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Biomedical subjects

Nancy Frasure-Smith

Publications and source records attributed to Nancy Frasure-Smith.

At least 19 recordsLinked to original sources

Depression, C-reactive protein and two-year major adverse cardiac events in men after acute coronary syndromes.

BACKGROUND: We investigated the impact of depression and inflammatory markers, assessed 2 months after acute coronary syndrome (ACS), on major adverse cardiac events over 2 years (MACEs; cardiac death, survived myocardial infarction, survived cardiac arrest, and nonelective revascularization). METHODS: Depression symptoms (Beck Depression Inventory-II; BDI-II), major depression, C-reactive protein (CRP), interleukin-6, and soluble intercellular adhesion molecule were assessed in 741 ACS patients (including 602 men). RESULTS: Some 102 (78 men) experienced at least one MACE. Beck Depression Inventory-II scores of > or =14 predicted MACEs (p = .007). The increase in risk was marked in men (hazard ratio [HR] = 1.96, 95% confidence interval [CI] = 1.24-3.09, p = .004), with little evidence of a relationship in women (p = .85). Subsequent analyses were limited to men. Results were similar after covariate adjustment (HR = 1.72, 95% CI = 1.07-2.77, p = .024). C-reactive protein levels were also associated with increased MACE risk (adjusted HR for CRP > or = 2.0 mg/L = 1.67, 95% CI = 1.07-2.62, p = .025). C-reactive protein levels and BDI-II scores interacted in predicting MACEs. Men with both BDI-II scores of > or =14 and CRP of > or =2.0 mg/L experienced an increase in risk similar to those with only one of these factors. CONCLUSIONS: In men assessed 2 months after ACS, depression and CRP are overlapping prognostic risks. Patients with either risk may benefit from similar therapies.

Adult↗

Recent evidence linking coronary heart disease and depression.

OBJECTIVES: To review the recent literature on the relation between depression and coronary heart disease (CHD), including both etiologic studies (that is, depression preceding development of CHD) and prognostic studies (that is, depression predicting prognosis in established CHD), and to assess the degree to which the literature supports a causal interpretation of the link between depression and CHD. METHOD: We searched the MEDLINE, Current Contents, and PsycINFO databases for articles published between December 15, 2003, and December 15, 2005, containing combinations of several key words related to CHD, prognosis, and depression. We reviewed papers for evidence of 6 rule-of-thumb criteria for making causal inferences: objective CHD outcome measures, prospective designs, results showing consistent and strong dose-response relations, adequate covariate adjustment, biological plausibility, and evidence from clinical trials that changing depression alters CHD risk. RESULTS: We found 8 recent etiologic studies, 16 prognostic studies, 2 publications with both types of data, and 23 review papers. Although there was much methodological variability concerning measurement of depression and assessment of cardiac outcomes, the recent etiologic studies increase the evidence of a role for depression. Recent prognostic data are less consistent. Small studies showing no link between depression and CHD prognosis continue to appear, despite lack of adequate statistical power. CONCLUSIONS: The recent literature continues to support both an etiologic and a prognostic role for depression in CHD. Despite this evidence, there have been few clinical trials of depression treatment in CHD patients and no clinical trials of depression prevention. Additional trials are needed.

Antidepressive Agents↗

Myocardial perfusion study of panic attacks in patients with coronary artery disease.

Panic disorder (PD) and panic-like anxiety have been associated with an increased risk of cardiovascular death. No study has specifically examined the association between panic attacks and ischemia in patients who have coronary artery disease (CAD). We hypothesized that panic attacks would induce myocardial perfusion defects in patients who have CAD and PD. Sixty-five patients who had CAD and positive results with nuclear exercise stress testing (35 with PD and 30 without PD served as controls) underwent a well-established panic challenge test (1 vital capacity inhalation of a gas mixture containing 35% carbon dioxide and 65% oxygen) and were injected with technetium-99m sestamibi at inhalation. Single-photon emission computed tomography was used to assess per-panic challenge perfusion defects, and heart rate, blood pressure, and 12-lead electrocardiogram were continuously measured during the procedure. Patients were not withdrawn from their cardiac medications. Patients who had PD were significantly younger than the controls; otherwise groups did not differ with respect to gender, cardiac medications, nuclear exercise test results, and baseline heart rate and blood pressure. Seventy-four percent of patients (26 of 35) who had PD had a panic attack at inhalation versus 6.7% of controls (2 of 30, p <0.001). As hypothesized, patients who had PD and demonstrated a panic attack were more likely to develop a reversible myocardial perfusion defect than were controls who did not have an attack (80.9% vs 46.4% p = 0.009). Thus, despite being on their cardiac medications, panic attacks preferentially induced significant perfusion defects in patients who had CAD and PD. In conclusion, panic attacks in patients who have CAD appear to be bad for the heart.

