Anxiety disorders increase risk for incident myocardial infarction in depressed and nondepressed Veterans Administration patients.

BACKGROUND: Depression is a risk factor for incident myocardial infarction (MI), but little is known about the independent or additive risk from anxiety disorders. METHODS: In a 7-year retrospective cohort design, we identified a cohort free of cardiovascular disease in fiscal years 1999 and 2000 that contained 96,612 patients between 25 and 80 years of age who had an International Classification of Diseases, Ninth Revision, Clinical Modification code indicating a diagnosis of depression in 2000 (baseline) and 259,387 patients without depression. Cox proportional hazards models stratified by depression were computed to test for a main effect of anxiety disorder unspecified, generalized anxiety disorder, panic disorder, social phobia, obsessive-compulsive disorder, and posttraumatic stress disorder (PTSD) on risk of incident MI. The models were adjusted for multiple MI risk factors and sociodemographics. RESULTS: Depressed as compared to nondepressed Veterans Administration patients were at increased risk for incident MI (HR 1.39; 95% CI 1.34-1.45). In nondepressed patients those with anxiety disorder unspecified (HR 1.34; 95% CI 1.21-1.47), panic disorder (HR 1.43; 95% CI 1.11-1.83), and PTSD (HR 1.25; 95% CI 1.16-1.36) were at increased risk for incident MI. The independent risk associated with anxiety disorders was reduced in patients comorbid for depression. CONCLUSIONS: In Veterans Administration patients free of heart disease in 1999 and 2000, those with depression, anxiety disorder unspecified, panic disorder, and PTSD were at increased risk of incident MI. Anxiety disorders are independent risk factors for MI. Depression partially accounts for the effect of anxiety disorders on risk of MI in patients with both conditions.

Genetic and environmental contributions to nicotine, alcohol and cannabis dependence in male twins.

AIMS: To compute the common and specific genetic and environmental contributions to nicotine dependence (ND) alcohol dependence (AD) and cannabis dependence (CD). DESIGN: Twin model. PARTICIPANTS: Data from 1874 monozygotic and 1498 dizygotic twin pair members of the Vietnam Era Twin Registry were obtained via telephone administration of a structured psychiatric interview in 1992. MEASUREMENTS: Data to derive life-time diagnoses of DSM-III-R ND, AD and CD were obtained via telephone administration of the Diagnostic Interview Schedule. FINDINGS: The best-fitting model allowed for additive genetic contributions and unique environmental influences that were common to all three phenotypes. Risks for ND and AD were also due to genetic and unique environmental influences specific to each drug. A specific shared environmental factor contributed to CD. CONCLUSIONS: These results suggest that the life-time co-occurrence of ND, AD and CD is due to common and specific genetic factors as well as unique environmental influences, and vulnerability for CD is also due to shared environmental factors that do not contribute to ND and AD. The majority of genetic variance is shared across drugs and the majority of unique environmental influences are drug-specific in these middle-aged men. Because differences between models allowing for specific genetic versus shared environment were small, we are most confident in concluding that there are specific familial contributions-either additive genetic or shared environment-to CD.

Common genetic liability to major depression and posttraumatic stress disorder in men.

BACKGROUND: Major depression (MD) and posttraumatic stress disorder (PTSD) are highly comorbid. The degree to which a common genetic liability explains the etiology of the MD-PTSD association has not been quantified and has important implications for research and prevention. METHODS: This paper presents an analysis of data from 6744 members of the Vietnam Era Twin Registry. MD and PTSD were assessed using the Diagnostic Interview Schedule-III-R in 1991-92. Bivariate twin modeling was conducted to determine the genetic and environmental etiology of the MD-PTSD association. RESULTS: The best-fitting model for the MD-PTSD association included a substantial genetic correlation (r=.77; 95% CI, .50-1.00) and a modest individual-specific environmental correlation (r=.34; 95% CI, .19-.48). Common genetic liability explained 62.5% of MD-PTSD comorbidity. Genetic influences common to MD explained 15% of the total variance in risk for PTSD and 58% of the genetic variance in PTSD. Individual-specific environmental influences common to MD explained only 11% of the individual-specific environmental variance in PTSD. LIMITATIONS: Our participants were male Vietnam era veterans and our findings may not generalize to civilians, females or other cohorts. CONCLUSIONS: MD-PTSD comorbidity is largely explained by common genetic influences. Substantial genetic overlap between MD and PTSD implies that genes implicated in the etiology of MD are strong candidates for PTSD and vice versa. Environmental influences on MD and PTSD explain less of their covariation and appear to be largely disorder-specific. Research is needed to identify environmental factors that influence the development of MD versus PTSD in the context of common genetic liability.

