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Background: The aim of the long-term Heinz Nixdorf Recall Study (observation period 20 years) was to establish the extent to which computed tomography (CT) improves the predictability of cardiovascular events relative to determination of risk factors alone. Methods: In the period 2000-2003, study staff examined 4355 probands (53% of them female) aged 45--75 years with no signs of cardiovascular disease. The Atherosclerotic Cardiovascular Disease (ASCVD) score was calculated on the basis of demographic data and cardiovascular risk factors. Cardiac CT was carried out over the same period and coronary artery calcification (CAC) was graded according to the Agatston score. Results: The median duration of follow-up was 18.2 years for men and 17.8 years for women. Myocardial infarction or stroke occurred in 458 (11%) of the 4154 participants with complete data. Overall, estimation of risk using a combination of ASCVD score and CAC grade was superior to the ASCVD score alone--even after 10 and 20 years. Classification into established risk categories improved by 12.2% (95% confidence interval: [5.3%; 18.1%]). In the highest ASCVD risk category, we observed occurrence of a cardiovascular event over 20 years for 14% [5.0%; 23.1%] of probands with a CAC score = 0 but for 34.2% [27.5%; 41.4%] of those with a CAC score ≥ 400. In the lowest ASCVD risk category, an event occurred in 2.4% [1.4%; 3.7%] of probands with a CAC score = 0 and in 23.5% [2.3%; 35.8%] of those with a CAC score ≥ 400. Conclusion: Even after 20 years, individual risk prediction is improved by addition of CT-based determination of coronary artery calcification to the ASCVD score. Therefore, assessment of ASCVD risk factors should be complemented more widely by cardiac CT in the primary prevention of cardiovascular disease. [ABSTRACT FROM AUTHOR]

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About 5-15% of patients with COVID(corona virus disease)-19 infection require intensive care surveillance and ventilatory support. In addition, similar to ventilator-induced lung damage (VILI), stress and strain on the lung associated with noninvasively generated high tidal volumes may also cause patient self-induced lung injury (P-SILI). In summary, ventilation of COVID-19 ICU patients is challenging because of the heterogeneous lung pathology that requires an individualized lung-protective ventilation strategy to improve outcome. [Extracted from the article]

Background: Atrial fibrillation (AF) and coronary artery disease (CAD) may be encountered coincidently in a large portion of patients. However, data on coronary artery calcium burden in such patients are lacking. Thus, we sought to determine the value of cardiac computed tomography (CCT) in patients presenting with new-onset AF associated with an intermediate pretest probability for CAD admitted to a chest pain unit (CPU). Methods: Calcium scores (CS) of 73 new-onset, symptomatic AF subjects without typical clinical, electrocardiographic, or laboratory signs of acute coronary syndrome (ACS) admitted to our CPU were analyzed. In addition, results from computed tomography angiography (CTA) were related to coronary angiography findings whenever available. Results: Calcium scores of zero were found in 25%. Median Agatston score was 77 (interquartile range: 1-270) with gender- and territory-specific dispersal. CS scores above average were present in about 50%, high (> 400)-to-very high (> 1000) CS scores were found in 22%. Overall percentile ranking showed a relative accordance to the reference percentile distribution. Additional CTA was performed in 47%, revealing stenoses in 12%. Coronary angiography was performed in 22% and resulted in coronary intervention or surgical revascularization in 7%. On univariate analysis, CS > 50th percentile failed to serve as an independent determinant of significant stenosis during catheterization. Conclusions: Within a CPU setting, relevant CAD was excluded or confirmed in almost 50%, the latter with a high proportion of coronary angiographies and subsequent coronary interventions, underlining the diagnostic value of CCT in symptomatic, non-ACS, new-onset AF patients when admitted to a CPU. [ABSTRACT FROM AUTHOR]

Aims: To compare the predictive value of coronary artery calcification (CAC), carotid intima-media thickness (CIMT) and ankle-brachial index (ABI) in a primary prevention cohort depending on risk factor profile to determine which of the three markers improves cardiovascular (CV) risk discrimination best in which risk group. Methods and results: We quantified CAC, CIMT, and ABI in 3108 subjects (mean age 59.2 ± 7.7, 47.1% male) without prevalent CV diseases from the population-based Heinz Nixdorf Recall study. Associations with incident major CV events (coronary event, stroke, CV death; n = 223) were assessed during a follow-up period of 10.3 ± 2.8 years with Cox proportional regressions in the total cohort and stratified by Framingham risk score (FRS) groups. Discrimination ability was evaluated with Harrell's C. All three markers were associated with CV events (hazard ratio [95% confidence interval (CI)]: CAC: 1.31 (1.23-1.39) per 1-unit increase in log(CAC + 1) vs. CIMT: 1.27 (1.13-1.43) per 1 SD vs. ABI: 1.30 (1.14-1.49) per 1 SD, in FRS adjusted models). Considering reclassification, CAC lead to highest reclassification in the total cohort, while also for CIMT and ABI significant improvement in net-reclassification was observed [NRI (95% CI): CAC: 0.55 (0.42-0.69); CIMT: 0.32 (0.19-0.45); ABI: 0.19 (0.10-0.28)]. Conclusion: Coronary artery calcification provides the best discrimination of risk compared with CIMT and ABI, particularly in the intermediate risk group, whereas CIMT may be an alternative measure for reassurance in the low risk group. [ABSTRACT FROM AUTHOR]

