Compared with patients who did not have diabetes, those with diabetes had an increased risk of heart failure (hazard ratio [HR] 2.17 [95% CI 1.37 3.44]).
A one standard deviation increase in patella and tibia lead concentrations was associated with greater risk for ischemic heart disease (Hazard Ratio for patella lead = 1.29; 95% CI, 1.02 1.62).
Lastly, after full adjustment, a 100 g increase in the consumption of fried food did not show an association with risk of coronary heart disease (hazard ratio 1.00, 0.90 to 1.11).
Among medical comorbidities, mortality risk was highest in those with congestive heart failure (hazard ratio, HR = 1.92; 95% CI 1.89-1.95), Lung disease (HR = 1.42; 95% CI 1.40-1.44) and cerebrovascular disease (HR = 1.39; 95% CI 1.37-1.40).
Over a 3-year period, AKI stage 1 and greater was associated with heart failure (hazard ratio 1.33), and AKI stages 2 and 3 were associated with myocardial infarction (hazard ratio 1.51).
No association was found between lipid lowering drug use and coronary heart disease (hazard ratio 1.12, 0.90 to 1.40).
In the same study, iron deficiency was an independent predictor of death or urgent heart transplantation (hazard ratio 1.58, 95% CI 1.14 2.17, P = 0.005).
In a pooled analysis, the increased risks of death from coronary heart disease (hazard ratio 1.33 (95% confidence interval 0.99 to 1.79); P=0.06; fig 3 ) and cardiovascular disease (1.27 (0.98 to 1.65); P=0.07; fig 4 ) approached significance.
Inclusion of these recovered data in an updated meta-analysis of linoleic acid intervention trials showed non-significant trends toward increased risks of death from coronary heart disease (hazard ratio 1.33 (0.99 to 1.79); P=0.06) and cardiovascular disease (1.27 (0.98 to 1.65); P=0.07).
Results Survivors of cancer were significantly more likely than siblings to report congestive heart failure (hazard ratio (HR) 5.9, 95% confidence interval 3.4 to 9.6; P<0.001), myocardial infarction (HR 5.0, 95% CI 2.3 to 10.4; P<0.001), pericardial disease (HR 6.3, 95% CI 3.3 to 11.9; P<0.001), or valvular abnormalities (HR 4.8, 95% CI 3.0 to 7.6; P<0.001).
To test if lifestyle improvement related to the start of statin treatment could explain why smokers showed a larger risk reduction with statins, we adjusted for smoking cessation within six months of the start of statin treatment, but this did not materially change the effect of statin treatment on coronary heart disease risk (hazard ratio 0.20 (0.15 to 0.26), P<0.001).
