Background Depressive symptoms are associated with heightened risk of heart failure (HF), but their association with cardiac function and with HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF) in late life is unclear. We aimed to determine the prevalence of depression in HFpEF and in HFrEF in late life, and the association of depressive symptoms with cardiac function and incident HFpEF and HFrEF. Methods and Results We studied 6025 participants (age, 75.3±5.1 years; 59% women; 20% Black race) in the ARIC (Atherosclerosis Risk in Communities) study at visit 5 who underwent echocardiography and completed the Center for Epidemiologic Studies Depression Scale questionnaire. Among HF‐free participants (n=5086), associations of Center for Epidemiologic Studies Depression Scale score with echocardiography and incident adjudicated HFpEF and HFrEF were assessed using multivariable linear and Cox proportional hazards regression. Prevalent HFpEF, but not HFrEF, was associated with a higher prevalence of depression compared with HF‐free participants (P<0.001 and P=0.59, respectively). Among HF‐free participants, Center for Epidemiologic Studies Depression Scale score was not associated with cardiac structure and function after adjusting for demographics and comorbidities (all P>0.05). Over 5.5‐year follow‐up, higher Center for Epidemiologic Studies Depression Scale score was associated with heightened risk of incident HFpEF (hazard ratio [HR] [95% CI], 1.06 [1.04–1.12]; P=0.02), but not HFrEF (HR [95% CI], 1.02 [0.96–1.08]; P=0.54), independent of echocardiographic measures, NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide), troponin, and hs‐CRP (high‐sensitivity C‐reactive protein) (HR [95% CI], 1.06 [1.00–1.12]; P=0.04). Conclusions Worse depressive symptoms predict incident HFpEF in late life, independent of common comorbidities, cardiac structure and function, and prognostic biomarkers. Further studies are necessary to understand the mechanisms linking depression to risk of HFpEF.

Several studies have demonstrated a positive relationship between vital exhaustion and incident coronary heart disease (CHD), but the association of exhaustion with recurrent cardiac events has not been established in large, epidemiologic studies. Vital exhaustion is considered the end-stage of prolonged psychological distress and is characterized by excessive fatigue, increased irritability, and a sense of demoralization. We assessed the hypothesis that vital exhaustion predicts recurrent cardiac events (myocardial infarction and CHD-related mortality) among middle-aged men and women with documented CHD. Participants were 589 black or white men and women (mean age = 59.8; range = 47 - 69 years) with a history of CHD at the 1990-1992 clinical examination of the ARIC Study. Vital exhaustion was measured at the same ARIC examination using the 21-item Maastricht Questionnaire, and scores were categorized into quartiles. Recurrent cardiac events were monitored in short term (0-5 years), mid- term (6-13 years), and long-term (14-19 years) follow-up. Cox proportional hazards regression models were adjusted for age, sex, race-center, educational level, body mass index, plasma LDL-and HDL-cholesterol levels, hypertension status, and pack-years of cigarette smoking. During short term follow-up, the risk for recurrent cardiac events among participants in the highest quartile of vital exhaustion was twice that of participants in the remainder of the sample (HR = 2.08; 95% C.I: 1.24 to 3.48). The risk was less strong but remained statistically significant in mid-term (HR = 1.77; 95% C.I: 1.26 to 2.48) and long-term (HR = 1.54; 95% C.I: 1.12 to 2.11) follow-up. In conclusion, vital exhaustion is positively associated with short-term and long-term risks for recurrent cardiac events among middle-aged men and women with established coronary heart disease, independent of the traditional biomedical risk factors.

BACKGROUND:Evidence regarding the association of anger proneness with incidence of heart failure is lacking. METHODS AND RESULTS:Anger proneness was ascertained among 13,171 black and white participants of the Atherosclerosis Risk in Communities (ARIC) study cohort with the use of the Spielberger Trait Anger Scale. Incident heart failure events, defined as occurrence of ICD-9-CM code 428.x, were ascertained from participants' medical records during follow-up in the years 1990-2010. Relative hazard of heart failure across categories of trait anger was estimated with the use of Cox proportional hazard models. Study participants (mean age 56.9 [SD 5.7] years) experienced 1,985 incident HF events during 18.5 (SD 4.9) years of follow-up. Incidence of HF was greater among those with high, as compared to those with low or moderate trait anger, with higher incidence observed for men than for women. The relative hazard of incident HF was modestly high among those with high trait anger, compared with those with low or moderate trait anger (age-adjusted hazard ratio for men: 1.44 (95% confidence interval [CI] 1.23-1.69). Adjustment for comorbidities and depressive symptoms attenuated the estimated age-adjusted relative hazard in men to 1.26 (95% CI 1.00-1.60). CONCLUSIONS:Assessment of anger proneness may be necessary in successful prevention and clinical management of heart failure, especially in men.

