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 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 1969, a Pacific Northwest American Indian community cohort (n = 100) was interviewed for the presence of physical and psychiatric illnesses. The same community was studied again in 1988. This study describes the outcome among the original 100 subjects. The schedule for Affective Disorders and Schizophrenia Lifetime Version (SADS-L) served as the basic interview instrument, supplemented by data from medical records, death certificates, and medical and community informants. Twenty-five subjects had died, 13 from cardiovascular disorders and seven from alcohol-related illnesses. Among the 46 subjects re-interviewed, hypertension, heart disease, and diabetes had become significant sources of medical morbidity. Alcoholism was the most significant cause of psychiatric morbidity, particularly among males. This study indicates that greater attention should be focused upon prevention and treatment of alcoholism, cardiovascular disorders, and diabetes in this community and in other American Indian populations.
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PMID:The natural history of medical and psychiatric disorders in an American Indian community. 130 32

A multidimensional relationship exists between cardiovascular disease and affective disorder that includes the observations that (1) there is a high rate of depression in the postmyocardial infarction period, (2) the presence of depressive illness adversely affects the prognosis of cardiac disease, and (3) depressed patients have a higher-than-expected rate of sudden cardiovascular death. The authors discuss these topics and the clinical management of depression in patients with significant preexisting heart disease. The cardiovascular effects of the tricyclic antidepressants and recently introduced nontricyclic antidepressants are reviewed with a focus on how the clinician can safely and effectively treat affective disorder in patients with severe cardiac disease.
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PMID:Treating the depressed patient with cardiovascular problems. 152 77

We studied the relation between mood disorder and hyperventilation (hypocapnia) before and during exercise treadmill testing in 113 chest pain patients attending a cardiac clinic and 30 healthy controls. In most patients end-tidal PCO2 (PCO2) rose in the normal way on exercise but in a subset of 24 (21 per cent) there was no rise: these patients with initial hyperventilation had significantly higher anxiety scores than those with a normal exercise-induced rise in PCO2. Two of the 24 had ischaemic heart disease and 10 (42 per cent) complained of recent panic anxiety compared with 12 (13 per cent) of the 89 with normal rise in PCO2 (p less than 0.05). Rates of psychiatric morbidity were similar in patients with 'typical' and 'atypical' chest pain. Resting hypocapnia occurred more often in patients with panic anxiety than in either anxious or non-anxious patients without panic. Panic patients also reported more symptoms of breathlessness and hyperventilation-related complaints than those without panic. Our findings confirm the important association between panic and hyperventilation in patients with chest pain. Furthermore, patients with exercise-induced hyperventilation are more likely to have a psychiatric than a cardiac disorder. Early detection and treatment of these patients may reduce the potential morbidity associated with unnecessary invasive investigations.
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PMID:Panic anxiety and hyperventilation in patients with chest pain: a controlled study. 327 82

Recent research suggests that affective disorder is associated with increased mortality and physical morbidity, but the reasons for this association remain uncertain. This report describes a 50-year prospective study of 240 men evaluated from the time they were university students in 1940-1942. A family history of mental illness was obtained and the men's habits, psychological adjustment, and marital and occupational satisfaction were followed every 2 years and their objective physical health was tracked every 5 years until age 70. Twenty-five men were identified as having affective spectrum disorder prior to age 53. Of the variables studied, the presence of affective spectrum disorder was the most powerful predictor of poor psychosocial outcome at age 65 and one of the most powerful predictors of poor physical health. Alcohol abuse and cigarette abuse accounted for the observed increased rates of heart disease and cancer. When alcohol abuse, smoking, and suicide were controlled for, affective disorder made a significant contribution to physical morbidity by age 70, but not to mortality from natural causes. Affective spectrum disorder, even in an educated population without antisocial trends, carries a profound negative risk to late-life physical and social adjustment.
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PMID:1995 IPA/Bayer Research Awards in Psychogeriatrics. Late-life consequences of affective spectrum disorder. 880 87

