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

Eight patients with major depression but otherwise healthy underwent radionuclide cardiography before and during nortriptyline treatment. The second examination was performed when the nortriptyline plasma concentration was within the therapeutic range (60-150 micrograms X l-1). Heart rate, arterial blood pressure, left ventricular ejection fraction, left ventricular volumes, systolic pressure-volume ratio, and cardiac output were determined. Heart rate increased in mean by 13% (P less than 0.05). All other variables were unchanged. We conclude that nortriptyline in therapeutic doses produces no major adverse effect on left ventricular function. Routine radionuclide cardiography might be a suitable method to detect among those treated with tricyclic antidepressants the occasional susceptible patient. This may particularly apply to patients with known heart disease and to elderly patients.
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PMID:The effect of the tricyclic antidepressant drug, nortriptyline on left ventricular ejection fraction and left ventricular volumes. 310 63

Seventy-four patients with chest pain and no prior history of organic heart disease were interviewed with a structured psychiatric interview immediately after coronary arteriography. The majority of patients with both negative and positive coronary angiographies had undergone previous exercise tolerance tests, but the patients with angiographic coronary artery disease were significantly more likely to have had positive results on a treadmill test. Patients with chest pain and negative coronary arteriograms were significantly younger; more likely to be female; more apt to have a higher number of autonomic symptoms (tachycardia, dyspnea, dizziness, and paresthesias) associated with chest pain, and more likely to describe atypical chest pain. Patients with chest pain and normal coronary arteriographic results also had significantly higher psychologic scores on indices of anxiety and depression and were significantly more likely to meet criteria of the Diagnostic and Statistical Manual of Mental Disorders, third edition, for panic disorder (43 percent versus 6.5 percent), major depression (36 percent versus 4 percent), and two or more phobias (36 percent versus 15 percent) than were patients with chest pain and a coronary arteriography study demonstrating coronary artery stenosis.
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PMID:Chest pain: relationship of psychiatric illness to coronary arteriographic results. 333 15

A total of 98 patients with chest pain and no prior history of organic heart disease underwent a structured psychiatric interview at the time of cardiac diagnostic testing, either coronary arteriography or exercise treadmill. Patients with negative cardiac test results were significantly younger and more likely to be female, endorsed a greater number of autonomic symptoms with their chest pain, and were more likely to report atypical chest pain. These patients had significantly higher scores on measures of anxiety and negative life events and significantly greater prevalences of DSM-III panic disorder (47% vs. 6%), major depression (39% vs. 8%), and two or more simple phobias (43% vs. 12%) than did patients with cardiac test results demonstrating coronary artery disease. Using logistic regression, a model was developed to estimate the probability of negative cardiac test results from patient characteristics and psychiatric diagnoses.
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PMID:Chest pain with negative cardiac diagnostic studies. Relationship to psychiatric illness. 337 97

The prevalence and significance of clinical heart disease and hypertension were compared in three groups of elderly patients. One group was diagnosed as dementia of an Alzheimer's type (AD), another as multiinfarct dementia (MID), and the third as major depression. Clinical heart disease and hypertension were uncommon in the AD group with the prevalence being lower than that reported in most epidemiologic studies. Four percent of the AD patients had a history of myocardial infarction, 5% angina, 1% arrhythmias, and 3% heart failure. Electrocardiographic changes of an old myocardial infarction were present in 9%, atrial fibrillation in 1%, and left ventricular hypertrophy in 3%. A history of hypertension was present in 24% of the AD patients. In comparison, a history of myocardial infarction, angina, and heart failure was five times greater, and electrocardiographic abnormalities were twice as prevalent in the MID group. A history of hypertension was three times more common and actual blood pressure readings were higher. In the depression group heart disease was not uncommon and the prevalence, in general, was comparable with the MID group. However, a history of increased blood pressure and actual increased blood pressure readings were statistically less than in the MID group.
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PMID:Prevalence and significance of cardiovascular disease and hypertension in elderly patients with dementia and depression. 401 97

Studies of dyspepsia show a 1% to 2% prevalence in adults, and 25% to 40% of these patients do not have a physical reason for their symptoms. These findings prompted us to do a retrospective follow-up study of 390 patients having motility studies for chest pain and gastrointestinal (GI) symptoms; 278 (71%) responded. Patients were asked to complete a self-rating symptom questionnaire regarding current GI symptoms and current symptoms of anxiety, panic, and depression; they were also asked to complete the Brief Symptom Inventory. Two groups were compared--those with known heart disease and those without heart disease. Substantial numbers of patients in both groups satisfied criteria for generalized anxiety disorders (> 70%), panic disorder (> 30%), and major depression (> 35%). GI symptoms compatible with nonulcer dyspepsia were strongly associated with a psychiatric diagnosis. Our data suggest that anxiety and depressive states are strongly associated with dyspepsia and other GI symptoms not caused by ulcer disease.
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PMID:Nonulcer dyspepsia associated with psychiatric disorder. 850 84

