Additional file 1: Table S1. of Dynamic high-sensitivity troponin elevations in atrial fibrillation patients might not be associated with significant coronary artery disease

Baseline characteristics, presentation and outcomes in the study population with CAD according to troponin subgroups. (XLSX 38 kb

Additional file 3: Table S3. of Dynamic high-sensitivity troponin elevations in atrial fibrillation patients might not be associated with significant coronary artery disease

Significance of clinically relevant background factors in predicting dynamic hsTnT elevation. Patients with stationary elevated hsTnT are excluded. (XLSX 10 kb

Baseline characteristics according to Genetic Risk Score (GRS) Quartiles and psychological stress.

<p>Baseline characteristics according to Genetic Risk Score (GRS) Quartiles and psychological stress.</p

A genetic risk score for CAD, psychological stress, and their interaction as predictors of CAD, fatal MI, non-fatal MI and cardiovascular death

<div><p>Background</p><p>Psychological stress is an independent risk factor for cardiovascular disease (CVD), but the mechanism by which stress is associated with CVD is not entirely understood. Although genetic factors are implied in both stress responsivity and cardiovascular reactivity, no studies to date have investigated their interactions with stress for cardiovascular end points. The objective was to elucidate the association and interactions between a genetic risk score (GRS), individual genetic variants and stress for three cardiovascular end points: coronary artery disease (CAD), fatal myocardial infarction (MI), non-fatal MI, and cardiovascular death.</p><p>Methods and findings</p><p>18,559 participants from the Malmö Diet Cancer Study, a population-based prospective study, were included in the analyses. Cox proportional hazards regression models were used and adjusted for a large number of known predictors of cardiovascular end points. Mean follow-up time in years was 14.6 (CAD; n = 1938), 14.8 (fatal MI; n = 436), 14.8 (non-fatal MI; n = 1108), and 15.1 (cardiovascular death; n = 1071) respectively. GRS was significantly associated with increased risks of CAD (top quartile hazard ratio [HR], 1.72; 95% confidence interval [CI], 1.51–1.96), fatal MI (top quartile HR, 1.62; 95%CI, 1.23–2.15), non-fatal MI (top quartile HR, 1.55; 95%CI, 1.31–1.84), and cardiovascular death (top quartile HR, 1.29; 95%CI, 1.08–1.53). Stress was not independently associated with any end point and did not interact with GRS. Four individual genetic variants interacted unfavorably with stress for end points with mortality outcomes.</p><p>Conclusion</p><p>A GRS composed of 50 SNPs and predictive of CAD was found for the first time to also strongly predict fatal MI, non-fatal MI and cardiovascular death. A stress-sensitive component of the GRS was isolated on the basis of individual genetic variants that interacted unfavorably with stress.</p></div

Cox proportional hazards regression models for the effect of interaction between psychological stress and quartiles of coronary artery disease (CAD) genetic risk score (GRS) on incident CAD, fatal myocardial infarction (MI), non-fatal MI, and cardiovascular death.

<p>Cox proportional hazards regression models for the effect of interaction between psychological stress and quartiles of coronary artery disease (CAD) genetic risk score (GRS) on incident CAD, fatal myocardial infarction (MI), non-fatal MI, and cardiovascular death.</p

Hazard Ratios (HR) and Confidence Intervals (CI) for the main effects of genetic risk score (GRS) and stress on incidence of coronary artery disease (CAD), fatal myocardial infarction (MI), non-fatal MI, and cardiovascular death.

<p>Hazard Ratios (HR) and Confidence Intervals (CI) for the main effects of genetic risk score (GRS) and stress on incidence of coronary artery disease (CAD), fatal myocardial infarction (MI), non-fatal MI, and cardiovascular death.</p

Salt induced change in 24 hour systolic ABP (salt sensitivity) in the carriers of the rs4149601 GG-genotype together with the rs2288774 CC-genotype vs. all other genotype combinations.

<p>Box plot presented as median and inter quartile range.</p

Flow chart of sample size.

The aim of this study was to explore the longitudinal association between reported baseline water intake and incidence of coronary artery disease (CAD) and type 2 diabetes in the Malmö Diet and Cancer Cohort (n = 25,369). Using cox proportional hazards models, we separately modelled the effect of plain and total (all water, including from food) water on CAD and type 2 diabetes risk, whilst adjusting for age, sex, diet collection method, season, smoking status, alcohol intake, physical activity, education level, energy intake, energy misreporting, body mass index, hypertension, lipid lowering medication, apolipoprotein A, apolipoprotein B, and dietary variables. Sensitivity analyses were run to assess validity. After adjustment, no association was found between tertiles of plain or total water intake and type 2 diabetes risk. For CAD, no association was found comparing moderate to low intake tertiles from plain or total water, however, risk of CAD increased by 12% (95% CI 1.03, 1.21) when comparing high to low intake tertiles of plain water, and by 17% (95% CI 1.07, 1.27) for high versus low tertiles of total water. Sensitivity analyses were largely in agreement. Overall, baseline water intake was not associated with future type 2 diabetes risk, whilst CAD risk was higher with higher water intakes. Our findings are discordant with prevailing literature suggesting higher water intakes should reduce cardiometabolic risk. These findings may be an artefact of limitations within the study, but future research is needed to understand if there is a causal underpinning.</div

Participant characteristics according to plain water intake.

Participant characteristics according to plain water intake.</p

Sensitivity analyses for type 2 diabetes and coronary artery disease.

Sensitivity analyses for type 2 diabetes and coronary artery disease.</p