Background and Purpose: Medical and endovascular treatment options for stroke prevention in patients with symptomatic intracranial stenosis have evolved over the past several decades, but the impact of 2 major multicenter randomized stroke prevention trials on physician practices has not been studied. We sought to determine changes in US physician treatment choices for patients with intracranial atherosclerotic stenosis (ICAS) following 2 NIH-funded clinical trials that studied medical therapies (antithrombotic agents and risk factor control) and percutaneous transluminal angioplasty and stenting (PTAS). Methods: Anonymous surveys on treatment practices in patients with ICAS were sent to physicians at 3 time points: before publication of the NIH-funded Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) trial (pre-WASID survey, 2004), 1 year after WASID publication (post-WASID survey, 2006) and 1 year after the publication of the NIH-funded Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis (SAMMPRIS) trial (post-SAMMPRIS survey, 2012). Neurologists were invited to participate in the pre-WASID survey (n = 525). Neurologists and neurointerventionists were invited to participate in the post-WASID (n = 598) and post-SAMMPRIS (n = 2,080) surveys. The 3 surveys were conducted using web-based survey tools delivered by E-mail, and a fax-based response form delivered by E-mail and conventional mail. Data were analyzed using the χ2 test. Results: Before WASID, there was equipoise between warfarin and aspirin for stroke prevention in patients with ICAS. The number of respondents who recommended antiplatelet treatment for ICAS increased across all 3 surveys for both anterior circulation (pre-WASID = 44%, post-WASID = 85%, post-SAMMPRIS = 94%) and posterior circulation (pre-WASID = 36%, post-WASID = 74%, post-SAMMPRIS = 83%). The antiplatelet agent most commonly recommended after WASID was aspirin, but after SAMMPRIS it was the combination of aspirin and clopidogrel. The percentage of neurologists who recommended PTAS in >25% of ICAS patients increased slightly from pre-WASID (8%) to post-WASID surveys (12%), but then decreased again after SAMMPRIS (6%). The percentage of neurointerventionists who recommended PTAS in >25% of ICAS patients decreased from post-WASID (49%) to post-SAMMPRIS surveys (17%). Conclusions: The surveyed US physicians' recommended treatments for ICAS differed over the 3 survey periods, reflecting the results of the 2 NIH-funded clinical trials of ICAS and suggesting that these clinical trials changed practice in the USA.

Though several large epidemiologic studies have demonstrated the positive association of anger with coronary heart disease (CHD) onset, a dearth of population-based evidence exists regarding the relationship of anger to the clinical course of CHD among people with established disease. Trait anger is conceptualized as a stable personality trait and defined as the tendency to experience frequent and intense anger. Therefore, it is plausible that the effects of trait anger on CHD are long standing. We assessed the hypothesis that trait anger predicts short-term and long-term risk for recurrent CHD among middle-aged men and women. Participants were 611 black or white men and women, ages 48 - 67, who had a history of CHD at the second clinical examination (1990-1992) of the Atherosclerosis Risk in Communities (ARIC) Study. They were followed for the recurrence of CHD (myocardial infarction or fatal CHD) from 1990 through three different time intervals: 1995, 2003, and 2009 (maximum follow-up = 19.0 years). Trait anger (measured at Visit 2) was assessed using the Spielberger Trait Anger Scale, with scores categorized as high, moderate, and low. Cox proportional hazards regression analyses were adjusted for age, sex, race-center, educational level, waist-to-hip ratio, plasma LDL-and HDL-cholesterol levels, hypertension, diabetes, cigarette smoking status, and pack-years of cigarette smoking. After 3 - 5 years of follow-up, the risk for recurrent CHD among participants with high trait anger was more than twice that of their counterparts with low trait anger (2.24 [95% C.I: 1.14 to 4.40]). After 11 - 13 years, the risk was 80% greater (1.80 [95% C.I: 1.17 to 2.78]) and after 17 - 19 years, it was 70% greater (1.70 [95% C.I: 1.15 to 2.52]). The risk for recurrent CHD was strongest in the first time interval but remained strong and statistically significant through 19 years of follow-up. In conclusion, the experience of frequent and intense anger increases short-term and long-term risk for recurrent CHD in middle-aged men and women.

