12881-020-01003-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7099786PMC
March 2020

Systematic Review of Aortic Dissection Detection Risk Score Plus D-dimer for Diagnostic Rule-out Of Suspected Acute Aortic Syndromes.

Acad Emerg Med 2020 10 21;27(10):1013-1027. Epub 2020 Apr 21.

S.C.U. Medicina d'Urgenza, Molinette Hospital, A.O.U. Città della Salute e della Scienza, Torino, Italy.

Objectives: In patients at low clinical probability of acute aortic syndromes (AASs), decision on advanced aortic imaging is cumbersome. Integration of the aortic dissection detection risk score (ADD-RS) with D-dimer (DD) provides a potential pipeline for standardized diagnostic rule-out. We systematically reviewed and summarized supporting data.

Methods: Cross-sectional studies assessing integration of ADD-RS with DD for diagnosis of AASs were identified on MEDLINE, EMBASE and Web Of Science databases. Two reviewers independently screened articles, assessed quality, and extracted data. The quality of design and reporting was evaluated with the QUADAS-2 and STARD tools. Individual patient data were obtained, to allow analysis of both conventional (500 ng/mL) and age-adjusted (DD ) DD cutoffs. Data were summarized for four diagnostic strategies combining ADD-RS = 0 or ≤ 1, with DD < 500 ng/mL or < DD . The statistical heterogeneity of the diagnostic variables was estimated with Higgins' I . Pooled values were calculated for variables showing nonsignificant heterogeneity.

Results: After screening of 680 studies, four articles (including a total of 3,804 patients) met inclusion criteria. One prospective study provided a low risk of bias/applicability concerns, while methodologic limitations were found in the other three retrospective studies. Statistical heterogeneity was negligible for sensitivity and negative likelihood ratio (LR) values and significant for specificity and positive LR values of all diagnostic strategies. Pooled sensitivity was 99.9% (95% confidence interval [CI] = 99.3% to 100%, I  = 0) for ADD-RS = 0 and DD < 500 ng/mL or < DD , 98.9% (95% CI = 97.9% to 99.9%, I  = 0) for ADD-RS ≤ 1 and DD < 500 ng/mL, and 97.6% (95% CI = 96.3% to 98.9%, I  = 0) for ADD-RS ≤ 1 and DD < DD .

Conclusions: Despite methodologic limitations, integration of ADD-RS = 0 or ≤ 1 with DD < 500 ng/mL shows negligible heterogeneity and consistently high sensitivity across studies, thus supporting reliability for diagnostic rule-out of AASs. Data supporting ADD-RS = 0 plus DD appear preliminary and require further scrutiny.
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http://dx.doi.org/10.1111/acem.13969DOI Listing
October 2020

Association of social relationships with incident cardiovascular events and all-cause mortality.

Heart 2020 09 12;106(17):1317-1323. Epub 2020 Mar 12.

Department of Neurology, University Hospital Essen, Essen, Germany

Objective: To examine how different aspects of social relationships are associated with incident cardiovascular events and all-cause mortality.

Methods: In 4139 participants from the population-based Heinz Nixdorf Recall study without previous cardiovascular disease (mean (SD) age 59.1 (7.7) years, 46.7% men), the association of self-reported instrumental, emotional and financial support and social integration at baseline with incident fatal and non-fatal cardiovascular events and all-cause mortality during 13.4-year follow-up was assessed in five different multivariable Cox proportional hazards regression models: minimally adjusted model (adjusting for age, sex, social integration or social support, respectively); biological model (minimally adjusted+systolic blood pressure, low-density and high-density lipoprotein cholesterol, glycated haemoglobin, body mass index, antihypertensive medication, lipid-lowering medication and antidiabetic medication); health behaviour model (minimally adjusted+alcohol consumption, smoking and physical activity); socioeconomic model (minimally adjusted+income, education and employment); and depression model (minimally adjusted+depression, antidepressants and anxiolytics).

Results: 339 cardiovascular events and 530 deaths occurred during follow-up. Lack of financial support was associated with an increased cardiovascular event risk (minimally adjusted HR=1.30(95% CI 1.01 to 1.67)). Lack of social integration (social isolation) was associated with increased mortality (minimally adjusted HR=1.47 (95% CI 1.09 to 1.97)). Effect estimates did not decrease to a relevant extent in any regression model.

Conclusions: Perceiving a lack of financial support is associated with a higher cardiovascular event incidence, and being socially isolated is associated with increased all-cause mortality. Future studies should investigate how persons with deficient social relationships could benefit from targeted interventions.
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http://dx.doi.org/10.1136/heartjnl-2019-316250DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7476279PMC
September 2020

[Evidence-based primary prevention : Where do we stand in 2020?]