IMPORTANCE The role of coronary artery calcium (CAC) testing for guiding preventive strategies among women at low cardiovascular disease (CVD) risk based on the American College of Cardiology and American Heart Association CVD prevention guidelines is unclear. OBJECTIVE To assess the potential utility of CAC testing for CVD risk estimation and stratification among low-risk women. DESIGN, SETTING, AND PARTICIPANTS Women with 10-year atherosclerotic CVD (ASCVD) risk lower than 7.5% from 5 large population-based cohorts: the Dallas Heart Study (United States), the Framingham Heart Study (United States), the Heinz Nixdorf Recall study (Germany), the Multi-Ethnic Study of Atherosclerosis (United States), and the Rotterdam Study (the Netherlands). The 5 cohorts were selected based on the availability of CAC data in a sizable group of low-risk women from the general population together with the long detailed follow-up data. Across the cohorts, events were assessed from the date of CAC scan (performed from 1998 through 2006) until January 1, 2012; January 1, 2014; or March 6, 2015. Fixed-effects meta-analysis was conducted to combine the results of the 5 studies. EXPOSURES CAC score by computed tomography. MAIN OUTCOMES AND MEASURES Main outcome was incident ASCVD, including nonfatal myocardial infarction, coronary heart disease (CHD) death, and stroke. Association of CAC with ASCVD was examined using Cox proportional hazards models. To assess whether CAC was associated with improved ASCVD risk predictions beyond the traditional risk factors, the C statistic and the continuous net reclassification improvement (cNRI) index were calculated. RESULTS Among 6739 women with low ASCVD risk from the 5 studies, mean age ranged from 44 to 63 years and CAC was present in 36.1%. Across the cohorts, median follow-up ranged from 7.0 to 11.6 years. A total of 165 ASCVD events occurred (64 nonfatal myocardial infarctions, 29 CHD deaths, and 72 strokes), with the ASCVD incidence rates ranging from 1.5 to 6.0 per 1000 person-years. Compared with the absence of CAC (CAC = 0), presence of CAC (CAC >0) was associated with an increased risk of ASCVD (incidence rates per 1000 person-years, 1.41 for CAC absence vs 4.33 for CAC presence; difference, 2.92 [95% CI, 2.02-3.83]; multivariable-adjusted hazard ratio, 2.04 [95% CI, 1.44-2.90]). The addition of CAC to traditional risk factors improved the C statistic from 0.73 (95% CI, 0.69-0.77) to 0.77 (95% CI, 0.74-0.81) and provided a cNRI of 0.20 (95% CI, 0.09-0.31) for ASCVD prediction. CONCLUSIONS AND RELEVANCE Among women at low ASCVD risk, CAC was present in approximately one-third and was associated with an increased risk of ASCVD and modest improvement in prognostic accuracy compared with traditional risk factors. Further research is needed to assess the clinical utility and cost-effectiveness of this additional accuracy. [ABSTRACT FROM AUTHOR]

Background: High resting heart rate (RHR) predicts cardiovascular outcomes in patients with vascular disease and heart failure. We evaluated the prognostic value of RHR in a large contemporary population-based, prospective cohort of individuals without known coronary artery disease. Methods and results: Resting heart rate (RHR) was determined in 4091 individuals (mean age 59.2 ± 7.7; 53 % women) from the Heinz Nixdorf RECALL study, of whom, 3348 were free of heart rate lowering medication. During 10.5 years of follow-up (median), 159 (3.9 %) individuals developed a coronary event and 398 (9.7 %) died of any cause. Persons without any event ( n = 3603) had similar heart rates as persons with coronary events (69.5 ± 11 versus 69.9 ± 11 bpm, p = 0.51) but lower heart rates than persons who died (72.3 ± 13 bpm, p < 0.0001). In individuals without heart rate lowering medication, an increase in heart rate by 5 bpm was associated with an increased hazard ratio (HR) for all-cause mortality of 13 % in unadjusted analysis and also upon adjustment for traditional cardiovascular risk factors, including coronary artery calcification [full model: HR (95 % CI) 1.13 (1.07-1.20), p < 0.0001], but not for coronary events [HR 1.02 (0.94-1.11), p = 0.60]. In individuals without heart rate lowering medication, the HR (full model) for heart rate ≥70 versus <70 bpm with regard to all-cause mortality and coronary events was 1.68 (1.30-2.18), p < 0.0001, and 1.20 (0.82-1.77), p = 0.35. Analysis of the entire cohort revealed a continuous relationship of heart rate with all-cause mortality [HR for lowest to highest heart rate quartile 1.64 (1.22-2.22), p = 0.001, full model] but not with coronary events [HR 1.04 (0.65-1.66), p = 0.86]. Conclusions: In the general population without known coronary artery disease and heart rate lowering medication, elevated RHR is an independent risk marker for all-cause mortality but not for coronary events. [ABSTRACT FROM AUTHOR]