Chronic obstructive pulmonary disease (COPD) affects over 16 million people in the United States and is a major cause of disability and death worldwide. Its prevalence and mortality are increasing disproportionately among the elderly, women, African-Americans, persons of lower socioeconomic status, and the populations of developing countries in which tobacco is aggressively marketed. In contrast to other major chronic diseases such as heart disease and cancer, medical treatments for COPD have not made decisive inroads into its morbidity or death rates over the last 20 years, resulting in continuing efforts to reduce disability in patients with established disease. Depression is a source of increased disability in COPD, and, as in other chronically ill patient populations, is often unrecognized and untreated in the primary and specialty care sectors. Nearly half of all patients experience some depressive symptoms and at least one-fifth have had one or more major depressive episodes, frequently of long duration. Evidence from randomized controlled trials supports the thesis that patients with mild depression improve with multidisciplinary rehabilitation, whereas patients with major depression may require specific pharmacotherapy to achieve significant improvement in mood disorder and day-to-day function. In addition to its impact on disability, depression may contribute indirectly to the etiology and progression of COPD through its relationship to addictive smoking. Mood disorder in adolescence and early adulthood contributes to early smoking and failure to quit, even after the onset of respiratory disease in later life. Patients with a history of major depression are more likely to fail in smoking cessation programs and to develop a major depressive episode when they do stop. This relationship calls for psychiatrically informed intervention models to improve long-term abstinence rates. The functional impairments associated with COPD are themselves potential promoters of depressive morbidity and chronicity, acting through complex causal pathways. Progressive hypoxia due to respiratory insufficiency leads to structural brain changes and neurocognitive deficits that impair day-to-day function and reduce adaptive potential; and oxygen therapy, as now practiced, offers minimal neurocognitive and mood benefits to most patients. Limited data from studies of experimental hypoxia in animals suggest that relatively mild lack of oxygen impairs the function and plasticity of critical neurotransmitter systems implicated in both cognition and mood, although current practice standards withhold oxygen therapy until late in the course of disease when the damaging effects of hypoxia on the brain have become well established. Neuropsychiatric approaches to the prevention, delay, and treatment of brain dysfunction should be a primary objective of research to improve patient outcomes. A comprehensive relational model that links pulmonary disease, hypoxia, neurocognitive impairment, and structural brain disease with depression provides a useful framework for the design of such studies. The near-term research agenda should include three components: (1) practical methods for improving physician and patient recognition of depression and neurocognitive impairment as targets for intervention; (2) additional trials of standard antidepressant treatment approaches for both major and minor depression; and (3) tests of the hypothesis that late-onset depression in patients with COPD is a marker for the presence of neurocognitive deficits and structural brain changes. The long-range research agenda must aim at preventive interventions designed to forestall brain deterioration. Controlled clinical trials of supplemental oxygen in patients with mild hypoxia and minimal cognitive deficits are needed to determine whether early treatment can reverse or moderate decline, reduce the incidence and chronicity of depression, and improve response to antidepressant treatment. Novel neuroprotective therapies such as antioxidant supplementation and modulation of monoaminergic neurotransmission, coupled with overall improvements in long-term respiratory disease management that minimize episodes of increased systemic oxidative stress, should be considered for multisite trials designed to define optimal treatment and prevention.
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PMID:Depression and Chronic Obstructive Pulmonary Disease: Treatment Trials. 1008 98

Coordinated efforts to identify susceptibility genes for unipolar major depressive disorder (MDD) and related disorders are now underway. These studies have focused on recurrent, early-onset MDD (RE-MDD), the most heritable form of this disorder. The goal of this study was to characterize the burden of MDD and other mood disorders, comorbid mental disorders, and excess mortality in RE-MDD families. A total of 81 families were identified through probands over the age of 18, who met criteria for recurrent (> or = 2 episodes), early-onset (< or = 25 years), nonpsychotic, unipolar MDD (RE-MDD), and included 407 first-degree relatives and 835 extended relatives. Psychiatric diagnoses for probands and their family members who provided blood samples were formulated from structured personal interviews, structured family history assessments, and available medical records. The remaining family members who participated and those who were deceased were evaluated through the family history method augmented by available medical records. Best estimate diagnoses were made during a consensus conference according to established diagnostic criteria. Approximately half of the first-degree relatives and a quarter of extended relatives of RE-MDD probands suffered from at least one mood disorder, typically MDD. As commonly observed for other oligogenic, multifactorial disorders, the severity of MDD reflected by age at onset and number of episodes attenuated with increasing familial/genetic distance from the proband. A substantial fraction of RE-MDD probands and their first-degree relatives met diagnostic criteria for additional psychiatric disorders that include prominent disturbances of mood. The deceased relatives of RE-MDD probands died at a median age that was 8 years earlier than for the local population; over 40% died before reaching age 65. These differences in mortality statistics resulted from a shift toward younger ages at death across the lifespan, including a fivefold increase in the proportion of individuals who died in the first year of life. Several-fold increases in the proportion of deaths by suicide, homicide, and liver disease were observed among the relatives of RE-MDD probands. However, the rank order of the three most common causes of death-heart disease, cancer, and stroke-remained unchanged and differences in the proportions of deaths from the remaining causes were small. RE-MDD is a strongly familial condition with a high rate of psychiatric comorbidity, whose malignant effects have a significant negative impact on the health and longevity of patients and their family members.
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PMID:Malignancy of recurrent, early-onset major depression: a family study. 1180 16