Herz 2020 Feb;45(1):1-2

Institut für Medizinische Informatik, Biometrie und Epidemiologie (IMIBE), Universitätsklinikum Essen (AöR), Essen, Deutschland.

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http://dx.doi.org/10.1007/s00059-019-04889-9DOI Listing
February 2020

No difference in medication regimes and dosing in study participants with and without blood pressure control: longitudinal data of the population-based Heinz Nixdorf Recall Study.

J Hypertens 2020 03;38(3):504-510

Institute for General Medicine, University Hospital Essen, University of Duisburg-Essen.

Background: To achieve blood pressure (BP) control adequate dosing of first-line antihypertensive medications is recommended in addition to life-style changes. Given observations that dosing of antihypertensive agents is frequently insufficient, we compared the changes of BP control rates and antihypertensive drug regimens in a prospective German population using a new strategy to analyze medication dosing.

Methods: This analysis is based on data of the baseline (2000-2003) and the first follow-up examination (2005-2008) of the population-based Heinz Nixdorf Recall study. Participants with hypertension at baseline (BP ≥140/90 mmHg or at least one antihypertensive agent) who participated in both examinations were included.

Results: Of the 4157 participants, 2289 (55.1%) had hypertension at baseline. The prevalence of participants on antihypertensive agents was 60.3% at baseline and increased to 75.1% at follow-up. The mean number of antihypertensive agents was 2 [±1 SD (standard deviation)] initially and at follow-up. The prevalence of medication-controlled BP did not improve over time (baseline: 54.5%, follow-up: 56.5%). When stratifying by medication-controlled BP, the medication dosing rate slightly increased over time without differences between groups [controlled versus uncontrolled BP: 40.9 versus 46.2% (baseline); 50.1 versus 51.9% (follow-up)].

Conclusion: Although the prevalence of antihypertensive medication use increased in the study period, the BP control rate did not. In contrast to clinical reasoning, participants with uncontrolled BP did neither receive more agents nor higher dosing despite outcome-relevant hypertension. Our approach to analyze medication dosing suggests a potential to improve cardiovascular outcomes by increasing dosages of antihypertensive agents.
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http://dx.doi.org/10.1097/HJH.0000000000002299DOI Listing
March 2020

Male-pattern baldness and incident coronary heart disease and risk factors in the Heinz Nixdorf Recall Study.

PLoS One 2019 19;14(11):e0225521. Epub 2019 Nov 19.

Institute for Medical Informatics, Biometry and Epidemiology, University Hospital Essen, Essen, Germany.

Male-pattern baldness (MPB) is characterized by a progressive hair loss from the frontal and vertex scalp that affects about 80% of men at the age of 80 years. Epidemiological studies show positive associations between MPB and coronary heart disease (CHD) and CHD related risk factors such as blood pressure (BP), diabetes mellitus (DM) or elevated blood lipid levels. The results however vary with regard to the pattern of hair loss (i.e. moderate, severe, frontal or vertex). Further, no study has investigated for a shared genetic determinant between MPB and CHD as well as CHD related risk factors. Using the longitudinal data from the population-based Heinz Nixdorf Recall study we aimed to systematically investigate the association between MPB and incident CHD and CHD risk factors on (i) an epidemiological (N = 1,673 males) and (ii) a genetic (N = 1,357 males) level. The prevalence of any baldness in our study population was 88% (mean age ± SD: 64±7.5 years). Compared to men with 'no baldness', in men with any kind of baldness a slightly increased risk for CHD (Hazard ratio [95% confidence interval (95%CI)] = 1.2 [0.8; 1.9]), a slightly higher extend of coronary artery calcification (CAC) (Beta [95%CI] = 0.2 [-0.1; 0.6]), a moderately increased risk for DM (prevalence ratio [95%CI] = 1.4 [0.9; 2.0]) and higher body mass index (BMI) (Beta [95%CI] = 0.6 [0.00003; 1.2]) seem to be indicated in the adjusted model. In contrast, the MPB genetic risk score did not show any association with CHD or CHD risk factors. Taken together, the results of our study suggest a weak association between MPB and a few CHD risk factors (CAC, DM and BMI) but do not point to MPB as a strong surrogate measure for CHD and CHD risk factors in general.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0225521PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6863534PMC
March 2020

Socioeconomic Position is Positively Associated with Monoclonal Gammopathy of Undetermined Significance in a Population-based Cohort Study.

Ann Hematol 2019 Dec 6;98(12):2761-2767. Epub 2019 Nov 6.

Institute for Medical Informatics, Biometry and Epidemiology, University of Duisburg-Essen, Hufelandstraße 55, 45122, Essen, Germany.