Differential etiology of posttraumatic stress disorder with conduct disorder and major depression in male veterans.

BACKGROUND: Epidemiologic studies reveal that posttraumatic stress disorder (PTSD) is highly comorbid with both conduct disorder and major depression in men. The genetic and environmental etiology of this comorbidity has not been examined. METHODS: Data were analyzed from 6744 middle-aged male-male monozygotic and dizygotic twins from the Vietnam Era Twin Registry. Conduct disorder, major depression, and PTSD were assessed via telephone interview using the Diagnostic Interview Schedule for the DSM-III-R in 1992. Structural equation modeling was used to estimate additive genetic, shared environmental, and individual-specific environmental effects common and specific to conduct disorder, major depression, and PTSD. RESULTS: The association between conduct disorder and PTSD was explained primarily by common shared environmental influences; these explained 10% (95% confidence interval: 6%-17%) of the variance in PTSD. The association between major depression and PTSD was largely explained by common genetic influences; these explained 19% (95% confidence interval: 11%-26%) of the variance in PTSD. CONCLUSIONS: Our findings suggest that different etiologic mechanisms explain the association of conduct disorder and major depression with PTSD in male veterans. If replicated in other populations, results suggest research aimed at identifying specific genetic and environmental factors that influence PTSD may benefit from starting with those that have been more consistently and strongly associated with major depression and conduct disorder.

Evidence for specificity of transmission of alcohol and nicotine dependence in an offspring of twins design.

Alcohol dependence (AD) and nicotine dependence (ND) have been shown to co-occur. Results from twin studies implicate the role of genetics in the etiology of both ND and AD with substantial, yet incomplete, overlap. To test for specificity of transmission of AD and ND in an offspring of twins sample we analyzed data from a study of adolescent and adult offspring of twin fathers ascertained from the Vietnam Era Twin Registry. This sample consists of 1213 twin fathers, 862 biologic or rearing mothers, and 1270 offspring. Offspring were allocated to one of four risk groups for AD based on twin fathers' zygosity and father's and cotwins AD history. Offspring DSM-IV AD and ND were measured by structured diagnostic interview. Paternal AD and ND were significantly associated with offspring AD and ND, respectively. Bivariate probit regression results suggest specificity for transmission of AD and ND. This remained constant after controlling for offspring demographics and psychopathology and maternal AD and ND. Despite the substantial genetic overlap between the two disorders, there is evidence for genetic effects specific for AD and ND.

Common genetic risk of major depression and nicotine dependence: the contribution of antisocial traits in a United States veteran male twin cohort.

Many studies that found associations between depression and nicotine dependence have ignored possible shared genetic influences associated with antisocial traits. The present study examined the contribution of genetic and environmental effects associated with conduct disorder (CD) and antisocial personality disorder (ASPD) to the comorbidity of major depression (MD) and nicotine dependence (ND). A telephone diagnostic interview, the Diagnostic Interview Schedule-III-R, was administered to eligible twins from the Vietnam Era Twin (VET) Registry in 1992. Multivariate genetic models were fitted to 3360 middle-aged and predominantly white twin pairs (1868 monozygotic, 1492 dizygotic pairs) of which both members completed the pertinent diagnostic interview sections. Genetic influences on CD accounted for 100%, 68%, and 50% of the total genetic variance in risk for ASPD, MD and ND, respectively. After controlling for genetic influences on CD, the partial genetic correlation between MD and ND was no longer statistically significant. Nonshared environmental contributions to the comorbidity among these disorders were not significant. This study not only demonstrates that the comorbidity between ND and MD is influenced by common genetic risk factors, but also further suggests that the common genetic risk factors overlapped with those for antisocial traits such as CD and ASPD in men.