Objectives: It appears that not only depression, but also low life satisfaction (LS), is related to sleep disorder in the general population. We evaluate whether the prevalence of sleep disorder attributable to depressed mood is greater among participants with low LS. Setting, participants and outcome measures: Analysis of cross-sectional data from 3880 cohort members from the German Heinz Nixdorf Recall study (2006-2008) aged 51-81 years. Standard mood (Center for Epidemiological Studies Depression scale (CES-D) for Depressive symptoms and a single-item life satisfaction measure) and sleep quality (Pittsburgh Sleep Quality Index, PSQI) measures were conducted as part of the survey. Multiple imputation was used to deal with missing data in outcome, exposures or covariates. Relative excess risk for interaction (RERI) and its 95% CIs were estimated using adjusted prevalence ORs. Owing to the study size, the precision of the measures of additive interaction is relatively low. Results: We observed an association between depressed mood (5-units increase in CES-D score) (POR=1.7 (95% CI 1.6 to 1.8)) and sleep disorder, and between low LS (not very satisfied vs very satisfied) (POR=1.5 (1.1 to 2.2)) and sleep disorder. Also, we observed a synergistic effect between lower level of LS (not very satisfied) and depressed mood (score =16) on prevalence of sleep disorders (RERI=3.7 (-0.2 to 7.1)). Furthermore, these findings were corroborated in sensitivity analysis carried out with the complete case data set and in sex-specific analyses (RERI=5.5 (-0.4 to 11.3), and RERI=2.4 (-2.5 to 7.4) for men and women, respectively). Conclusions: Both depressed mood and LS are notably associated with sleep quality, and these relationships are best captured by considering their joint effects. Depression and LS need to be taken into consideration when analysing sleep quality. [ABSTRACT FROM AUTHOR]

BACKGROUND: In several studies, exposure to fine particulate matter (PM) has been associated with inflammation, with inconsistent results. We used repeated measurements to examine the association of long-term fine and ultrafine particle exposure with several blood markers of inflammation and coagulation. METHODS: We used baseline (2000-2003) and follow-up (2006-2008) data from the Heinz Nixdorf Recall Study, a German population-based prospective cohort of 4814 participants. A chemistry transport model was applied to model daily surface concentrations of PM air pollutants (PM10, PM2.5) and particle number on a grid of 1 km(2). Applying mixed regression models, we analysed associations of long-term (mean of 365days prior to blood draw) particle exposure at each participant's residence with the level of high-sensitivity C reactive protein (hs-CRP), fibrinogen, platelet and white cell count (WCC), adjusting for short-term PM exposure (moving averages of 1-7days), personal characteristics, season, ambient temperature (1-5days), ozone and time trend. RESULTS: We analysed 6488 observations: 3275 participants with baseline data and 3213 with follow-up data. An increase of 2.4ug/m(3) in long-term PM2.5 was associated with an adjusted increase of 5.4% (95% CI 0.6% to 10.5%) in hs-CRP and of 2.3% (95% CI 1.4% to 3.3%) in the platelet count. Fibrinogen and WCC were not associated with long-term particle exposure. CONCLUSIONS: In this population-based cohort, we found associations of long-term exposure to PM with markers of inflammation (hs-CRP) and coagulation (platelets). This finding supports the hypothesis that inflammatory processes might contribute to chronic effects of air pollution on cardiovascular disease. [ABSTRACT FROM AUTHOR]

Background In several studies, exposure to fine particulate matter (PM) has been associated with inflammation, with inconsistent results. We used repeated measurements to examine the association of long-term fine and ultrafine particle exposure with several blood markers of inflammation and coagulation. Methods We used baseline (2000-2003) and follow-up (2006-2008) data from the Heinz Nixdorf Recall Study, a German population-based prospective cohort of 4814 participants. A chemistry transport model was applied to model daily surface concentrations of PM air pollutants (PM10,PM2.5) and particle number on a grid of 1 km². Applying mixed regression models, we analysed associations of long-term (mean of 365 days prior to blood draw) particle exposure at each participant's residence with the level of high-sensitivity C reactive protein (hs-CRP), fibrinogen, platelet and white cell count (WCC), adjusting for short-term PM exposure (moving averages of 1-7 days), personal characteristics, season, ambient temperature (1-5 days), ozone and time trend. Results We analysed 6488 observations: 3275 participants with baseline data and 3213 with follow-up data. An increase of 2.4 mg/m³ in long-term PM2.5 was associated with an adjusted increase of 5.4% (95% CI 0.6% to 10.5%) in hs-CRP and of 2.3% (95% CI 1.4% to 3.3%) in the platelet count. Fibrinogen and WCC were not associated with long-term particle exposure. Conclusions In this population-based cohort, we found associations of long-term exposure to PM with markers of inflammation (hs-CRP) and coagulation (platelets). This finding supports the hypothesis that inflammatory processes might contribute to chronic effects of air pollution on cardiovascular disease. [ABSTRACT FROM AUTHOR]