Psychological depression is shown to be associated with several aspects of coronary artery disease (CAD), including arrhythmias, myocardial infarction, heart failure and sudden death. The physiological mechanisms accounting for this association are unclear. Hypothalamic-pituitary-adrenal dysregulation, diminished heart rate variability, altered blood platelet function and noncompliance with medial treatments have been proposed as mechanisms underlying depression and cardiovascular disease. Recent evidence also suggests that reduced baroreflex sensitivity, impaired immune function, chronic fatigue and the co-morbidity of depression and anxiety may be involved in the relationship between depression and cardiovascular dysregulation. An experimental strategy using animal models for investigating underlying physiological abnormalities in depression is presented. A key to understanding the bidirectional association between depression and heart disease is to determine whether there are common changes in brain systems that are associated with these conditions. Such approaches may hold promise for advancing our understanding of the interaction between this mood disorder and CAD.
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PMID:Biological mechanisms in the relationship between depression and heart disease. 1266 98

This study investigated the relationship of executive impairment and heart disease burden to remission of major depression among elderly patients. A total of 112 elderly subjects suffering from major depression received treatment with citalopram at a target daily dose of 40 mg for 8 weeks. Diagnosis was assigned using the Research Diagnostic Criteria and the DSM-IV Criteria after an interview with the Schedule for Affective Disorders and Schizophrenia. Executive dysfunction was assessed with the Initiation/Perseveration subscale of the Dementia Rating Scale (DRS) and the Color-Word Stroop test. Medical burden, including heart disease burden, was rated with the Cumulative Illness Rating Scale, and disability with Philadelphia Multilevel Instrument. Both abnormal initiation/perseveration and abnormal Stroop scores were associated with low remission rates of geriatric depression. Similarly, heart disease burden and baseline severity of depression also predicted low remission rates. The relationship of heart disease burden to remission was not mediated by executive dysfunction. Impairment in other DRS cognitive domains, disability, medical burden unrelated to heart disease did not significantly influence the outcome of depression in this sample. Executive dysfunction and heart disease burden constitute independent vulnerability factors that increase the risk for chronicity of geriatric depression. The findings of this study provide the rationale for investigation of the role of specific frontostriatal-limbic pathways in predisposing to geriatric depression or worsening its course.
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PMID:Executive dysfunction, heart disease burden, and remission of geriatric depression. 1534 Mar 93

The number of uninsured Texas residents who rely on the medical emergency department as their primary health care provider continues to increase. Unfortunately, little information about the characteristics of this group of emergency department users is available. Using an administrative billing database, we conducted a descriptive study to examine the demographic and clinical features of 17,110 consecutive patients without medical insurance who presented to the emergency department of the University of Texas Medical Branch in Galveston over a 12-month period. We also analyzed the risk of multiple emergency department visits or hospitalization according to demographic characteristics. Twenty percent of the study population made two or more emergency department visits during the study period; 19% of the population was admitted to the hospital via the emergency department. The risk of multiple emergency department visits was significantly elevated among African Americans and increased in a stepwise fashion according to age. The risk of being hospitalized was significantly reduced among females, African Americans, and Hispanics. There was an age-related monotonic increase in the risk of hospitalization. Abdominal pain, cellulitis, and spinal disorders were the most common primary diagnoses in patients who made multiple emergency department visits. Hospitalization occurred most frequently in patients with a primary diagnosis of chest pain, nonischemic heart disease, or an affective disorder. Additional studies of emergency department usage by uninsured patients from other regions of Texas are warranted. Such data may prove helpful in developing effective community-based alternatives to the emergency department for this growing segment of our population. Local policymakers who are responsible for the development of safety net programs throughout the state should find this information particularly useful.
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PMID:Emergency department usage by uninsured patients in Galveston County, Texas. 1862 70

Matrix metalloproteinase-9 (MMP-9) plays a role in many pathological conditions (e.g., cancer and heart disease). Recently, MMP-9 has been implicated in various aspects of brain functions (e.g., neuroplasticity and epileptogenesis) and thus, we hypothesized that MMP-9 gene may be associated with bipolar mood disorder. The study was performed on 416 patients with bipolar mood disorder, including 75 patients with bipolar II type of the illness, and in 558 healthy control persons. A functional -1562C/T polymorphism of the MMP-9 gene was genotyped in all subjects. Patients with bipolar mood disorder had significant preponderance of T allele versus C allele of 1562C/T polymorphism of the MMP-9 gene, compared to healthy control subjects. The higher frequency of T allele compared to healthy subjects was especially evident in a subgroup of patients with bipolar disorder, type II. The results may provide the first evidence for an involvement of the MMP-9 gene in the pathogenesis of bipolar mood disorder. They may also contribute to explaining genetic connection between bipolar mood disorder and some somatic illnesses. In the light of our results obtained with this polymorphism in schizophrenia, we speculate that the MMP-9 gene may be a common susceptibility gene to major psychoses with different allelic variants occurring in bipolar illness and schizophrenia.
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PMID:Matrix metalloproteinase-9 gene and bipolar mood disorder. 1953 54


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