Nicotine dependence subtypes: association with smoking history, diagnostic criteria and psychiatric disorders in 5440 regular smokers from the Vietnam Era Twin Registry.

Studies suggest empirically derived subtypes of nicotine dependence exist in young adult populations with short smoking careers. It is not known if classes of dependence exist in middle aged smokers with longer smoking careers and whether these classes reflect quantitative or qualitative differences. It is not known if psychiatric disorders are associated with classes of nicotine dependence. Nicotine dependence symptoms were obtained from a 1992 administration of the Diagnostic Interview Schedule. Latent Class Analyses (LCA) was computed using data from 5440 members of the Vietnam Era Twin Registry. LCA was used to derive significantly different classes of nicotine dependence, which were assessed for their association with smoking history, nicotine dependence, and other psychiatric disorders. The LCA model which best fit the data was a 4 class solution characterized by severity. Age onset of regular smoking decreased with more severe classes. Cigarette consumption, failed cessation and psychiatric disorders were associated with more severe classes. Empirically derived subtypes of nicotine dependence are mostly characterized by increasing severity. Suggestions for refinement of nicotine dependence diagnostic criteria are discussed.

Training practitioners in evidence-based chronic disease prevention for global health.

Too often, public health decisions are based on short-term demands rather than long-term research and objectives. Policies and programmes are sometimes developed around anecdotal evidence. The Evidence-Based Public Health (EBPH) programme trains public health practitioners to use a comprehensive, scientific approach when developing and evaluating chronic disease programmes. Begun in 2002, the EBPH programme is an international collaboration. The course is organized in seven parts to teach skills in: 1) assessing a community's needs; 2) quantifying the issue; 3) developing a concise statement of the issue; 4) determining what is known about the issue by reviewing the scientific literature; 5) developing and prioritizing programme and policy options; 6) developing an action plan and implementing interventions; and 7) evaluating the programme or policy. The course takes an applied approach and emphasizes information that is readily available to busy practitioners, relying on experiential learning and includes lectures, practice exercises, and case studies. It focuses n using evidence-based tools and encourages participants to add to the evidence base in areas where intervention knowledge is sparse. Through this training programme, we educated practitioners from 38 countries in 4 continents. This article describes the evolution of the parent course and describes experiences implementing the course in the Russian Federation, Lithuania, and Chile. Lessons learned from replication of the course include the need to build a "critical mass" of public health officials trained in EBPH within each country and the importance of international, collaborative networks. Scientific and technologic advances provide unprecedented opportunities for public health professionals to enhance the practice of EBPH. To take full advantage of new technology and tools and to combat new health challenges, public health practitioners must continually improve their skills.

Exposure to paternal alcoholism does not predict development of alcohol-use disorders in offspring: evidence from an offspring-of-twins study.

