Introduction

Erectile dysfunction (ED) is associated with cardiovascular disease (CVD); however, the association between change in ED status over time and future underlying CVD risk is unclear.

Aim

The aim of this study was to investigate the association between change in ED status and Framingham CVD risk, as well change in Framingham risk.

Methods

We studied 965 men free of CVD in the Boston Area Community Health (BACH) Survey, a longitudinal cohort study with three assessments. ED was assessed with the five-item International Index of Erectile Function at BACH I (2002-2005) and BACH II (2007-2010) and classified as no ED/transient ED/persistent ED. CVD risk was assessed with 10-year Framingham CVD risk algorithm at BACH I and BACH III (2010-2012). Linear regression models controlled for baseline age, socio-demographic and lifestyle factors, as well as baseline Framingham risk. Models were also stratified by age (≥/< 50 years).

Main outcome measures

Framingham CVD risk and change in Framingham CVD risk were the main outcome measures.

Results

Transient and persistent ED was significantly associated with increased Framingham risk and change in risk over time in univariate and age-adjusted models. In younger men, persistent ED was associated with a Framingham risk that was 1.58 percentage points higher (95% confidence interval [CI]: 0.11, 3.06) and in older men, a Framingham risk that was 2.54 percentage points higher (95% CI: -1.5, 6.59), compared with those without ED. Change in Framingham risk over time was also associated with transient and persistent ED in men <50 years, but not in older men.

Conclusions

Data suggest that even after taking into account other CVD risk factors, transient and persistent ED is associated with Framingham CVD risk and a greater increase in Framingham risk over time, particularly in younger men. Findings further support clinical assessment of CVD risk in men presenting with ED, especially those under 50 years.

Objectives

Links between arrhythmias and particulate matter exposures have been found among sensitive populations. We examined the relationship between personal particulate matter ≤2.5 µm aerodynamic diameter (PM2.5) exposures and ectopy in a panel study of healthy welders.

Methods

Simultaneous ambulatory ECG and personal PM2.5 exposure monitoring with DustTrak Aerosol Monitor was performed on 72 males during work and non-work periods for 5-90 h (median 40 h). ECGs were summarised hourly for supraventricular ectopy (SVE) and ventricular ectopy (VE). PM2.5 exposures both work and non-work periods were averaged hourly with lags from 0 to 7 h. Generalised linear mixed-effects models with a random participant intercept were used to examine the relationship between PM2.5 exposure and the odds of SVE or VE. Sensitivity analyses were performed to assess whether relationships differed by work period and among current smokers.

Results

Participants had a mean (SD) age of 38 (11) years and were monitored over 2993 person-hours. The number of hourly ectopic events was highly skewed with mean (SD) of 14 (69) VE and 1 (4) SVE. We found marginally significant increases in VE with PM2.5 exposures in the sixth and seventh hour lags, yet no association with SVE. For every 100 μg/m(3) increase in sixth hour lagged PM2.5, the adjusted OR (95% CI) for VE was 1.03 (1.00 to 1.05). Results persisted in work or non-work exposure periods and non-smokers had increased odds of VE associated with PM2.5 as compared with smokers.

Conclusions

A small increase in the odds of VE with short-term PM2.5 exposure was observed among relatively healthy men with environmental and occupational exposures.

Background

To better understand the mechanism(s) of particulate matter (PM) associated cardiovascular effects, research priorities include identifying the responsible PM characteristics. Evidence suggests that metals play a role in the cardiotoxicity of fine PM (PM2.5) and in exposure-related decreases in heart rate variability (HRV). We examined the association between daytime exposure to the metal content of PM2.5 and night HRV in a panel study of boilermaker construction workers exposed to metal-rich welding fumes.

Methods

Twenty-six male workers were monitored by ambulatory electrocardiogram (ECG) on a workday while exposed to welding fume and a non-workday (baseline). From the ECG, rMSSD (square root of the mean squared differences of successive intervals) was summarized over the night (0:00-7:00). Workday, gravimetric PM2.5 samples were analyzed by x-ray fluorescence to determine metal content. We used linear mixed effects models to assess the associations between night rMSSD and PM2.5 metal exposures both with and without adjustment for total PM2.5. Matched ECG measurements from the non-workday were used to control for individual cardiac risk factors and models were also adjusted for smoking status. To address collinearity between PM2.5 and metal content, we used a two-step approach that treated the residuals from linear regression models of each metal on PM2.5 as surrogates for the differential effects of metal exposures in models for night rMSSD.