Background: Increased left ventricular (LV) size is associated with cardiovascular mortality and morbidity. Once noncontrast cardiac computed tomography (CT) is performed for other purposes, information of LV size is readily available. Purpose: To determine the association of gated CT-derived LV size with cardiovascular risk factors and coronary artery calcification (CAC) and to describe age- and gender-specific normative values in a general population cohort. Material and Methods: LV area was quantified from non-contrast-enhanced CT in axial, end-diastolic images at a midventricular slice in participants of the population-based Heinz Nixdorf Recall Study, free of known cardiovascular disease. LV index (LVI) was calculated by the quotient of LV area and body surface area (BSA). Crude and adjusted regression analyses were used to determine the association of LVI with risk factors and CAC. Results: Overall, 3926 subjects (age 59 ± 8 years, 53% women) were included in this analysis. From quantification in end-diastolic phase, men had larger LV index (2232 ± 296 mm²/m² vs. 2088 ± 251 mm²/m², both P<0.0001). LVI was strongly correlated systolic blood pressure (men, PE [95% CI]: 22.8 [15.5-30.2] mm²/10 mmHg; women, 23.4 [18.1- 28.6]), and antihypertensive medication (men, 45.2 [14.7-75.8] mm²; women: 46.5 [22.7-70.2], all P<0.005). Cholesterol levels were associated with LVI in univariate analysis, however, correlations were low (R² ± 0.04). In multivariable regression, blood pressure, antihypertensive medication and cholesterol levels, remained associated with LVI (P<0.05). LVI was linked with CAC in unadjusted (men, increase of CACþ1 by 13.0% [1.4-25.8] with increased LVI by 1 standard deviation of LVI, P=0.03; women, 20.7% [10.0-32.3], P<0.0001) and risk factor adjusted models (men, 14.6% [3.7-26.6], P=0.007); women, 17.4% [7.8-27.8], P=0.0002). Conclusion: Non-contrast cardiac CT derived LV index is associated with body size and hypertension. LVI is weakly linked with CAC-score. Further studies need to evaluate whether assessment of LV dimensions from cardiac CT helps identifying subjects with increased cardiovascular risk. [ABSTRACT FROM AUTHOR]

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

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

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. [ABSTRACT FROM PUBLISHER]

Background: Left atrial (LA) size is associated with cardiovascular mortality and morbidity. Once cardiac computed tomography (CT) is performed, information on LA size is readily available without additional contrast media or radiation exposure. Purpose: To determine the association of CT-derived LA area and body surface area-adjusted (BSA) LA index with cardiovascular risk factors and describe age- and gender-specific normative values in a general population cohort. Material and Methods: This study included 3945 participants (mean age, 59 ± 8 years; 53% women) from the community-based Heinz Nixdorf Recall Study. LA area in an axial image at the level of the mitral valve was quantified from non-contrast-enhanced electron-beam CT by manual delineations of the boundaries of the LA with exclusion of subjects with prevalent cardiovascular disease. Definition of normative values was performed in subjects without predictors of LA enlargement. Results: LA quantification was feasible in all subjects. Men had larger LA size (1856 mm(2) vs. 1677 mm(2), P < 0.0001), while after adjustment for BSA, this effect was inverted (910 mm(2)/m(2) vs. 933 mm(2)/m(2) for men and women, P < 0.0001). Determinants of body size were major predictors of LA size (body mass index [BMI]: R(2) = 0.195, BSA: R(2 )= 0.216, both P < 0.0001). Blood pressure was associated with LA size (parameter-estimate [95% confidence interval] = 51.0 (4.9-57.1) mm(2)/10 mmHg for systolic, 31.4 (25.4-37.4) mm(2)/5 mmHg for diastolic blood pressure, 214.6 (186.9-242.3) mm(2) for antihypertensive medication, P < 0.0001 for all). Cholesterol levels, lipid-lowering therapy, and diabetes were associated with LA in univariable analysis, however, correlations were low (r(2 )≤ 0.026). Current smoking was associated with reduced LA size (-115.9 [-149.0 - -82.8] mm(2), P < 0.0001). In multivariable regression, BMI, blood pressure, antihypertensive medication, and smoking remained associated with LA size (P < 0.005). Conclusion: Non-contrast-enhanced cardiac CT enables LA quantification with body size, hypertension, and smoking status being predictors of LA size. [ABSTRACT FROM AUTHOR]

The article presents information on a study to conducted to determine the association of computed topography (CT)-derived left atrial (LA) area and index of body surface area-adjusted (BSA) LA with risk factors of cardiovascular disease. The study was conducted on 3945 participants. It has been concluded that CT of non-contrast-enhanced cardiac enables LA quantification with body size, hypertension, and smoking status are predictors of LA size.