OBJECTIVE: Using an offspring-of-twins design, we tested the hypothesis that exposure to paternal alcoholism during the child's first 12 years will increase offspring risk for subsequent alcohol-use disorders (AUD). METHOD: Structured psychiatric interviews assessed history of psychiatric and substance-use disorders in Vietnam Era Twin Registry fathers (n = 512), their offspring (n = 877), and mothers of the offspring (n = 507). Exposure was defined as the fathers' endorsement of any Diagnostic and Statistical Manual of Mental Disorders (DSM), Fourth Edition, AUD symptom, according to the Lifetime Drinking History assessment (administered in 1999), at any time between off- spring ages 0-12 years; all fathers had satisfied DSM, Third Edition, Revised (DSM-III-R), criteria for alcohol dependence in a 1992 diagnostic interview. Cox proportional hazards models were fit to predict time to first symptom of abuse/dependence in offspring. RESULTS: Off- spring exposed to paternal alcoholism were significantly more likely to develop an AUD when compared with offspring of nonalcoholic fathers (hazard ratio [HR] = 1.51; 95% confidence interval [CI]: 1.10-2.07). Although offspring unexposed to paternal alcoholism did not significantly differ from control offspring (HR = 1.50, 95% CI: 0.93-2.41), the magnitude of association was similar to that in the exposed offspring. There were no significant differences in AUD between offspring of alcoholics who were exposed and those who were not exposed to paternal alcoholism, as long as fathers had satisfied DSM-III-R criteria for alcohol dependence at some point in their lives. CONCLUSIONS: There does not appear to be a relationship between exposure to paternal alcoholism during childhood and development of an AUD in offspring. Genetic and high-risk environmental factors that are correlated with lifetime paternal alcoholism may be stronger predictors of offspring AUD than fathers' problem drinking. Future research should be encouraged, using more comprehensive analyses, to examine the role of family genetic influences and other family environmental influences on offspring alcohol outcomes.

Shared genetic risk of major depression, alcohol dependence, and marijuana dependence: contribution of antisocial personality disorder in men.

BACKGROUND: Little is known about genetic factors that underlie the interrelationships among antisocial personality disorder (ASPD), major depression (MD), alcohol dependence (AD), and marijuana dependence (MJD). We examined the contribution of genetic effects associated with ASPD to the comorbidity of MD and substance use disorders. METHODS: The Vietnam Era Twin Registry is a general population registry of male veteran twins constructed from computerized Department of Defense files and other sources. A telephone diagnostic interview was administered to eligible twins from the Registry in 1992. Of 5150 twin pairs who served on active military duty during the Vietnam era, 3360 pairs (1868 monozygotic and 1492 dizygotic) in which both members completed the pertinent diagnostic interview sections were included. The main outcome measures were lifetime DSM-III-R ASPD, MD, AD, and MJD. RESULTS: Structural equation modeling was performed to estimate additive genetic, shared environmental, and nonshared environmental effects common and specific to each disorder. The heritability estimates for lifetime ASPD, MD, AD, and MJD were 69%, 40%, 56%, and 50%, respectively. Genetic effects on ASPD accounted for 38%, 50%, and 58% of the total genetic variance in risk for MD, AD, and MJD, respectively. After controlling for genetic effects on ASPD, the partial genetic correlations of MD with AD and with MJD were no longer statistically significant. Genetic effects specific to MD and AD and familial effects specific to MJD remained statistically significant. Nonshared environmental contributions to the comorbidity in these disorders were small. CONCLUSIONS: In this sample, the shared genetic risk between MD and both AD and MJD was largely explained by genetic effects on ASPD, which in turn was associated with increased risk of each of the other disorders.

Subjective reactions to cocaine and marijuana are associated with abuse and dependence.

Subjective effects of marijuana and cocaine use are associated with amount of drug use and potentially with risk of abuse and dependence. We used Latent Class Analyses (LCA) to examine subjective responses to two categories of drugs and link these to abuse and dependence. In 1992, subjective responses were queried of 2506 marijuana and 661 cocaine lifetime users who were members of the Vietnam Era Twin Registry. LCA was used to identify classes of subjective effects. Multinomial logistic regression models were computed to test for an association between classes and marijuana and cocaine abuse or dependence. The best LCA solution for marijuana identified 6 distinct classes characterized as positive, relaxed, reactive, adverse, low and very reactive. The best LCA solution for cocaine identified 5 distinct classes characterized as positive, alert, adverse, low and very reactive. Marijuana abuse and dependence were significantly associated with each latent class. Cocaine abuse was associated with the reactive class (OR=3.9; 95% CI: 1.6-9.5). Cocaine dependence was associated with reactive (OR=15.3; 95% CI: 7.1-32.6), adverse (OR=9.7; 95% CI: 4.5-21.0) and very reactive (OR=18.7; 95% CI: 5.6-62.6) classes. We found evidence for both qualitative and quantitative subjective effect profiles. Subjective effects, both positive and adverse are associated with lifetime risk for marijuana and cocaine dependence.

