Impact of Left Atrial Appendage Amputation on Left Atrial Morphology and Rhythm after Off-Pump CABG.

OBJECTIVES: Left atrial appendage (LAA) amputation concomitant to coronary artery bypass grafting (CABG) has become an increasingly performed technique in patients with atrial fibrillation (AF) or with sinus rhythm and a CHA2DS2-VASc score ≥2. However, LAA amputation has come under suspicion to cause postoperative atrial fibrillation (POAF) due to left atrial (LA) dilation. This study aims to assess this assumption in patients undergoing CABG in off-pump technique with and without amputation of the LAA. METHODS: Patients who underwent isolated CABG in off-pump technique without history of AF were retrospectively examined. Cohorts were divided according to the concomitant execution of LAA amputation. LA volume was measured by transthoracic echocardiography and rhythm was analyzed by electrocardiography, medication protocol, and visit documentation. Propensity score (PS) matching was performed based on 20 preoperative risk variables to correct for selection bias. RESULTS: A total of 1,522 patients were enrolled, with 1,267 in the control group and 255 in the LAA amputation group. Occurrence of POAF was compared in 243 PS-matched patient pairs. Neither the unmatched cohort (odds ratio [OR] 0.82; 95% confidence interval or CI [0.61; 1.11], p = 0.19) nor the PS-matched cohort (OR 0.94; 95% CI [0.62; 1.41], p = 0.75) showed significant differences in POAF occurrence. Subgroup analysis of sex, use of ß-blockers, pulmonary disease, ejection fraction, and CHA2DS2-VASc-Score also showed no tendencies. LA volume did not change significantly (p = 0.18, 95% CI [-0.29; 1.51]). CONCLUSION: Surgical amputation of the LAA concomitant to CABG did not lead to LA dilation and has no significant impact on the occurrence of POAF.

Impact of Immunosuppressive Agents on Clinical Manifestations and Outcome of Staphylococcus aureus Bloodstream Infection: A Propensity Score-Matched Analysis in 2 Large, Prospectively Evaluated Cohorts.

BACKGROUND: Staphylococcus aureus bloodstream infection (SAB) is a common, life-threatening infection. The impact of immunosuppressive agents on the outcome of patients with SAB is incompletely understood. METHODS: Data from 2 large prospective, international, multicenter cohort studies (Invasive Staphylococcus aureus Infections Cohort [INSTINCT] and International Staphylococcus aureus Collaboration [ISAC]) between 2006 and 2015 were analyzed. Patients receiving immunosuppressive agents were identified and a 1:1 propensity score-matched analysis was performed to adjust for baseline characteristics of patients. Overall survival and time to SAB-related late complications (SAB relapse, infective endocarditis, osteomyelitis, or other deep-seated manifestations) were analyzed by Cox regression and competing risk analyses, respectively. This approach was then repeated for specific immunosuppressive agents (corticosteroid monotherapy and immunosuppressive agents other than steroids [IMOTS]). RESULTS: Of 3188 analyzed patients, 309 were receiving immunosuppressive treatment according to our definitions and were matched to 309 nonimmunosuppressed patients. After propensity score matching, baseline characteristics were well balanced. In the Cox regression analysis, we observed no significant difference in survival between the 2 groups (death during follow-up: 105/309 [33.9%] immunosuppressed vs 94/309 [30.4%] nonimmunosuppressed; hazard ratio [HR], 1.20 [95% confidence interval {CI}, .84-1.71]). Competing risk analysis showed a cause-specific HR of 1.81 (95% CI, .85-3.87) for SAB-related late complications in patients receiving immunosuppressive agents. The cause-specific HR was higher in patients taking IMOTS (3.69 [95% CI, 1.41-9.68]). CONCLUSIONS: Immunosuppressive agents were not associated with an overall higher mortality. The risk for SAB-related late complications in patients receiving specific immunosuppressive agents such as IMOTS warrants further investigations.

Short-term exposure to ultrafine and fine particulate matter with multipollutant modelling on heart rate variability among seniors and children from the CorPuScula (coronary, pulmonary, sanguis) longitudinal study in Germany.