Aims Epicardial adipose tissue (EAT) is increased in subjects with atrial fibrillation (AF). Likewise, EAT is associated with left atrial (LA) size, as itself is a strong predictor of AF. We aimed to determine the association of EAT and LA size as computed tomography (CT)-derived measures with prevalent and incident AF and investigated whether both measures independently predict AF. Methods and results Participants from the Heinz Nixdorf Recall study without known cardiovascular disease were included. At baseline, EAT, defined as fat volume inside the pericardial sac, and LA size, defined as an axial area at the level of the mitral valve, were quantified from non-contrast enhanced cardiac CT. AF was determined from electrocardiogram at baseline and also at 5-year follow-up examination. Overall, 3467 participants (age: 58.9 ± 7.6 years, 47% male) were included. Ninety-six subjects had AF (46 prevalent and 50 incident). A 1-standard deviation (SD) change of EAT was associated with nearly two-fold increased prevalence of AF in univariate analysis, which persisted after adjustment for AF risk factors [odds ratio (OR) (95% confidence interval, 95% CI): 1.38 (1.11–1.72), P = 0.003]. Ancillary adjusting for LA reduced the effect [1.26 (0.996–1.60), P = 0.054]. For incident AF, no relevant effect was observed for EAT when adjusting for risk factors [1.19 (0.88–1.61), P = 0.26]. In contrast, a 1-SD chance of LA was strongly associated with AF independently of EAT and risk factors [2.70 (2.22–2.20), P < 0.0001]. LA but not EAT as non-contrast CT-derived measures improved the prediction of AF over risk factors (receiver operating characteristics: 0.810–0.845, P = 0.025). Conclusion LA size from non-contrast CT is strongly associated with prevalent and incident AF and ultimately diminishes the link of EAT with AF. [ABSTRACT FROM PUBLISHER]

Background: Bilirubin is a product of heme oxygenase and an antioxidant per se. In selected cohorts and patient studies, bilirubin was associated with decreased risk for cardiovascular events. We aimed to determine the association of serum bilirubin with coronary artery calcification (CAC) and incident cardiovascular disease in the unselected general population. Methods: Participants without prior coronary heart or liver disease were drawn from the population-based Heinz Nixdorf Recall study. CAC was measured from electron beam computed tomography and quantified using the Agatston method. Incident major cardiovascular events (coronary events, stroke, cardiovascular death) were assessed during follow-up. The association of bilirubin with CAC score and incident events was calculated using regression analysis. Results: A total of 3,553 subjects (mean age 59.4 years, 44 % male) were included. Bilirubin was inversely correlated with CAC in men [estimated % change in (CAC + 1) per each gender-specific standard deviation of bilirubin [95 % confidence interval (CI): −6.1 (−11.6; −1.7) %, p = 0.032] but less so in women [−3.6 (−7.7; 0.2) %, p = 0.065], when adjusting for age only. With adjustment for traditional cardiovascular risk factors, the association was less pronounced [men: −2.5 (−7.5; 2.6) %, p = 0.35, women: −0.2 (−4.1; 3.5) %, p = 0.9]. Likewise, higher bilirubin by one standard deviation was associated with 19 % lower frequency of incident cardiovascular events in age- and gender-adjusted Cox regression analysis [hazard ratio (95 % CI): 0.81 (0.68; 0.96), p = 0.014]; this effect was slightly attenuated after adjustment for traditional cardiovascular risk factors [0.87 (0.73; 1.04), p = 0.13]. Conclusion: Our data from a general population suggest that a potential protective role of bilirubin in the atherosclerosis process is largely secondary to a more beneficial risk factor profile. [ABSTRACT FROM AUTHOR]

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

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

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. [ABSTRACT FROM AUTHOR]

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

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

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

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

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Stent implantation into atherosclerotic coronary arteries releases particulate debris and soluble substances that contribute to impaired microvascular perfusion. Here we addressed the potential for microvascular obstruction in patients with stenotic native right coronary arteries (nRCA) compared with saphenous vein grafts on right coronary arteries (SVG-RCA). We enrolled symptomatic, male patients with stable angina pectoris and a flow-limiting stenosis in their nRCA or SVG-RCA (n = 18/18). Plaque volume and composition were analyzed using intravascular ultrasound before stent implantation. Coronary aspirate was retrieved during stent implantation under protection with a distal occlusion/aspiration device and divided into particulate debris and plasma. The release of catecholamines, endothelin, serotonin, thromboxane B2, and tumor necrosis factor-α was measured. The response of rat mesenteric arteries with intact (+E) and denuded (-E) endothelium to aspirate plasma (without and with selective endothelin receptor blockade) was normalized to that by potassium chloride (KClmax = 100%). Plaque volume and composition were not different between nRCA and SVG-RCA. There was less particulate debris (65 ± 8 vs. 146 ± 23 mg; P < 0.05) and more endothelin release (5.8 ± 0.8 vs. 1.3 ± 0.7 pg/ml; P < 0.05) in nRCA than in SVG-RCA, whereas the release of the other mediators was not different. Aspirate from nRCA induced stronger vasoconstriction than that from SVG-RCA [nRCA, 78 ± 6% (+E)/84 ± 5% (-E); SVG-RCA, 59 ± 6% (+E)/68 ± 3% (-E); P < 0.05 nRCA vs. SVG-RCA], which was attenuated by a nonspecific endothelin and a specific endothelin receptor A antagonist. Thus coronary aspirate from stented nRCA is characterized by less debris but more endothelin and stronger vasoconstrictor response than that from SVG-RCA. [ABSTRACT FROM AUTHOR]