A twin study of depression symptoms, hypertension, and heart disease in middle-aged men.

OBJECTIVE: Epidemiological and clinical studies have established an association between major depression and cardiovascular disease. We utilized a twin design to test whether there are common genetic and environmental risk factors underlying depression symptoms, hypertension and heart disease. METHODS: Association studies were conducted with 6,903 male-male twins from the Vietnam Era Twin Registry who responded to both a 1990 health questionnaire and a 1992 telephone administration of a structured psychiatric interview. Data from 2,731 complete twin pairs were used to fit genetic models which determined the extent to which lifetime depression symptoms, heart disease and hypertension shared genetic and/or environmental factors. RESULTS: Heart disease was significantly associated with 1-4 symptoms and 5 or more symptoms of depression (odds ratio [OR] = 2.62; 95% confidence interval [CI]: 1.54-4.46 and OR = 4.02; 95% CI: 2.16-7.46). Hypertension was significantly associated with 1 to 4 symptoms and 5 or more symptoms of depression (OR = 1.29; 95% CI: 1.11-1.50 and OR = 1.49; 95% CI: 1.21-1.83). The genetic correlations were significant between depression symptoms and hypertension (r =.19), and between depression symptoms and heart disease (r =.42). Of the total variance in depression, 8% was common to hypertension and heart disease, 7% of the variance in hypertension was common with depression symptoms and heart disease, and 64% of the variance in heart disease was common with depression symptoms and hypertension. CONCLUSIONS: Men who reported cardiovascular disease were significantly more likely to have depression symptoms. The lifetime co-occurrence of these phenotypes is partly explained by common genetic risk factors.

Does marijuana use have residual adverse effects on self-reported health measures, socio-demographics and quality of life? A monozygotic co-twin control study in men.

AIMS: To assess the effects of former heavy marijuana use on selected aspects of health. DESIGN: A monozygotic co-twin control design was used to compare the health of former heavy marijuana using male monozygotic twins to that of their co-twins who never used marijuana significantly. SETTING: In-person survey and questionnaires. PARTICIPANTS: Fifty-six marijuana use discordant monozygotic twin pair members of the Vietnam Era Twin (VET) Registry. MEASUREMENTS: Current socio-demographic characteristics; current nicotine and alcohol use; life-time nicotine and alcohol abuse/dependence; past 5-year physical and mental health services utilization; and health-related quality of life. FINDINGS: The mean number of days on which the marijuana user twin used marijuana in his life-time was 1085, while the non-marijuana user used marijuana a maximum of 5 days. Marijuana was last used a mean of 20 years previously. No significant differences were found between the former marijuana user twins and their siblings for current socio-demographic characteristics; current nicotine or alcohol use; life-time nicotine or alcohol abuse/dependence; past 5-year out-patient or emergency room visits, hospitalizations or medication use for medical problems; past 5-year mental health out-patient use or hospitalizations; or health-related quality of life. CONCLUSIONS: Previous heavy marijuana use a mean of 20 years earlier by a group of men who reported no other significant illicit drug use does not appear to be associated with adverse socio-demographic, physical or mental health adverse effects. The conclusions of the study are limited by possible participation and recall biases, relatively small sample size and the absence of a physical health examination.

Are substance use, abuse and dependence associated with study participation? Predictors of offspring nonparticipation in a twin-family study.

