Dataset Information

Midday naps and the risk of coronary artery disease: results of the Heinz Nixdorf Recall Study.

ABSTRACT:

Study objectives

Several studies have assessed the association between midday nap and cardiovascular outcomes and reported heterogenous results. Concern exists that confounding might have distorted these results and contributed to discrepancies among them. This study prospectively examines the association between midday nap habits and the occurrence of coronary artery disease in a non-Mediterranean population.

Participants

The baseline examination of 4,123 participants aged 45-75 years.

Measurements

Measurements included interviews, physical examinations, laboratory tests, and electron beam computed tomography. We studied the influence of midday nap habits on risk of coronary artery disease. We adjusted for several potential confounders including measures of subclinical atherosclerosis-such as coronary calcium score and ankle brachial index-at baseline. Cardiac events during a median follow-up of 8.1 years were defined as nonfatal myocardial infarction and sudden cardiac death.

Results

Overall, 135 of 4,123 subjects (3.3%) either suffered from acute myocardial infarction (81 subjects) or died due to a sudden cardiac death (54 subjects) during follow-up. After adjustment for several confounders including measures of subclinical atherosclerosis, regular long (> 60 min) midday nap was associated with an increased hazard ratio of cardiac events (hazard ratio 2.12, 95% confidence interval 1.11-4.05).

Conclusions

As our detailed confounder analyses showed, confounding is not the sole explanation for this finding. Future research on midday naps should focus on biological mechanisms that may be responsible for increasing the risk of coronary artery disease among subjects taking regular long midday naps.

SUBMITTER: Stang A

PROVIDER: S-EPMC3490363 | biostudies-literature | 2012 Dec

REPOSITORIES: biostudies-literature

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Publications

Midday naps and the risk of coronary artery disease: results of the Heinz Nixdorf Recall Study.

Stang Andreas A Dragano Nico N Moebus Susanne S Möhlenkamp Stefan S Schmermund Axel A Kälsch Hagen H Erbel Raimund R Jöckel Karl-Heinz KH

Sleep 20121201 12

<h4>Study objectives</h4>Several studies have assessed the association between midday nap and cardiovascular outcomes and reported heterogenous results. Concern exists that confounding might have distorted these results and contributed to discrepancies among them. This study prospectively examines the association between midday nap habits and the occurrence of coronary artery disease in a non-Mediterranean population.<h4>Participants</h4>The baseline examination of 4,123 participants aged 45-75 ...[more]

PMID: 23204613

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Project description: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.

Project description:ObjectivesExposure to manganese (Mn) may cause movement disorders, but less is known whether the effects persist after the termination of exposure. This study investigated the association between former exposure to Mn and fine motor deficits in elderly men from an industrial area with steel production.MethodsData on the occupational history and fine motor tests were obtained from the second follow-up of the prospective Heinz Nixdorf Recall Study (2011-2014). The study population included 1232 men (median age 68 years). Mn in blood (MnB) was determined in archived samples (2000-2003). The association between Mn exposure (working as welder or in other at-risk occupations, cumulative exposure to inhalable Mn, MnB) with various motor functions (errors in line tracing, steadiness, or aiming and tapping hits) was investigated with Poisson and logistic regression, adjusted for iron status and other covariates. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated for substantially impaired dexterity (errors >90th percentile, tapping hits <10th percentile).ResultsThe median of cumulative exposure to inhalable Mn was 58 µg m-3 years in 322 men who ever worked in at-risk occupations. Although we observed a partly better motor performance of exposed workers at group level, we found fewer tapping hits in men with cumulative Mn exposure >184.8 µg m-3 years (OR 2.15, 95% CI 1.17-3.94). MnB ≥ 15 µg l-1, serum ferritin ≥ 400 µg l-1, and gamma-glutamyl transferase ≥74 U l-1 were associated with a greater number of errors in line tracing.ConclusionsWe found evidence that exposure to inhalable Mn may carry a risk for dexterity deficits. Whether these deficits can be exclusively attributed to Mn remains to be elucidated, as airborne Mn is strongly correlated with iron in metal fumes, and high ferritin was also associated with errors in line tracing. Furthermore, hand training effects must be taken into account when testing for fine motor skills.

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Dataset Information

Midday naps and the risk of coronary artery disease: results of the Heinz Nixdorf Recall Study.

Study objectives

Participants

Measurements

Results

Conclusions

Publications

Midday naps and the risk of coronary artery disease: results of the Heinz Nixdorf Recall Study.

Similar Datasets

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