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

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

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

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

Atherosclerotic coronary arteries are more calcified in patients with than without chronic kidney disease (CKD). We addressed the potential for coronary microvascular obstruction in patients with and without CKD during stenting for saphenous vein aorto-coronary graft (SVG) stenosis under protection with a distal occlusion/aspiration device. In patients with and without CKD ( n = 20/20), SVG plaque composition was analyzed from virtual histology using intravascular ultrasound analysis before stent implantation. There was more dense calcium and more necrotic core in patients with than without CKD (14 ± 3 vs. 3 ± 1 % and 21 ± 3 vs. 12 ± 2 % of plaque volume, respectively). Coronary aspirate was retrieved during stent implantation and divided into particulate debris and plasma. Patients with CKD had more particulate debris and calcium release than patients without CKD. In contrast, the release of serotonin was less in patients with than without CKD (0.4 ± 0.1 vs. 1.2 ± 0.3 μmol/L), whereas that of catecholamines, endothelin, tissue factor, thromboxane, tumor necrosis factor α, and C reactive protein was not significantly different. Confirming the biochemical results, aspirate plasma from patients with CKD induced less vasoconstriction of rat mesenteric arteries than that from patients without CKD (with endothelium (+E), 26 ± 7 %; without endothelium (−E): 28 ± 7 % vs. +E, 68 ± 12 %; −E: 95 ± 16 % of maximum KCl-induced vasoconstriction). Graft atherosclerosis of patients with CKD is more degenerated and releases more particulate debris and calcium, but the aspirate has surprisingly less serotonin and vasoconstrictor potential. [ABSTRACT FROM AUTHOR]

As high-sensitivity C-reactive protein (hsCRP) seems to be associated with an increased risk of cognitive decline, this nested case-control study examined the relation of hsCRP and mild cognitive impairment (MCI) at different time points. 148 MCI cases (106 amnestic, 42 non-amnestic (aMCI/naMCI)) and 148 matched controls were identified from a prospective population based cohort study of 4,359 participants (aged 50-80). HsCRP levels were measured 5 years before (baseline) and at the time of neuropsychological testing (follow-up). Odds ratios (OR) for hsCRP quartiles serum levels were calculated for the two time points using logistic regression analyses and were adjusted for cardiovascular covariates. In the fully adjusted model, baseline hsCRP levels were significantly associated with both MCI and aMCI (OR = 2.29, 95% confidence interval (CI), 1.01-5.15, first versus fourth quartile, respective OR = 2.73, 95% CI, 1.09-6.84). At follow-up, the fourth hsCRP quartile was associated with MCI (OR = 3.60, 95% CI, 1.55-8.33), aMCI (OR = 3.73, 95% CI, 1.52-9.17) and naMCI (OR = 3.66, 95% CI, 1.00-13.77). Elevated hsCRP levels, even detected five years before diagnosis, are associated with an at least twofold increased probability of MCI. These findings suggest that inflammation plays an important role in the development and presence of cognitive impairment. [ABSTRACT FROM AUTHOR]

BACKGROUND: Recent studies have shown an association of short-term exposure to fine particulate matter (PM) with transient increases in blood pressure (BP), but it is unclear whether long-term exposure has an effect on arterial BP and hypertension. OBJECTIVES: We investigated the cross-sectional association of residential long-term PM exposure with arterial BP and hypertension, taking short-term variations of PM and long-term road traffic noise exposure into account. METHODS: We used baseline data (2000.2003) on 4,291 participants, 45.75 years of age, from the Heinz Nixdorf Recall Study, a population-based prospective cohort in Germany. Urban background exposure to PM with aerodynamic diameter ≤ 2.5 μm (PM2.5) and ≤10 μm (PM10) was assessed with a dispersion and chemistry transport model. We used generalized additive models, adjusting for short-term PM, meteorology, traffic proximity, and individual risk factors. RESULTS: An interquartile increase in PM2.5 (2.4 μg/m3) was associated with estimated increases in mean systolic and diastolic BP of 1.4 mmHg [95% confidence interval (CI): 0.5, 2.3] and 0.9 mmHg (95% CI: 0.4, 1.4), respectively. The observed relationship was independent of long-term exposure to road traffic noise and robust to the inclusion of many potential confounders. Residential proximity to high traffic and traffic noise exposure showed a tendency toward higher BP and an elevated prevalence of hypertension. CONCLUSIONS: We found an association of long-term exposure to PM with increased arterial BP in a population-based sample. This finding supports our hypothesis that long-term PM exposure may promote atherosclerosis, with air-pollution.induced increases in BP being one possible biological pathway. [ABSTRACT FROM AUTHOR]