OBJECTIVE: Although epidemiologic studies have reported that problem drinking is associated with nonresponse to surveys, it is unclear whether parents' alcoholism is associated with nonresponse in their offspring. This question is particularly important to family studies of alcoholism. In the current study we constructed a model of offspring nonparticipation in a twin-family design and computed weights to recapture the distribution of offspring alcohol abuse and dependence. METHOD: In 1999, the first wave of a longitudinal study of offspring of alcoholic twins was conducted via telephone interview with members of the Vietnam Era Twin Registry. The target offspring sample consisted of 2,096 male and female children, of whom 1,270 were successfully interviewed. Offspring response status was classified as participation, refusal or unavailable/no consent. Stepwise logistic regression models were used to identify variables that were significantly associated with one or both types of offspring nonparticipation. A multinomial logit procedure with backward deletion was then used to build a model of the three levels of child response. RESULTS: Paternal alcoholism was not significantly associated with offspring nonresponse, although offspring nonparticipation because of not being located, or being deceased, disabled or unavailable was associated with current paternal smoking, paternal divorce and paternal marital status (after adjustment for other predictor variables). CONCLUSIONS: The most important conclusion to be drawn from current results is that the alcohol abuse and dependence history of fathers should not bias analyses in family studies of alcoholism when data are collected via telephone interview. Study limitations and directions for future research are discussed.

Lifetime and 12-month prevalence of psychiatric disorders in 8,169 male Vietnam War era veterans.

OBJECTIVE: This study reports the prevalence of psychiatric disorders among a nationally distributed sample of Vietnam Era veterans assessed using standardized psychiatric interviewing methods. METHODS: In 1992, the National Institute of Mental Health Diagnostic Interview Schedule was administered by telephone to 8,169 middle-aged males who served in the military during the Vietnam era (1965-1975). RESULTS: Approximately 72% of respondents reported a lifetime history and 36% reported a 12-month history of at least one psychiatric disorder. The most prevalent psychiatric disorders included alcohol abuse and/or dependence (54% lifetime, 17% 12 month), nicotine dependence (48% lifetime, 22% 12 month), and posttraumatic stress disorder (10% lifetime, 4.5% 12 month). CONCLUSIONS: Because of possible participation bias, these results likely represent conservative estimates of psychiatric disorder prevalences among the more than eight million Vietnam Era veterans and reinforces the major public health challenge of preventing, identifying, and treating psychiatric illness in American veterans.

Increased risk of myocardial infarction in depressed patients with type 2 diabetes.

OBJECTIVE: To investigate major depressive disorder (MDD), which complicates the course of type 2 diabetes and is associated with an increased risk of cardiovascular disease and death. This risk may be due to a greater susceptibility for myocardial infarction (MI) in depressed patients with type 2 diabetes compared with nondepressed patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: Veterans Administration electronic medical records were analyzed to identify a cohort free of cardiovascular disease in fiscal years 1999 and 2000, aged 25 to 80 years. ICD-9-CM codes were used to create a four-level risk group indicating 1) neither diabetes nor MDD (n = 214,749), 2) MDD alone (n = 77,568), 3) type 2 diabetes alone (n = 40,953), and 4) comorbid MDD and type 2 diabetes (n = 12,679). Age-adjusted Cox proportional hazards models were computed before and after adjusting for baseline sociodemographic and time-dependent covariates. RESULTS: After adjusting for covariates, patients with type 2 diabetes alone and patients with MDD alone were at ∼30% increased risk for MI, and patients with type 2 diabetes and MDD were at 82% increased risk for MI (hazard ratio 1.82 [95% CI 1.69-1.97]) compared with patients without either condition. CONCLUSIONS: Compared with patients with only diabetes or only MDD, individuals with type 2 diabetes and MDD are at increased risk for new-onset MI. Monitoring cardiovascular health in depressed patients with type 2 diabetes may reduce the risk of MI in this especially high-risk group.

Antidepressant drug compliance: reduced risk of MI and mortality in depressed patients.