Background: Short-term exposure particulate matter with a diameter of 10 µm or less (PM10) and fine particulate matter (PM2.5) has been associated with heart rate variability (HRV), but exposure to ultrafine particles (UFP) has been less well examined. We investigated the associations between the HRV outcomes and short-term exposure to UFP, PM10 and PM2.5 among school-aged children and seniors. Methods: CorPuScula (Coronary, Pulmonary and Sanguis) is a longitudinal, repeated-measure panel study conducted in 2000-2002 in Munich, Germany including 52 seniors (58-94 years old) with 899 observations and 50 children (6-10 years old) with 925 observations. A 10-min resting electrocardiogram was performed to assess resting HRV outcomes [Standard Deviation of Normal to Normal Intervals (SDNN), Root Mean Square of Successive Differences between Normal Heartbeats (RMSSD), Low Frequency power (LF), High Frequency power (HF), ration between low and high frequency (LF/HF)]. UFP and PM exposures were measured near the care home and school yard for seniors and children, respectively. Mean exposures during the day of examination (9-21 h) as well as 3-h, 12-h, 24-h, one-day, and two-day lags were assessed. Linear mixed-effect models were used to investigate the associations between short-term air pollution and HRV outcomes separately in children and seniors. The models were adjusted for sex, age, weather conditions (temperature, precipitation, and water vapor pressure), BMI, lifestyle and medical information. Two and multipollutant models adjusted for NO2 and O3 were performed. Results: Among seniors, we observed increases in SDNN, LF, HF and LF/HF ratio after short-term exposure to UFP (hourly and daily lags) in contrast to decreases in SDNN and RMSSD after exposure to PM10. Associations were generally robust to two- and multipollutant adjustment. Among children, we observed increases of the LF/HF ratio after short-term exposures to UFP at lags 12 and 24 h. In contrast, we observed decreases of the ratio after exposure to PM2.5 and PM10. Results were largely unchanged for multipollutant modelling, however we found a more pronounced increase in SDNN and LF/HF (UFP lag 12 and 24 h) after adjusting for NO2. Conclusions: Overall, among seniors, we observed associations of UFP and PM10 exposure with sympathetic responses of the ANS, which play an important role in sudden heart attacks or arrhythmia. Among children we found more inconsistent associations between UFP and a delayed increase in HRV. Adjusting for co-pollutants including NO2 and O3 yielded robust results.

Long-term exposure to air pollution and prevalent nonalcoholic fatty liver disease.

Background: Nonalcoholic fatty liver disease (NAFLD) is a disease characterized by lipid accumulation within hepatocytes, ranging from simple steatosis to steatohepatitis, in the absence of secondary causes of hepatic fat accumulation. Although air pollution (AP) has been associated with several conditions related to NAFLD (e.g., metabolic syndrome, type 2 diabetes mellitus), few studies have explored an association between AP and NAFLD. The aim of the study was to investigate whether exposure to AP is associated with NAFLD prevalence. Methods: We used baseline cross-sectional data (2000-2003) of the Heinz-Nixdorf-Recall cohort study in Germany (baseline n = 4,814), a prospective population-based cohort study in the urbanized Ruhr Area. Mean annual exposure to size-fractioned particulate matter (PM10, PM2.5, PMcoarse, and PM2.5abs), nitrogen dioxide, and particle number was assessed using two different exposure models: a chemistry transport dispersion model, which captures urban background AP exposure on a 1 km2 grid at participant's residential addresses, and a land use regression model, which captures point-specific AP exposure at participant's residential addresses. NAFLD was assessed with the fatty liver index (n = 4,065), with NAFLD defined as fatty liver index ≥60. We estimated ORs of NAFLD per interquartile range of exposure using logistic regression, adjusted for socio-demographic and lifestyle variables. Results: We observed a NAFLD prevalence of 31.7% (n = 1,288). All air pollutants were positively associated with NAFLD prevalence, with an OR per interquartile range for PM2.5 of 1.11 (95% confidence interval [CI] = 1.00, 1.24) using chemistry transport model, and 1.06 (95% CI = 0.94, 1.19) using the land use regression model, respectively. Conclusion: There was a positive association between long-term AP exposure and NAFLD.

Long-term air pollution, noise, and structural measures of the Default Mode Network in the brain: Results from the 1000BRAINS cohort.

BACKGROUND: While evidence suggests that long-term air pollution (AP) and noise may adversely affect cognitive function, little is known about whether environmental exposures also promote structural changes in underlying brain networks. We therefore investigated the associations between AP, traffic noise, and structural measures of the Default Mode Network (DMN), a functional brain network known to undergo specific changes with age. METHODS: We analyzed data from 579 participants (mean age at imaging: 66.5 years) of the German 1000BRAINS study. Long-term residential exposure to particulate matter (diameter ≤10 µm [PM10]; diameter ≤2.5 µm [PM2.5]), PM2.5 absorbance (PM2.5abs), nitrogen dioxide (NO2), and accumulation mode particulate number concentration (PNAM) was estimated using validated land use regression and chemistry transport models. Long-term outdoor traffic noise was modeled at participants' homes based on a European Union's Environmental Noise Directive. As measures of brain structure, cortical thickness and local gyrification index (lGI) values were calculated for DMN regions from T1-weighted structural brain images collected between 2011 and 2015. Associations between environmental exposures and brain structure measures were estimated using linear regression models, adjusting for demographic and lifestyle characteristics. RESULTS: AP exposures were below European Union standards but above World Health Organization guidelines (e.g., PM10 mean: 27.5 µg/m3). A third of participants experienced outdoor 24-h noise above European recommendations. Exposures were not consistently associated with lGI values in the DMN. We observed weak inverse associations between AP and cortical thickness in the right anterior DMN (e.g., -0.010 mm [-0.022, 0.002] per 0.3 unit increase in PM2.5abs) and lateral part of the posterior DMN. CONCLUSION: Long-term AP and noise were not consistently associated with structural parameters of the DMN in the brain. While weak associations were present between AP exposure and cortical thinning of right hemispheric DMN regions, it remains unclear whether AP might influence DMN brain structure in a similar way as aging.

