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Aim: Intraindividual body weight variability (BWV), that is, the degree of weight fluctuations over time, is associated with an increased risk of cardiovascular diseases (CVDs) in multiple settings. The impact of BWV on cardiovascular risk in type 1 diabetes (T1D) remains unclear, despite the issues relative to weight management in individuals with this condition., Materials and Methods: Using data from the Swedish National Diabetes Register, we identified individuals with T1D and without CVD at baseline with at least three measurements of body weight taken over three consecutive years. We estimated BWV as quartiles of the standard deviation of weight measures and explored its longitudinal association with the incidence of CVD during a 12.7 ± 4.6 year follow-up through adjusted Cox regression models. The primary endpoint was the composite of nonfatal myocardial infarction, nonfatal stroke and all-cause mortality. We modelled the function of risk in relation to the magnitude of BWV, testing also whether weight trends, that is, increasing, stable or decreasing, age, sex and glycaemic control modified the association between BWV and the outcome., Results: Among the 36 333 individuals with T1D in the register, we identified 19 373 individuals with at least three measures of body weight and without CVD at baseline. Participants with the highest BWV had a 42% increased risk of reaching the primary endpoint compared to those with the lowest BWV (hazard ratio [HR] = 1.42, 95% confidence interval [CI]: 1.24-1.62). In addition, high BWV was significantly associated with a 51% increased risk of all-cause mortality (HR = 1.51, 95% CI: 1.28-1.78), a 37% increased risk of peripheral artery disease (HR = 1.37, 95% CI: 1.06-1.77) and a 55% increased risk of hospitalization for heart failure (HR = 1.55, 95% CI: 1.20-2.01). BWV showed a quasi-linear association with the primary endpoint. No interaction was observed when comparing subgroups for weight trends, sex or degree of glycaemic control. In the subgroup of elderly individuals, the association of BWV with the primary endpoint was no longer significant., Conclusions: High BWV is associated with an increased risk of CVD and all-cause mortality in individuals with T1D, independently of canonical risk factors. Weight trends, sex and glycaemic control do not modify such association while older age attenuates it., (© 2024 The Author(s). Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd.)

Background: Type 2 diabetes (T2D) and peripheral artery disease (PAD) are recognized as independent risk factors contributing to excess mortality. Contemporary observational studies exploring the associations of risk factors, and risk of all-cause and atherosclerotic cardiovascular disease mortality in persons with T2D following the onset of incident peripheral artery disease are limited. The objectives of this study were to investigate the associations of risk factors, and assess mortality risks in people with T2D compared with controls without T2D after the onset of PAD., Methods: All persons with T2D (n = 150,215) registered in the Swedish National Diabetes Register between 2005 and 2009 were included, along with 346,423 controls without T2D matched for sex and age. Data were retrieved from several national registries, capturing information on risk factors, onset of incident peripheral artery disease, other comorbidities, socioeconomic factors, and outcomes. To compare persons with T2D and controls following the onset of peripheral artery disease regarding the risk of all-cause, and atherosclerotic cardiovascular disease mortality, Cox proportional hazard models and Kaplan-Meier curves were employed. A gradient-boosting model was utilized to estimate the relative statistical contribution of risk factors to the modeling of incident mortality risk in people with both T2D and peripheral artery disease., Results: Crude rates of incident all-cause mortality were higher in individuals with T2D compared with controls, following the onset of PAD (600.4 (95% CI, 581.4-619.8) per 10,000 person-years versus 549.1 (95% CI, 532.1-566.5) per 10,000 person-years). Persons with T2D had an adjusted hazard ratio (HR) for all-cause mortality of 1.12 (95% CI, 1.05-1.19, P < 0.01) compared with controls after onset of incident PAD. The comparable adjusted HR for cardiovascular mortality was 1.13 (95% CI, 1.07-1.19, P < 0.01). High age and hyperglycemia at baseline played a significant role in contributing to the predictive models for incident all-cause and cardiovascular mortality among individuals with both T2D and PAD., Conclusions: The presence of T2D with concomitant PAD is related to an increased risk of both all-cause and cardiovascular mortality compared with individuals with only PAD. This argues for implementing optimized and intensive treatment strategies for individuals with both conditions., (© 2024. The Author(s).)