BACKGROUND: The long-term risk of myocardial infarction (MI) associated with use of antidepressants is uncertain, especially for nontricyclic antidepressants. The present study uses a national Veterans Affairs cohort to test whether antidepressants increase or decrease risk of MI and all-cause mortality. METHODS: US Department of Veterans Affairs patient records were analyzed to identify a cohort free of cardiovascular disease in fiscal years 1999 and 2000, aged 25-80 years, who had an International Classification of Diseases, Ninth Revision, Clinical Modification code indicating an episode of depression (n=93,653). Incident MI and all-cause mortality were modeled in patients who received 12 weeks or more of antidepressant pharmacotherapy as compared with 0-11 weeks during follow-up. Age-adjusted Cox proportional hazard models were computed before and after adjusting for baseline sociodemographics and time-dependent covariates. RESULTS: Receipt of 12 or more weeks of continuous antidepressant therapy was associated with significantly reduced rates of incident MI across classes of antidepressants: selective serotonin reuptake inhibitor (SSRIs) (hazard ratio [HR] 0.48; 95% confidence interval [CI], 0.44-0.52), serotonin-norepinephrine reuptake inhibitors (SNRIs) (HR 0.35; 95% CI, 0.32-0.40), tricyclic antidepressants (TCAs) (HR 0.39; 95% CI, 0.34-0.44), and "Other" (HR 0.41; 95% CI, 0.37-0.45). Risk of all-cause mortality also was decreased with receipt of 12 weeks of pharmacotherapy with all classes of antidepressants (SSRI, SNRI, TCA, Other), with HRs ranging from 0.50 to 0.66. CONCLUSIONS: Across classes of antidepressants, 12 weeks of pharmacotherapy appears to be safe in terms of MI risk. Although the mechanism for this association remains uncertain, it is possible that compliance with pharmacotherapy for depression reflects compliance with cardiovascular medications. It also is possible that a direct drug effect or improved depressed mood may attenuate the risk of MI in depressed patients.

Commentary: the role of mentored internships for systems engineering in improving health care delivery.

The authors advise the adoption of mentored internships in systems engineering, conducted at academic hospitals, directed by physicians, epidemiologists, and health administrators and overseen by faculty at attendant schools of engineering. Such internships are anticipated to directly address the immediate objectives of administrators and clinicians. Additionally, this affords future generations of health care engineers the opportunity to learn the language and methodology of the medical sciences to provide a common ground for the analysis and understanding of medical systems. In turn, this should foster collaboration between the principal stakeholders in health care delivery--practitioners, administrators, engineers, and researchers--in the collective efforts to improve the quality of services provided.

Depression increases risk of incident myocardial infarction among Veterans Administration patients with rheumatoid arthritis.

OBJECTIVE: This study evaluates whether depression is a risk factor for incident myocardial infarction (MI) in Department of Veterans Affairs (VA) patients with rheumatoid arthritis (RA) between 30 and 79 years of age. METHODS: We used a retrospective cohort study of 15,634 patients with RA. Diagnoses and sociodemographic data were obtained from VA administrative and pharmacy databases between fiscal years 1999 and 2006. Entry into the cohort required 2 years of patient time with no evidence of cardiovascular disease. Cox proportional hazard models with time-dependent covariates were computed to determine whether RA patients with depression as compared to RA patients without depression were at increased risk for MI during the maximum 6-year follow-up period. RESULTS: Unadjusted analyses indicated depressed RA patients were 1.4 times more likely than nondepressed RA patients to have an MI during follow-up. These results remained significant (HR=1.4; 95% CI: 1.1-1.8) in the adjusted Cox proportional hazards model which included the effects of sociodemographics and known physical risks (e.g., diabetes) for MI. CONCLUSIONS: Depressed RA patients, without a history of cardiovascular disease, are 40% more likely to have a heart attack as compared to those without depression. These data demonstrate a rapid (within 6 years) transition to MI following onset of depression in RA patients. Increased monitoring of depression and heart disease status in this patient population may be warranted which in turn may result in longer duration of life.