There is evidence that anger and hostility are positively associated with the metabolic syndrome. In turn, the metabolic syndrome mediates the association between anger and hostility and adverse cardiac events. Very little is known about these associations in African-American populations. We assessed the hypothesis that anger and hostility are positively associated with the metabolic syndrome in an African-American cohort. Participants were 2,732 African-American men and women, ages 45 – 95, who were enrolled in the Jackson Heart Study at baseline. Anger was measured using the Spielberger State-Trait Anger Inventory, and hostility was measured using the Cook-Medley Hostility Scale. The metabolic syndrome was defined by the National Cholesterol Education Program, Adult Treatment Panel III criteria. Overall anger, components anger-in and anger-out, and hostility scores were entered into separate logistic regression models as continuous variables. In models adjusted for age, sex, educational level, and physical activity, higher levels of overall anger (β = 0.024, p = 0.006), anger-in (β = 0.028, p = 0.04), anger-out (β = 0.037, p = 0.04), and hostility (β = 0.021, p = 0.04) were associated with an increased prevalence of the metabolic syndrome. The correlation between anger and hostility was statistically significant but not strong (r = 0.38, p <0.0001). In men, 5 of the 16 individual anger items were significantly associated with the metabolic syndrome. The strongest was “I lose my temper” (β = 0.395, p = 0.003) and “I tend to harbor grudges” (β = 0.314, p = 0.008). In women, only 1 anger item, “I make sarcastic remarks” (β = 0.189, p = 0.04) was associated with the metabolic syndrome. In conclusion, higher levels of overall anger, anger-in, anger-out, and hostility were associated with an increased prevalence of the metabolic syndrome in middle- and older-aged African-American men and women. In men, an angry temperament and a tendency to hold grudges were particularly strong correlates of the metabolic syndrome. Increased understanding of the negative emotions anger and hostility among African-Americans may provide greater insights into cardiovascular disease risk in their population.

BackgroundAlthough modest effect estimates have been observed for the association of anger proneness with the risk of coronary heart disease and stroke, few prospective studies have evaluated the association of anger proneness with the risk of heart failure. We examined association of trait anger with incidence of heart failure (HF) among 13,212 participants (age range 46-70 years) of a large bi-racial cohort, the Atherosclerosis Risk in Communities (ARIC) Study cohort.MethodsIncident hospitalized HF was established from medical records. Anger proneness was measured using the Spielberger Trait Anger Scale (range 10-40) and defined as a categorical variable of low (10-14), moderate (15-21) and high (22-40) trait anger. Cox proportional hazard regression analysis was used to determine the relative hazard of HF across categories of anger proneness.ResultsHigh trait anger was associated with increased age-adjusted incidence of heart failure (Figure 1). During the median 14.5 years of follow-up, the age, gender, and race adjusted risk of incident HF among those with high as compared to low trait anger (Hazard Ratio, HR=1.48 [95% CI 1.25, 1.76]) was attenuated in analyses adjusted for education and median household income (HR = 1.39 [95% CI 1.16, 1.66]). Adjustment for depression further attenuated estimates to statistically non-significant levels. The average number of hospital readmissions post incident HF event increased from 4.7 for those with low or moderate anger to 5.9 for those with high anger (p<0.05).Conclusions BackgroundAlthough modest effect estimates have been observed for the association of anger proneness with the risk of coronary heart disease and stroke, few prospective studies have evaluated the association of anger proneness with the risk of heart failure. We examined association of trait anger with incidence of heart failure (HF) among 13,212 participants (age range 46-70 years) of a large bi-racial cohort, the Atherosclerosis Risk in Communities (ARIC) Study cohort. Although modest effect estimates have been observed for the association of anger proneness with the risk of coronary heart disease and stroke, few prospective studies have evaluated the association of anger proneness with the risk of heart failure. We examined association of trait anger with incidence of heart failure (HF) among 13,212 participants (age range 46-70 years) of a large bi-racial cohort, the Atherosclerosis Risk in Communities (ARIC) Study cohort. MethodsIncident hospitalized HF was established from medical records. Anger proneness was measured using the Spielberger Trait Anger Scale (range 10-40) and defined as a categorical variable of low (10-14), moderate (15-21) and high (22-40) trait anger. Cox proportional hazard regression analysis was used to determine the relative hazard of HF across categories of anger proneness. Incident hospitalized HF was established from medical records. Anger proneness was measured using the Spielberger Trait Anger Scale (range 10-40) and defined as a categorical variable of low (10-14), moderate (15-21) and high (22-40) trait anger. Cox proportional hazard regression analysis was used to determine the relative hazard of HF across categories of anger proneness. ResultsHigh trait anger was associated with increased age-adjusted incidence of heart failure (Figure 1). During the median 14.5 years of follow-up, the age, gender, and race adjusted risk of incident HF among those with high as compared to low trait anger (Hazard Ratio, HR=1.48 [95% CI 1.25, 1.76]) was attenuated in analyses adjusted for education and median household income (HR = 1.39 [95% CI 1.16, 1.66]). Adjustment for depression further attenuated estimates to statistically non-significant levels. The average number of hospital readmissions post incident HF event increased from 4.7 for those with low or moderate anger to 5.9 for those with high anger (p<0.05). High trait anger was associated with increased age-adjusted incidence of heart failure (Figure 1). During the median 14.5 years of follow-up, the age, gender, and race adjusted risk of incident HF among those with high as compared to low trait anger (Hazard Ratio, HR=1.48 [95% CI 1.25, 1.76]) was attenuated in analyses adjusted for education and median household income (HR = 1.39 [95% CI 1.16, 1.66]). Adjustment for depression further attenuated estimates to statistically non-significant levels. The average number of hospital readmissions post incident HF event increased from 4.7 for those with low or moderate anger to 5.9 for those with high anger (p<0.05). Conclusions