Knowledge of social inequalities in monoclonal gammopathy of undetermined significance (MGUS) will contribute to understanding multiple myeloma (MM) etiology, as MGUS consistently precedes MM. The aim of the present study was to examine whether socioeconomic position (SEP) is associated with MGUS in a population-based cohort including information on potential MGUS risk factors. Overall, 4787 study participants aged 45-75 years with information on MGUS were included. SEP indicators (education, income) and potential risk factors (i.e., body mass index, diabetes, smoking, dietary factors) were assessed at baseline. Overall, 260 MGUS cases were detected at baseline and prospectively over a 10-year follow-up. In age-adjusted logistic regression models, a lower chance of having MGUS at baseline or developing MGUS during 10 years of follow-up was indicated for groups of low SEP with odds ratios (OR) of 0.39 (95% confidence interval [95%-CI] 0.19-0.76) for women and 0.48 (95% CI 0.10-1.16) for men in the lowest compared to the highest educational group. After additionally including potential mediating risk factors in the regression models, the estimated ORs changed only slightly in magnitude. Similar results were obtained for income. Current smoking and low fruit consumption were associated with MGUS independently of SEP in women, but not in men. The present study indicates a lower MGUS risk in lower SEP groups. Supporting evidence is given that smoking and diet play a role in the development of MGUS independently of SEP, while it has to be assumed that risk factors unknown to date are responsible for the observed social inequalities in MGUS.
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http://dx.doi.org/10.1007/s00277-019-03825-5DOI Listing
December 2019

One simple claudication question as first step in Peripheral Arterial Disease (PAD) screening: A meta-analysis of the association with reduced Ankle Brachial Index (ABI) in 27,945 subjects.

PLoS One 2019 4;14(11):e0224608. Epub 2019 Nov 4.

DZHK (German Centre for Cardiovascular Research), partner site Greifswald, Greifswald, Germany.

Purpose And Methods: A meta-analysis using data from seven German population-based cohorts was performed by the German Epidemiological consortium of Peripheral Arterial Disease (GEPArD) to investigate whether one question about claudication is more efficient for PAD screening than established questionnaires. Claudication was defined on the basis of the answer to one question asking for pain in the leg during normal walking. This simple question was compared with established questionnaires, including the Edinburgh questionnaire. The associations of claudication with continuous ABI values and decreased ABI were analyzed by linear and logistic regression analysis, respectively. The results of the studies were pooled in a random effect meta-analysis, which included data from 27,945 individuals (14,052 women, age range 20-84 years).

Results: Meta-analysis revealed a significant negative association between claudication and ABI, which was stronger in men (β = -0.07; 95%CI -0.10, -0.04) than in women (β = -0.02; 95%CI -0.02, -0.01). Likewise, the presence of claudication symptoms was related to an increased odds of a decreased ABI in both men (Odds ratio = 5.40; 95%CI 4.20, 6.96) and women (Odds ratio = 1.99; 95%CI 1.58, 2.51).

Conclusions: Asking only one question about claudication was able to identify many individuals with a high likelihood of a reduced ABI with markedly higher sensitivity and only slightly reduced specificity compared to more complex questionnaires. At least in men, this question should be established as first screening step.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0224608PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6827909PMC
April 2020

Cardiovascular Risk and Atherosclerosis Progression in Hypertensive Persons Treated to Blood Pressure Targets.

Hypertension 2019 12 4;74(6):1436-1447. Epub 2019 Nov 4.

From the Department of Neurology, University Hospital Essen, Germany (J.G., R.K., C.W., D.M.H.).

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.
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http://dx.doi.org/10.1161/HYPERTENSIONAHA.119.13827DOI Listing
December 2019

HDAC9 is implicated in atherosclerotic aortic calcification and affects vascular smooth muscle cell phenotype.

Nat Genet 2019 11 28;51(11):1580-1587. Epub 2019 Oct 28.

National Heart, Lung, and Blood Institute Framingham Heart Study, Framingham, MA, USA.

Aortic calcification is an important independent predictor of future cardiovascular events. We performed a genome-wide association meta-analysis to determine SNPs associated with the extent of abdominal aortic calcification (n = 9,417) or descending thoracic aortic calcification (n = 8,422). Two genetic loci, HDAC9 and RAP1GAP, were associated with abdominal aortic calcification at a genome-wide level (P < 5.0 × 10). No SNPs were associated with thoracic aortic calcification at the genome-wide threshold. Increased expression of HDAC9 in human aortic smooth muscle cells promoted calcification and reduced contractility, while inhibition of HDAC9 in human aortic smooth muscle cells inhibited calcification and enhanced cell contractility. In matrix Gla protein-deficient mice, a model of human vascular calcification, mice lacking HDAC9 had a 40% reduction in aortic calcification and improved survival. This translational genomic study identifies the first genetic risk locus associated with calcification of the abdominal aorta and describes a previously unknown role for HDAC9 in the development of vascular calcification.
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http://dx.doi.org/10.1038/s41588-019-0514-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6858575PMC
November 2019
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