In the choice of an antidepressant drug the clinician must often consider the presence of a cardiovascular comorbidity in depressed patients. In the present study the cardiovascular effects of fluvoxamine and maprotiline were compared in a double-blind trial in which the quantitative changes in ECGs were assessed before and during a 3-week treatment. A total of 33 patients (mean age 44 years; range 20-65 years) with major depressive disorder (RDC) who were free from clinically relevant organic diseases were investigated. After a 7-day wash-out period, a 3 week treatment phase was started with 200 mg daily of either fluvoxamine (n = 18) or maprotiline (n = 15). On days 0, 7, 14 and 21 a 12-lead standard ECG was performed and the drug plasma levels were determined. All ECGs were analysed in a blind fashion by an internist. Maprotiline caused a significant prolongation of the PR interval (P < 0.001) and of the QRS interval (P < 0.01) was well as an increase in heart rate (P < 0.001). The QTc interval was only tendentially prolonged (P < 0.10) and the P-wave duration and T-wave amplitude were not affected by maprotiline. No significant changes in ECG parameters were observed during treatment with fluvoxamine; and there was a nonsignificant trend (P < 0.10) for a lower heart rate during treatment. Blood pressure was not affected by treatment with either antidepressant. In both groups no significant correlations were found between ECG findings and the plasma levels of the drugs. Our results confirm that fluvoxamine in therapeutic dose causes no alteration in surface ECG regarding cardiac conduction and repolarization. Conversely, maprotiline caused a significant prolongation of atrioventricular and intraventricular conduction and a rise in heart rate. Although these effects were not clinically relevant in our sample of patients without overt heart disease, they should be taken into account when treating depressed patients with concomitant cardiac disease.
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PMID:Cardiovascular effects of fluvoxamine and maprotiline in depressed patients. 877 12

This study examines the degree to which untreated anxiety disorders and major depressive disorder, occurring either singly or in combination, reduce functioning and well-being among primary care patients. Adult patients were screened using the SCL-52 to identify those with clinically significant anxiety symptoms. They also completed the Rand Short-Form (SF-36) to measure self-reported patient functioning and well-being. Patients with untreated disorders were identified using the Q-DIS-III-R to diagnose six DIS-anxiety disorders (generalized anxiety disorder, post-traumatic stress disorder (PTSD), simple phobia, social phobia, panic/agoraphobia, obsessive/compulsive disorder) and major depression. Of 319 patients identified, 137 (43%) had a single disorder and 182 (57%) had multiple disorders. Regression models estimated the relative effects of these disorders on health status (SF-36) by comparing patients with the disorders to patients screened as being not-anxious. Estimates of these effects were consistent with available national norms. The estimated effect of each single disorder on all subscales for physical, social and emotional functioning was negative, often as much as a 20-30 point reduction on this 100-point scale. Major depression had the greatest negative impact, followed by PTSD and panic/ agoraphobia. For patients with multiple disorders, the presence of major depression was associated with the greatest reduction in functioning status. The impact of untreated anxiety disorders and major depressive disorder on functioning was comparable to, or greater than, the effects of medical conditions such as low back pain, arthritis, diabetes and heart disease.
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PMID:The functioning and well-being of patients with unrecognized anxiety disorders and major depressive disorder. 916 80

This article reviews the burgeoning literature on the relationship of mood disorders and heart disease. Major depression and depressive symptoms, although commonly encountered in medical populations, are frequently underdiagnosed and undertreated in patients with cardiovascular disease (CVD). This is of particular importance because several studies have shown depression and its associated symptoms to be a major risk factor for both the development of CVD and death after an index myocardial infarction. This review of the extant literature is derived from MEDLINE searches (1966-1997) using the search terms "major depression," "psychiatry," "cardiovascular disease," and "pathophysiology." Studies investigating pathophysiological alterations related to CVD in depressed patients are reviewed. The few studies on treatment of depression in patients with CVD are also described. Treatment of depression in patients with CVD improves their dysphoria and other signs and symptoms of depression, improves quality of life, and perhaps even increases longevity. Recommendations for future research are proposed.
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PMID:The relationship of depression to cardiovascular disease: epidemiology, biology, and treatment. 967 48

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

The purpose of this study was to determine the threshold at which depression becomes important for the daily functioning of patients with heart disease. Data from a 1-year prospective cohort study of health maintenance organization patients undergoing coronary angiography for coronary heart disease were analyzed for differences in a standardized composite measure of functioning. Patients with major depression (N = 19) and patients with minor depression (N = 28) were significantly more functionally impaired at baseline and at 1-year follow-up than those with no depression (N = 110). The major and minor depression groups did not differ significantly. The significance of the depression group differences was reduced, but not eliminated, when controlling for differences in reported heart symptoms.
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PMID:Depression in coronary heart disease. What is the appropriate diagnostic threshold? 1040 72


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