Background: Air pollution is associated with cardiovascular morbidity and mortality, but its role in the development of congestive heart failure (CHF) and the role of different pollution sources in cardiovascular disease remain uncertain., Methods: Participants were enrolled in the Malmö Diet and Cancer cohort in 1991-1996 with information on lifestyle and clinical indicators of cardiovascular disease. The cohort participants were followed through registers until 2016. Annual total and local source-specific concentrations of particulate matter less than 10 μm and 2.5 μm (PM 10 and PM 2.5 ), black carbon (BC), and nitrogen oxides (NO x ) from traffic, residential heating, and industry were assigned to each participant's address throughout the study period. Cox proportional hazards models adjusted for possible confounders was used to estimate associations between air pollution 1-5 years prior to outcomes of incident CHF, fatal myocardial infarction (MI), major adverse coronary events (MACE), and ischemic stroke., Results: Air pollution exposure levels (mean annual exposures to PM 2.5 of 11 μg/m 3 and NO x of 26 μg/m 3 ) within the cohort were moderate in terms of environmental standards. After adjusting for confounders, we observed statistically significant associations between NO x and CHF (hazard ratio [HR] 1.11, 95% confidence interval [CI] 1.01-1.22) and NO x and fatal MI (HR 1.10, 95%CI 1.01-1.20) per interquartile range (IQR) of 9.6 μg/m 3 . In fully adjusted models, the estimates were similar, but the precision worse. In stratified analyses, the associations were stronger in males, ever-smokers, older participants, and those with baseline carotid artery plaques. Locally emitted and traffic-related air pollutants generally showed positive associations with CHF and fatal MI. There were no associations between air pollution and MACE or stroke., Discussion/conclusion: In an area with low to moderate air pollution exposure, we observed significant associations of long-term residential NO x with increased risk of incident CHF and fatal MI, but not with coronary events and stroke., (Copyright © 2022. Published by Elsevier Inc.)

Long-term air pollution exposure increases the risk for cardiovascular disease, but little is known about the temporal relationships between exposure and health outcomes. This study aims to estimate the exposure-lag response between air pollution exposure and risk for ischemic heart disease (IHD) and stroke incidence by applying distributed lag non-linear models (DLNMs). Annual mean concentrations of particles with aerodynamic diameter less than 2.5 µm (PM 2.5 ) and black carbon (BC) were estimated for participants in five Swedish cohorts using dispersion models. Simultaneous estimates of exposure lags 1-10 years using DLNMs were compared with separate year specific (single lag) estimates and estimates for lag 1-5- and 6-10-years using moving average exposure. The DLNM estimated no exposure lag-response between PM 2.5 total, BC, and IHD. However, for PM 2.5 from local sources, a 20% risk increase per 1 µg/m 3 for 1-year lag was estimated. A risk increase for stroke was suggested in relation to lags 2-4-year PM 2.5 and BC, and also lags 8-9-years BC. No associations were shown in single lag models. Increased risk estimates for stroke in relation to lag 1-5- and 6-10-years BC moving averages were observed. Estimates generally supported a greater contribution to increased risk from exposure windows closer in time to incident IHD and incident stroke.