Exposure to military combat has been associated with myriad adverse health effects. Mechanisms are not well understood, but may include negative emotional states. The authors investigated the relationship between combat and trait anger and vital exhaustion among 5,347 middle-aged male participants in the Atherosclerosis Risk in Communities Study. Combat was significantly associated with trait anger, although results were limited to men of the Korean and Vietnam War eras. Among men of the Korean War era, combat- and noncombat veterans, compared to their nonveteran counterparts, reported more trait anger. Compared to their noncombat and nonveteran counterparts, Vietnam War era combat veterans reported more trait anger. Noncombat veterans from the World War II and Vietnam War eras reported lower vital exhaustion compared to nonveterans. Anger proneness may be a mechanism through which combat stress is associated with adverse health outcomes.

Vital exhaustion, defined as excessive fatigue, feelings of demoralization, and increased irritability, has been identified as a risk factor for incident and recurrent cardiac events, but there are no population-based prospective studies of this association in US samples. We examined the predictive value of vital exhaustion for incident myocardial infarction or fatal coronary heart disease in middle-aged men and women in 4 US communities. Participants were 12,895 black or white men and women enrolled in the Atherosclerosis Risk In Communities (ARIC) study cohort and followed for the occurrence of cardiac morbidity and mortality from 1990 through 2002 (maximum follow-up 13.0 years). Vital exhaustion was assessed using the 21-item Maastricht Questionnaire and scores were partitioned into approximate quartiles for statistical analyses. High vital exhaustion (fourth quartile) predicted adverse cardiac events in age-, gender-, and race-center-adjusted analyses (1.69, 95% confidence interval 1.40 to 2.05) and in analyses further adjusted for educational level, body mass index, plasma low-density lipoprotein and high-density lipoprotein cholesterol levels, systolic and diastolic blood pressure levels, diabetes mellitus, cigarette smoking status, and pack-years of cigarette smoking (1.46, 95% confidence interval 1.20 to 1.79). Risk for adverse cardiac events increased monotonically from the first through the fourth quartile of vital exhaustion. Probabilities of adverse cardiac events over time were significantly higher in people with high vital exhaustion compared to those with low exhaustion (p = 0.002). In conclusion, vital exhaustion predicts long-term risk for adverse cardiac events in men and women, independent of established biomedical risk factors.