Results

The median PM2.5 exposure was 650 microg/m3; median metal exposures for iron, manganese, aluminum, copper, zinc, chromium, lead, and nickel ranged from 226 microg/m3 to non-detectable. We found inverse linear associations in exposure-response models with increased metal exposures associated with decreased night rMSSD. A statistically significant association for manganese was observed, with a decline of 0.130 msec (95% CI: -0.162, -0.098) in night rMSSD for every 1 microg/m3 increase in manganese. However, even after adjusting for individual metals, increases in total PM2.5 exposures were associated with declines in night rMSSD.

Conclusion

These results support the cardiotoxicity of PM2.5 metal exposures, specifically manganese. However the metal component alone did not account for the observed declines in night HRV. Therefore, results suggest the importance of other PM elemental components.

Background

Although studies have documented the association between heart rate variability (HRV) and ambient particulate exposures, the association between HRV, especially at night, and metal-rich, occupational particulate exposures remains unclear.

Objective

Our goal in this study was to investigate the association between long-duration HRV, including nighttime HRV, and occupational PM(2.5) exposures.

Methods

We used 24-hr ambulatory electrocardiograms (ECGs) to monitor 36 male boilermaker welders (mean age of 41 years) over a workday and nonworkday. ECGs were analyzed for HRV in the time domain; rMSSD (square root of the mean squared differences of successive intervals), SDNN (SD of normal-to-normal intervals over entire recording), and SDNN(i) (SDNN for all 5-min segments) were summarized over 24-hr, day (0730-2130 hours), and night (0000-0700 hours) periods. PM(2.5) (particulate matter with an aerodynamic diameter ResultsMean (+/- SD) PM(2.5) exposure was 0.73 +/- 0.50 mg/m(3) and ranged from 0.04 to 2.70 mg/m(3). We observed a consistent inverse exposure-response relationship, with a decrease in all HRV measures with increased PM(2.5) exposure. However, the decrease was most pronounced at night, where a 1-mg/m(3) increase in PM(2.5) was associated with a change of -8.32 [95% confidence interval (CI), -16.29 to -0.35] msec nighttime rMSSD, -14.77 (95% CI, -31.52 to 1.97) msec nighttime SDNN, and -8.37 (95% CI, -17.93 to 1.20) msec nighttime SDNN(i), after adjusting for nonworking nighttime HRV, age, and smoking.

Conclusion

Metal-rich particulate exposures were associated with decreased long-duration HRV, especially at night. Further research is needed to elucidate which particulate metal constituent is responsible for decreased HRV.

We sought to determine whether posttraumatic stress disorder (PTSD) was associated with sexual health in returned warzone-deployed veterans from the recent Iraq and Afghanistan conflicts. We studied 1,581 males and females from the Veterans After-Discharge Longitudinal Registry, a gender-balanced U.S. Department of Veterans Affairs registry of health care-seeking veterans with and without PTSD. Approximately one quarter (25.1%) of males (n = 198) and 12.7% of females (n = 101) had a sexual dysfunction diagnosis and/or prescription treatment for sexual dysfunction. Both genders were more likely to have a sexual dysfunction diagnosis and/or prescription treatment if they had PTSD compared with those without PTSD (male: 27.3% vs. 21.1%, p = .054; female: 14.9% vs. 9.4%, p = .022). Among the 1,557 subjects analyzed here, males with PTSD had similar levels of sexual activity compared to those without PTSD (71.2% vs. 75.4%, p = .22), whereas females with PTSD were less likely to be sexually active compared to females without PTSD (58.7% vs. 72.1%, p < .001). Participants with PTSD were also less likely to report sex-life satisfaction (male: 27.6% vs. 46.0%, p < .001; female: 23.0% vs. 45.7%, p < .001) compared with those without PTSD. Although PTSD was not associated with sexual dysfunction after adjusting for confounding factors, it was significantly negatively associated with sex-life satisfaction in female veterans with a prevalence ratio of .71, 95% confidence interval [.57, .90].