Background: Secondhand smoke (SHS) consists of fine particulate matter, carcinogens, and various toxins that affect large parts of the population. SHS increases the risk for acute cardiovascular events and may contribute to the development of atherosclerosis. Objectives: We investigated the association of SHS with coronary artery calcification (CAC). Methods: In this cross-sectional analysis, we used baseline data (2000-2003) from 1,766 never-smokers without clinically manifested coronary heart disease, 45-75 years of age, from the Heinz Nixdorf Recall Study, an ongoing, prospective, population-based cohort study in Germany. Self-reported frequent SHS at home, at work, and in other places was assessed by questionnaire. CAC scores were derived based on electron-beam computed tomography. We conducted multiple linear regression analysis using exposure to SHS as the explanatory variable and In(CAC+1) as the response variable. We conducted logistic regression to estimate the odds ratio (OR) for presence of any CAC. Results: Frequent exposure to SHS was reported by 21.5% of participants. After adjustment forage, sex, and socioeconomic status, CAC + 1 was 21.1% [95% confidence interval (CI): -5.5%, 55.2%] higher in exposed than in unexposed participants. After adjusting for other cardiovascular risk factors, the association was attenuated (15.4%; 95% CI: -9.6%, 47.2%). SHS exposure was also associated with a CAC score > 0 (fully adjusted OR = 1.38; 95% CI: 1.03, 1.84). Conclusions: Self-reported frequent exposure to SHS was associated with subclinical coronary atherosclerosis in our cross-sectional study population. Considering the widespread exposure and the clinical relevance of coronary atherosclerosis, this result, if confirmed, is of public health importance. [ABSTRACT FROM AUTHOR]

Aim: Irregular meal intakes have several harmful effects on health and yet it is largely unknown which factors are related to irregular meal intakes. In order to understand variations in regularity of meal intakes, associations between sociodemographics, health conditions, health behaviours, work characteristics and meal intakes were studied. Subject and methods: Cross-sectional data of 2,395 men and 2,419 women (45-75 years) participating in the Heinz Nixdorf Recall Study, a population-based prospective cohort study in Germany, were analysed. Information on the regularity of breakfast, lunch and supper intake was obtained from a self-reported questionnaire. Multivariate ordinal regression models were run to estimate associations between sociodemographics, health conditions, health behaviours, work characteristics and meal intakes. Results: Findings confirm an association between age [odds ratio (OR) 0.95, 95% confidence interval (CI) 0.95-0.97], number of household members (OR 0.86, 95% CI 0.79-0.95), diabetes (OR 0.65, 95% CI 0.50-0.84), fruit and vegetable consumption (OR 0.63, 95% CI 0.54-0.73) and regular meal intakes. High body mass index (OR 1.03, 95% CI 1.01-1.06), being divorced, separated or widowed (OR 1.57, 95% CI 1.17-2.10), smoking (OR 1.79, 95% CI 1.51-2.11) and daily working hours (OR 1.06, 95% CI 1.03-1.08) were related to irregular meal intakes. Conclusion: These results indicate that indicators of social support such as number of household members or marital status, other health behaviours and work conditions influence the regularity of meal intakes rather than socioeconomic conditions per se. [ABSTRACT FROM AUTHOR]

Non-contrast-enhanced computed tomography (CT) imaging of the heart enables noninvasive quantification of coronary artery calcification (CAC), a surrogate marker of the atherosclerotic burden in the coronary artery tree. Multiple studies have underlined the ability of CAC score for individual risk stratification and, accordingly, the American Heart Association recommended cardiac CT for risk assessment in individuals with an intermediate risk of cardiovascular events as measured by Framingham Risk Score. However, limitations in transcribing risk stratification algorithms based on American cohort studies into European populations have been acknowledged in the past. Moreover, data on implications for reclassification into higher- or lower-risk groups based on CAC scores were lacking. The Heinz Nixdorf Recall (HNR) study is a population-based cohort study that investigated the ability of CAC scoring in risk prediction for major cardiovascular events above and beyond traditional cardiovascular risk factors. According to Heinz Nixdorf Recall findings, CAC can be used for reclassification, especially in those in the intermediate-risk group, to advise on lifestyle changes for the reclassified low-risk category, or to implement intensive treatments for the reclassified high-risk individuals. This article discusses the present findings of the Heinz Nixdorf Recall Study with respect to the current literature, risk stratification algorithms, and current European guidelines for risk prediction. [ABSTRACT FROM AUTHOR]