Dental schools around the world face new challenges that raise issues with regard to how they are governed, led and managed. With rapid societal changes, including globalization and consumerism, the roles of universities and their funding have become intensely debated topics. When financial burdens on universities increase, so does the pressure on dental schools. This is exacerbated by the relative expense of running dental schools and also by the limited understanding of both university managers and the public of the nature and scope of dentistry as a profession. In these circumstances, it is essential for dental schools to have good systems of leadership and management in place so that they can not only survive in difficult times, but flourish in the longer term. This paper discusses the concept of governance and how it relates to leadership, management and administration in dental schools and hospitals. Various approaches to governance and management in dental schools on different continents and regions are summarized and contrasted. A number of general governance and leadership issues are addressed. For example, a basic principle supported by the Working Group is that an effective governance structure must link authority and responsibility to performance and review, i.e. accountability, and that the mechanism for achieving this should be transparent. The paper also addresses issues specific to governing, leading and managing dental schools. Being a dean of a modern dental school is a very demanding role and some issues relating to this role are raised, including: dilemmas facing deans, preparing to be dean and succession planning. The importance of establishing a shared vision and mission, and creating the right culture and climate within a dental school, are emphasized. The Working Group advocates establishing a culture of scholarship in dental schools for both teaching and research. The paper addresses the need for effective staff management, motivation and development, and highlights the salience of good communication. The Working Group suggests establishing an advisory board to the dean and school, including lay persons and other external stakeholders, as one way of separating governance and management to some extent and providing some checks and balances within a dental school. Several other suggestions and recommendations are made about governance, management and leadership issues, including the need for schools to promote an awareness of their roles by good communication and thereby influence perceptions of others about their roles and values.

Background and Purpose— Atherosclerotic intracranial stenosis is an important cause of stroke in blacks, yet there are limited data on vascular risk factors and outcome. We analyzed the vascular risk factors and outcomes of blacks and whites in the Warfarin versus Aspirin for Symptomatic Intracranial Disease (WASID) trial. Methods— Baseline characteristics and outcomes (ischemic stroke, brain hemorrhage, or vascular death combined and ischemic stroke alone) were compared between blacks (n=174) and whites (n=331) using univariate and multivariate analyses. Results— Blacks were significantly ( P <0.05) more likely than whites to be/have: female, hypertension history, diabetes history, higher LDL, higher total cholesterol, lower triglycerides, unmarried, unemployed, nonprivate insurance, no insurance, stroke as qualifying event, <70% stenosis, symptomatic anterior circulation vessel, no antithrombotic medication before qualifying event, and no family history of myocardial infarction. Blacks more frequently reached an end point of ischemic stroke, brain hemorrhage or vascular death (28% versus 20%; hazard ratio of 1.49, 95% CI 1.03 to 2.17, P =0.03), had a higher 2-year event rate (0.28 versus 0.19), and reached the end point of ischemic stroke alone (25% versus 16% at 2 years; hazard ratio of 1.62, P =0.017). In multivariate analysis, race was associated with ischemic stroke ( P =0.0488) but not with the end point ischemic stroke, brain hemorrhage or vascular death ( P =0.188). Conclusions— Blacks with intracranial stenosis are at higher risk of stroke recurrence than whites. This risk warrants additional study of factors contributing to stroke in blacks and highlights the need for aggressive risk factor management in blacks to prevent recurrence.

BACKGROUND AND PURPOSE:There are limited and conflicting data on gender differences in clinical outcomes among patients with symptomatic intracranial arterial stenosis. This study examined gender differences in patients enrolled in the Warfarin-Aspirin Symptomatic Intracranial Disease (WASID) Study.METHODS:Participants were 569 men and women with symptomatic intracranial arterial stenosis. They were followed-up for the occurrence of ischemic stroke and the combined end point of stroke or vascular death from February 1999 through July 2003 (mean follow-up, 1.8 years).RESULTS:Two-year rates of the primary end point were 28.4% and 16.6% for women and men, respectively. Cumulative probabilities of the outcomes over time were estimated by the Kaplan-Meier product-limit method and were compared between men and women with the use of the log-rank test. Cox proportional hazards regression analyses were used to estimate the hazard ratio of gender (women to men) for ischemic stroke and for the primary end point. The probabilities of ischemic stroke (P=0.005) and of the combined end point of stroke or vascular death (P=0.017) over time were significantly higher in women than men. Women had a greater multivariate-adjusted risk for ischemic stroke (HR, 1.85; 95% CI, 1.14 to 3.01; P=0.013) and for the combined end point of stroke or vascular death (HR, 1.58; 95% CI, 1.01 to 2.48; P=0.045).CONCLUSIONS:Women with symptomatic intracranial arterial stenosis are at significantly greater risk for ischemic stroke and for the combined end point of stroke or vascular death. These findings suggest the need for vigorous screening of risk factors and for aggressive management of risk factors and stroke in women. They also suggest the need to ensure adequate numbers of women in clinical trials designed to explore new and promising therapies for intracranial arterial stenosis.