Association between Long-Term Air Pollution, Chronic Traffic Noise, and Resting-State Functional Connectivity in the 1000BRAINS Study.

BACKGROUND: Older adults show a high variability in cognitive performance that cannot be explained by aging alone. Although research has linked air pollution and noise to cognitive impairment and structural brain alterations, the potential impact of air pollution and noise on functional brain organization is unknown. OBJECTIVE: This study examined the associations between long-term air pollution and traffic noise with measures of functional brain organization in older adults. We hypothesize that exposures to high air pollution and noise levels are associated with age-like changes in functional brain organization, shown by less segregated brain networks. METHODS: Data from 574 participants (44.1% female, 56-85 years of age) in the German 1000BRAINS study (2011-2015) were analyzed. Exposure to particulate matter (PM10, PM2.5, and PM2.5 absorbance), accumulation mode particle number (PNAM), and nitrogen dioxide (NO2) was estimated applying land-use regression and chemistry transport models. Noise exposures were assessed as weighted 24-h (Lden) and nighttime (Lnight) means. Functional brain organization of seven established brain networks (visual, sensorimotor, dorsal and ventral attention, limbic, frontoparietal and default network) was assessed using resting-state functional brain imaging data. To assess functional brain organization, we determined the degree of segregation between networks by comparing the strength of functional connections within and between networks. We estimated associations between air pollution and noise exposure with network segregation, applying multiple linear regression models adjusted for age, sex, socioeconomic status, and lifestyle variables. RESULTS: Overall, small associations of high exposures with lesser segregated networks were visible. For the sensorimotor networks, we observed small associations between high air pollution and noise and lower network segregation, which had a similar effect size as a 1-y increase in age [e.g., in sensorimotor network, -0.006 (95% CI: -0.021, 0.009) per 0.3 ×10-5/m increase in PM2.5 absorbance and -0.004 (95% CI: -0.006, -0.002) per 1-y age increase]. CONCLUSION: High exposure to air pollution and noise was associated with less segregated functional brain networks. https://doi.org/10.1289/EHP9737.

Impact of neutropenia on clinical manifestations and outcome of Staphylococcus aureus bloodstream infection: a propensity score-based overlap weight analysis in two large, prospectively evaluated cohorts.

OBJECTIVES: This study aimed to investigate whether neutropenia influenced mortality and long-term outcomes of Staphylococcus aureus bloodstream (SAB) infection. METHODS: Data from two prospective, multicentre cohort studies (INSTINCT and ISAC) conducted at 20 tertiary care hospitals in six countries between 2006 and 2015 were analyzed. Neutropenic and severely neutropenic patients (defined by proxy of total white blood cell count <1000/µl and <500/µl, respectively, at onset of SAB infection) were compared with a control group using a propensity score model and overlapping weights to adjust for baseline characteristics. Overall survival and time to SAB infection-related late complications (SAB infection recurrence, infective endocarditis, osteomyelitis, or other deep-seated manifestations) were analyzed with Cox regression and competing risk analyses, respectively. RESULTS: Of the 3187 included patients, 102 were neutropenic and 70 severely neutropenic at the time of SAB infection onset. Applying overlap weights yielded two groups of 83 neutropenic and 220 nonneutropenic patients, respectively. The baseline characteristics of these groups were exactly balanced. In the Cox regression analysis, we observed no significant difference in survival between the two groups (death during follow up: 36.1% in neutropenic vs. 30.6% in nonneutropenic patients; hazard ratio (HR): 1.21; 95% CI, 0.79-1.83). This finding remained unchanged when we considered severely neutropenic patients (HR: 1.08; 95% CI, 0.60-1.94). A competing risk analysis showed a cause-specific HR of 0.39 (95% CI, 0.11-1.39) for SAB infection-related late complications in neutropenic patients. DISCUSSION: Neutropenia was not associated with a higher survival rate during follow up. The lower rate of SAB infection-related late complications in neutropenic patients should be validated in other cohorts.