Volcanic ash contributed significantly to particulate matter (PM) in Iceland following the eruptions in Eyjafjallajökull 2010 and Grímsvötn 2011. This study aimed to investigate the association between different PM sources and emergency hospital visits for cardiorespiratory causes from 2007 to 2012. Indicators of PM10 sources; "volcanic ash", "dust storms", or "other sources" (traffic, fireworks, and re-suspension) on days when PM10 exceeded the daily air quality guideline value of 50 µg/m3 were entered into generalized additive models, adjusted for weather, time trend and co-pollutants. The average number of daily emergency hospital visits was 10.5. PM10 exceeded the air quality guideline value 115 out of 2191 days; 20 days due to volcanic ash, 14 due to dust storms (two days had both dust storm and ash contribution) and 83 due to other sources. High PM10 levels from volcanic ash tended to be significantly associated with the emergency hospital visits; estimates ranged from 4.8% (95% Confidence Interval (CI): 0.6, 9.2%) per day of exposure in unadjusted models to 7.3% (95% CI: -0.4, 15.5%) in adjusted models. Dust storms were not consistently associated with daily emergency hospital visits and other sources tended to show a negative association. We found some evidence indicating that volcanic ash particles were more harmful than particles from other sources, but the results were inconclusive and should be interpreted with caution.

In the aftermath of the Icelandic volcano Grimsvötn's eruption on 21 May 2011, volcanic ash reached Northern Europe. Elevated levels of ambient particles (PM) were registered in mid Sweden. The aim of the present study was to investigate if the Grimsvötn eruption had an effect on mortality in Sweden. Based on PM measurements at 16 sites across Sweden, data were classified into an ash exposed data set (Ash area) and an unexposed data set (No ash area). Data on daily all-cause mortality were obtained from Statistics Sweden for the time period 1 April through 31 July 2011. Mortality ratios were calculated as the ratio between the daily number of deaths in the Ash area and the No ash area. The exposure period was defined as the week following the days with elevated particle concentrations, namely 24 May through 31 May. The control period was defined as 1 April through 23 May and 1 June through 31 July. There was no absolute increase in mortality during the exposure period. However, during the exposure period the mean mortality ratio was 2.42 compared with 2.17 during the control period, implying a relatively higher number of deaths in the Ash area than in the No ash area. The differences in ratios were mostly due to a single day, 31 May, and were not statistically significant when tested with a Mann-Whitney non-parametric test (p > 0.3). The statistical power was low with only 8 days in the exposure period (24 May through 31 May). Assuming that the observed relative differences were not due to chance, the results would imply an increase of 128 deaths during the exposure period 24-31 May. If 31 May was excluded, the number of extra deaths was reduced to 20. The results of the present study are contradicting and inconclusive, but may indicate that all-cause mortality was increased by the ash-fall from the Grimsvötn eruption. Meta-analysis or pooled analysis of data from neighboring countries might make it possible to reach sufficient statistical power to study effects of the Grimsvötn ash on morbidity and mortality. Such studies would be of particular importance for European societies preparing for future large scale volcanic eruptions in Iceland.

Background: Air pollution exposure is associated with hospital admissions and emergency room visits for cardiopulmonary disease and stroke. Iceland's capital area, Reykjavik, has generally low air pollution levels, but traffic and natural sources contribute to pollution levels. The objective of this study was to investigate temporal associations between emergency hospital visits and air pollutants ozone (O3), nitrogen dioxide (NO2), and particulate matter (PM10) in the Icelandic capital area., Methods: We constructed a time series of the daily number of adults who visited the emergency room, or were acutely admitted for stroke or cardiorespiratory causes to Landspitali University Hospital 1 January 2003 - 31 December 2009 from the hospital in-patient register. We used generalized additive models assuming Poisson distribution, to analyze the daily emergency hospital visits as a function of the pollutant levels, and adjusted for meteorological variables, day of week, and time trend with splines., Results: Daily emergency hospital visits increased 3.9% (95% confidence interval (CI) 1.7-6.1%) per interquartile (IQR) change in average O3 the same and two previous days. For females, the increase was 7.8% (95% CI 3.6-12.1) for elderly (70+), the increase was 3.9% (95% CI 0.6-7.3%) per IQR increase of NO2. There were no associations with PM10., Conclusions: We found an increase in daily emergency hospital visits associated with O3, indicating that low-level exposure may trigger cardiopulmonary events or stroke.