Cardiovascular events remain one of the most frequent causes of mortality and morbidity worldwide. The majority of cardiac events occur in individuals without known coronary artery disease (CAD) and in low- to intermediate-risk subjects. Thus, the development of improved preventive strategies may substantially benefit from the identification, among apparently intermediate-risk subjects, of those who have a high probability for developing future cardiac events. Cardiac computed tomography and myocardial perfusion scintigraphy (MPS) by single photon emission computed tomography may play a role in this setting. In fact, absence of coronary calcium in cardiac computed tomography and inducible ischaemia in MPS are associated with a very low rate of major cardiac events in the next 3–5 years. Based on current evidence, the evaluation of coronary calcium in primary prevention subjects should be considered in patients classified as intermediate-risk based on traditional risk factors, since high calcium scores identify subjects at high-risk who may benefit from aggressive secondary prevention strategies. In addition, calcium scoring should be considered for asymptomatic type 2 diabetic patients without known CAD to select those in whom further functional testing by MPS or other stress imaging techniques may be considered to identify patients with significant inducible ischaemia. From available data, the use of MPS as first line testing modality for risk stratification is not recommended in any category of primary prevention subjects with the possible exception of first-degree relatives of patients with premature CAD in whom MPS may be considered. However, the Working Group recognizes that neither the use of computed tomography for calcium imaging nor of MPS have been proven to significantly improve clinical outcomes of primary prevention subjects in prospective controlled studies. This information would be crucial to adequately define the role of imaging approaches in cardiovascular preventive strategies. [ABSTRACT FROM PUBLISHER]

Implantation of bare metal stents (BMS) induces the release not only of particulate debris, but also of soluble vasoconstrictors which contribute to microvascular impairment. So this study aimed at addressing the potential attenuation of such vasoconstriction using paclitaxel eluting stents (PES). Using a distal protection/aspiration device, coronary arterial blood was retrieved before and during stent [ n = 14 BMS, n = 14 PES, n = 3 sirolimus eluting stents (SES)] implantation in patients with saphenous vein aorto-coronary bypass stenosis and analyzed for plasma serotonin and thromboxane B concentrations. The vasoconstriction of rat mesenteric arteries with intact (+E) and denuded (−E) endothelium in response to coronary arterial or aspirate plasma was quantified and normalized to that by potassium chloride (KCl = 100%). Coronary arterial plasma before stent implantation induced a vasoconstriction of 30-43%, which was independent of endothelial integrity. Serotonin-release was 2.2 ± 0.5 μmol/l with BMS and 2.0 ± 0.4 μmol/l with PES, thromboxane B-release was 26 ± 5 pg/ml with BMS and 22 ± 8 pg/ml with PES. BMS- and SES-aspirate plasma induced a vasoconstriction of 68 ± 18% (+E)/93 ± 14% (−E) and 81 ± 17% (+E)/124 ± 14% (−E), respectively. In contrast, PES-aspirate plasma induced only minor vasoconstriction of 8 ± 3% (+E)/12 ± 5% (−E). Addition of paclitaxel to BMS-aspirate plasma attenuated vasoconstriction. PES-aspirate induced microtubular condensation in immunofluorescence microscopy. Results indicate that aspirate from PES implantation attenuates vasoconstriction, possibly secondary to microtubular stabilization. Such acute downstream vascular paralysis could be beneficial in preventing a no-reflow phenomenon in patients undergoing stenting. [ABSTRACT FROM AUTHOR]

Background: The value of assessing coronary artery calcium (CAC) with regard to characterizing unstable coronary artery disease remains controversial. Purpose: To evaluate the amount of CAC in patients with an acute marker-positive coronary syndrome in segments containing the culprit lesion compared with the remote coronary segments. Material and Methods: Thirty-two patients with a marker-positive acute coronary syndrome were examined using electron-beam computed tomography (EBCT), selective coronary angiography and, in some, intravascular ultrasound. The coronary anatomy was analyzed according to the segmental classification proposed by the American Heart Association (AHA). Results: The total EBCT coronary artery calcium score (CAC, Agatston method) was 251±371 (range 0-1629). In 81% of the patients, a greater CAC score was observed than expected on the basis of age and gender. In 30 patients, significant stenoses were detected. The CAC score of the culprit vessel was 108±163 vs 78±134 in the non-culprit vessels and did not differ significantly (P=0.4). The mean CAC score of the coronary segment (AHA classification) containing the culprit lesion was 51±82 vs 29±45 in the other coronary artery segments (P=0.14). Of the two patients with no CAC detected by EBCT, one had no coronary atherosclerosis (confirmed by intravascular ultrasound) and one had one vessel coronary artery disease. Conclusion: Coronary calcium related to the culprit lesion in patients with a marker-positive acute coronary syndrome showed a tendency for an increased amount but was not statistically different from the amount of coronary calcium in remote vessel segments. [ABSTRACT FROM AUTHOR]