This paper examines the association between trait anger and subclinical carotid artery atherosclerosis among 14,098 Black or White men and women, aged 48-67 years, in the Atherosclerosis Risk in Communities Study cohort, 1990-1992. Trait anger was assessed using the 10-item Spielberger Trait Anger Scale. Carotid atherosclerosis was determined by an averaged measure of the wall intimal-medial thickness (IMT) of the carotid bifurcation and of the internal and common carotids, measured by high-resolution B-mode ultrasound. In the full study cohort, trait anger and carotid IMT were significantly and positively associated (p = 0.04). In race-gender stratified analysis, the association was strongest and independent only in Black men, among whom a significant trait anger-carotid IMT relation was observed for both the overall trait anger measure (p = 0.004) and the anger reaction dimension (p = 0.001). In Black men, carotid IMT levels increased across categories of overall trait anger and anger reaction, resulting in clinically significant differences (67 microm (95% confidence interval: 23, 110) and 82 microm (95% confidence interval: 40, 125), respectively) from low to high anger. Sociodemographic, lifestyle, anthropometric, and biologic cardiovascular disease risk factors appear to mediate the relation in Black women, White men, and White women. In conclusion, these findings document disparate race-gender patterns in the association of trait anger with subclinical carotid artery atherosclerosis.

The cross-sectional association between trait anger and stiffness of the left common carotid artery was examined in 10,285 black or white men or women, 48-67 years of age, from the Atherosclerosis Risk in Communities (ARIC) study cohort. Trait anger was assessed using the 10-item Spielberger Trait Anger Scale. Arterial stiffness was assessed by pulsatile arterial diameter change (PADC) derived from echo-tracking ultrasound methods; the smaller the PADC, the stiffer the common carotid artery. In men, trait anger was significantly associated with PADC, independent of the established cardiovascular disease risk factors (p=0.04). PADC decreased from the first (lowest anger group) to the second quintile of anger, but there was no progressive decrease thereafter. Also observed was a 13-microm (95% confidence interval [CI], 1-25) difference in the magnitude of PADC from the lowest to the uppermost quintile of anger (PADC [standard error], 421 [4] microm vs. 408 [5] microm). In women, the association was marginally significant (p=0.07). The low-high difference in the magnitude of PADC (PADC [standard error], 397 [3] microm vs. 406 [4] microm) was inverse (-9 microm 95% CI, -19 to 2). Conclusions indicate that very high trait anger is associated with arterial stiffness in men.

Objective: Trait anger has been shown to predict coronary heart disease; however, there are no prior studies evaluating anger as a risk factor for type 2 diabetes. The objective of this study was to determine if anger proneness predicted type 2 diabetes using prospective analyses.Methods: We analyzed data on trait anger, assessed by questionnaire, in a longitudinal, bi-racial cohort study of 11,615 initially non-diabetic adults aged 48-67, who were subsequently followed for 6 years for the development of type 2 diabetes.Results: There was no relation between overall trait anger and the subsequent risk of diabetes; however, individuals in the highest tertile of trait anger temperament scores had a 34% increased risk of developing diabetes compared to those in the lowest tertile (Relative hazard [RH]=1.34; 95% confidence interval: 1.10, 1.62), following adjustment for age, race, gender, and education. The relation between anger temperament and diabetes remained significant following adjustment for behavioral factors (smoking, physical activity, and caloric intake) (RH = 1.31; 95% Cl: 1.08, 1.60) but was non-significant after additional adjustment for waist-to-hip ratio and body-mass index (RH = 1.18; 95% Cl: 0.97, 1.44).Conclusions: While we found no relation between overall trait anger and incident diabetes, persons who had higher anger temperament subscale scores had a slightly increased risk of type 2 diabetes, which was largely explained by adiposity. Anger temperament may deserve further attention as a potential risk factor for type 2 diabetes. (C) 2005 Elsevier Ltd. All rights reserved.

