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Leukocyte telomere length has been proposed as a biomarker of cellular aging and atherosclerosis. The aim of this study was to determine whether leukocyte telomere length is independently associated with incident coronary heart disease (CHD) in the general population. Telomere length was measured using a polymerase chain reaction method for participants enrolled in the 1995 Nova Scotia Health Survey (NSHS95; n = 1,917). The primary end point was the first occurrence of a fatal or nonfatal CHD event. During a mean follow-up period of 8.7 years, 164 fatal or nonfatal CHD events occurred. Compared with participants in the longest tertile of telomere length, those in the middle and shortest tertiles had increased incidence of CHD events (6.2, 11.2, and 12.2 per 1,000 person-years, respectively). After adjustment for demographics, traditional risk factors, and inflammatory markers including high-sensitivity C-reactive protein, interleukin-6, and soluble intercellular adhesion molecule-1, those in the middle tertile had significantly elevated risk for incident CHD (hazard ratio 1.63, 95% confidence interval 1.07 to 2.51, p = 0.02) compared with the longest tertile, whereas the risk for those in the shortest tertile was nonsignificantly elevated (hazard ratio 1.25, 95% confidence interval 0.82 to 1.90, p = 0.30). In conclusion, these findings do not support a linear association between leukocyte telomere length and incident CHD risk in the general population., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Background: Premature shortening of leukocyte telomere length has been proposed as a novel mechanism by which depression may confer increased risk of adverse cardiovascular events. Prior studies demonstrating associations of depression and depressive symptoms with shorter leukocyte telomere length were small, included selected psychiatric outpatients, were based on convenience samples, and/or adjusted for a limited number of possible confounding factors., Methods and Findings: We examined the associations of depressive symptoms, probable depressive disorder, and specific depressive symptom clusters, as assessed by the Center for Epidemiological Studies--Depression (CES-D) scale, with leukocyte telomere length, measured by using a real-time PCR method, in 2,225 apparently healthy participants from the 1995 Nova Scotia Health Survey population-based study. The mean age was 48.2 ± 18.9 years; 49.9% of participants were female; and the mean CES-D score was 7.4 ± 7.9. The mean telomere length was 5,301 ± 587 base pairs. In an unadjusted model, depressive symptoms were significantly associated with longer leukocyte telomere length (B = 27.6 base pairs per standard deviation increase in CES-D, 95% confidence interval [CI] = 3.1-52.1, p = 0.027). This association was no longer significant after adjustment for age and sex (B = 9.5, 95% CI = -14.6-33.6, p = 0.44) or after further adjustment for body mass index, Framingham risk score and previous history of ischemic heart disease (all p's ≥ 0.37). Neither probable depressive disorder nor specific depressive symptom clusters were independently associated with leukocyte telomere length., Conclusions: Concurrent depressive symptoms were not associated with leukocyte telomere length in a large, representative, population-based study.

Objectives: The aim of this study was to examine the relation between hostility and incident ischemic heart disease (IHD) and to determine whether observed hostility is superior to patient-reported hostility for the prediction of IHD in a large, prospective observational study., Background: Some studies have found that hostile patients have an increased risk of incident IHD. However, no studies have compared methods of hostility assessment or considered important psychosocial and cardiovascular risk factors as confounders. Furthermore, it is unknown whether all expressions of hostility carry equal risk or whether certain manifestations are more cardiotoxic., Methods: We assessed the independent relationship between baseline observed hostility and 10-year incident IHD in 1,749 adults of the population-based Canadian Nova Scotia Health Survey., Results: There were 149 (8.5%) incident IHD events (140 nonfatal, 9 fatal) during the 15,295 person-years of observation (9.74 events/1,000 person-years). Participants with any observed hostility had a greater risk of incident IHD than those without (p = 0.02); no such relation was found for patient-reported hostility. Those with any observed hostility had a significantly greater risk of incident IHD (hazard ratio: 2.06, 95% confidence interval: 1.04 to 4.08, p = 0.04), after adjusting for cardiovascular (age, sex, Framingham Risk Score) and psychosocial (depression, positive affect, patient-reported hostility, and anger) risk factors., Conclusions: The presence of any observed hostility at baseline was associated with a 2-fold increased risk of incident IHD over 10 years of follow-up. Compared with patient-reported measures, observed hostility is a superior predictor of IHD., (Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Numerous studies have found that depression was a strong independent risk factor for incident coronary heart disease (CHD), with increasing risk in those with higher levels of depressive symptoms. The association between measures of inflammation (C-reactive protein, interleukin-6, and soluble intracellular adhesion molecule-1), depressive symptoms, and CHD incidence was examined in 1,794 subjects of the population-based Canadian Nova Scotia Health Survey. There were 152 incident CHD events (8.5%; 141 nonfatal, 11 fatal) during the 15,514 person-years of observation (incidence rate 9.8 events/1,000 person-years). Depression and inflammation were correlated at baseline and each significantly predicted CHD in separate models. When both risk factors were in the same model, each remained significant. The association between depressed group by the Center for Epidemiological Studies-Depression scale (score > or =10 vs 0 to 9) and CHD incidence (hazard rate 1.60, 95% confidence interval 1.12 to 2.27) was not reduced by the addition of inflammatory markers to the model (hazard rate 1.59, 95% confidence interval 1.12 to 2.26). Findings were similar after adjustment for aspirin, lipid-lowering medication, or antidepressant use, and the association did not vary by gender, smoking status, age, obesity, cardiovascular medication use, or antidepressant use. In conclusion, increased inflammation explained only a very small proportion of the association between depression and incident CHD.