There is mounting evidence to suggest that psychosocial factors, including anger proneness, depression and social isolation, are risk factors for cardiovascular disease. Nevertheless, evidence relating these factors to peripheral arterial disease (PAD) and intermittent claudication remains sparse. Using data from the Atherosclerosis Risk in Communities Study, we analyzed the relationship of psychosocial variables (Spielberger anger score, depression score from the Maastricht questionnaire, and a perceived social support scale) at study visit 2 with incident PAD (ankle-brachial index ≤0.9; a hospital discharge diagnosis of PAD, leg amputation, or leg revascularization procedures; or intermittent claudication). In 12 965 middle-aged adults with no prior history of PAD, 854 developed PAD over a mean follow-up time of 9.7 years, yielding an incidence rate of 6.8 per 1000 person years. A modest, monotonic dose-response, positive association between anger proneness and incident PAD was observed in a multivariable model: relative risk (RR) = 1.15 (95% confidence interval (CI) 0.99-1.38) in the moderate anger group and RR = 1.38 (95% CI 1.08-1.76) in the high anger group, compared with the low anger group. When compared with a low level of depressive symptoms, moderate and high levels of depressive symptoms were also associated with greater incident PAD, with multivariable RRs of 1.20 (95% CI 0.99-1.45) and 1.44 (95% CI 1.19-1.74) respectively. There was no association of perceived level of social support with the occurrence of PAD. Anger proneness and depressive symptoms may be associated with the occur-rence of PAD, as for other atherosclerotic syndromes. These findings may warrant confirmation in further studies and, if causal, could serve as a unique target for a PAD prevention trial.

Background— The purpose of this study was to assess the relation of adverse childhood experiences (ACEs), including abuse, neglect, and household dysfunction, to the risk of ischemic heart disease (IHD) and to examine the mediating impact on this relation of both traditional IHD risk factors and psychological factors that are associated with ACEs. Methods and Results— Retrospective cohort survey data were collected from 17 337 adult health plan members from 1995 to 1997. Logistic regression adjusted for age, sex, race, and education was used to estimate the strength of the ACE–IHD relation and the mediating impact of IHD risk factors in this relation. Nine of 10 categories of ACEs significantly increased the risk of IHD by 1.3- to 1.7-fold versus persons with no ACEs. The adjusted odds ratios for IHD among persons with ≥7 ACEs was 3.6 (95% CI, 2.4 to 5.3). The ACE–IHD relation was mediated more strongly by individual psychological risk factors commonly associated with ACEs than by traditional IHD risk factors. We observed significant association between increased likelihood of reported IHD (adjusted ORs) and depressed affect (2.1, 1.9 to 2.4) and anger (2.5, 2.1 to 3.0) as well as traditional risk factors (smoking, physical inactivity, obesity, diabetes and hypertension), with ORs ranging from 1.2 to 2.7. Conclusions— We found a dose-response relation of ACEs to IHD and a relation between almost all individual ACEs and IHD. Psychological factors appear to be more important than traditional risk factors in mediating the relation of ACEs to the risk of IHD. These findings provide further insights into the potential pathways by which stressful childhood experiences may increase the risk of IHD in adulthood.

Aims The Framingham risk equations are widely used to estimate risk of coronary heart disease (CHD). The purpose of this study was to evaluate the reliability of these equations in predicting CHD risk in people with diabetes and the reliability of using imputed mean HDL-cholesterol values.Methods Data describing the baseline characteristics of recognized CHD risk factors for 938 people aged 30-74 years were extracted from the Cardiff Diabetes Database. Data describing CHD events were available for up to 4 years following the baseline year (1996). Several mathematical techniques were used to assess the reliability of predictions provided by the Framingham equations in this population.Results Thirty-four percent of males and 25% of females who experienced CHD events had a predicted 10-year CHD risk greater than or equal to 30%. Seventy-five percent of males and 58% of females had a predicted 10-year CHD risk greater than or equal to 20%. Using imputed HDL-cholesterol values, 26% of males and 6% of females who later developed CHD events had a 10-year CHD risk greater than or equal to 30%. Using imputed HDL-cholesterol values, the CHD risk predicted by the Framingham equations consistently underestimated the actual risk of CHD events. However, refitting the Framingham risk equations to the Cardiff data resulted in only marginal improvements in discriminatory capabilities.Conclusions The Framingham risk equations can be unreliable when applied to the diabetic population, tending to underestimate an individual's probability of progressing to CHD; the equations perform marginally better in women than in men. The use of imputed mean HDL-cholesterol values improved the reliability of the estimates of risk.