Adult↗

Mood disorders in the medically ill: scientific review and recommendations.

OBJECTIVE: The purpose of this review is to assess the relationship between mood disorders and development, course, and associated morbidity and mortality of selected medical illnesses, review evidence for treatment, and determine needs in clinical practice and research. DATA SOURCES: Data were culled from the 2002 Depression and Bipolar Support Alliance Conference proceedings and a literature review addressing prevalence, risk factors, diagnosis, and treatment. This review also considered the experience of primary and specialty care providers, policy analysts, and patient advocates. The review and recommendations reflect the expert opinion of the authors. STUDY SELECTION/DATA EXTRACTION: Reviews of epidemiology and mechanistic studies were included, as were open-label and randomized, controlled trials on treatment of depression in patients with medical comorbidities. Data on study design, population, and results were extracted for review of evidence that includes tables of prevalence and pharmacological treatment. The effect of depression and bipolar disorder on selected medical comorbidities was assessed, and recommendations for practice, research, and policy were developed. CONCLUSIONS: A growing body of evidence suggests that biological mechanisms underlie a bidirectional link between mood disorders and many medical illnesses. In addition, there is evidence to suggest that mood disorders affect the course of medical illnesses. Further prospective studies are warranted.

Acquired Immunodeficiency Syndrome↗

Major depression is associated with lower omega-3 fatty acid levels in patients with recent acute coronary syndromes.

BACKGROUND: Polyunsaturated fatty acids (PUFAs) are intrinsic cell membrane components and closely involved in neurotransmission and receptor function. Lower omega-3 levels are associated with increased risk of coronary artery disease (CAD), increases in cardiac events in CAD patients, and depression. We sought to examine relationships between depression and serum levels of omega-3 and omega-6 PUFAs in patients recovering from acute coronary syndromes (ACS). METHODS: We carried out a case-control study of serum PUFA levels and current major depression in 54 age- and sex-matched pairs approximately 2 months following ACS. RESULTS: Depressed patients had significantly lower concentrations of total omega-3 and docosahexaenoic acid (DHA), and higher ratios of arachidonic acid (AA) to DHA, AA to eicosapentaenoic acid (EPA), and n-3 to n-6 than controls. There were no baseline differences in any potential risk or protective factors for depression. CONCLUSIONS: Results are consistent with previous reports in depressed patients without CAD, and with literature concerning omega-3 levels and risk of CAD events. Dietary, genetic, and hormonal factors may all play a role in both depression and CAD. Both prospective studies and randomized trials are needed to help clarify the interrelationships.

Acute Coronary Syndrome↗

Are exercise stress tests appropriate for assessing myocardial ischemia in patients with major depressive disorder?

BACKGROUND: Major depressive disorder (MDD) disproportionately affects patients with coronary artery disease (CAD). Evidence of myocardial ischemia with electrocardiography (ECG) or single-photon-emission-computed-tomography (SPECT) assessments during exercise testing is an important determinant of CAD prognosis. However, many key symptoms of MDD, such as reduced interest in daily activities, lack of energy, and fatigue, may affect exercise performance and the detection of ischemia in patients with MDD. This study evaluated the extent to which MDD and depressive symptomatology moderate exercise test performance and compared the ability of ECG versus SPECT for detecting ischemia in 1367 consecutive patients who underwent exercise testing. METHODS: All patients underwent a brief, structured psychiatric interview (PRIME-MD) and completed the Beck Depression Inventory (BDI) on the day of their exercise (treadmill) test. RESULTS: A total of 183 patients (13%) met diagnostic criteria for MDD. Patients with MDD achieved a significantly lower percent of maximal predicted heart rate (%MPHR), exhibited lower peak exercise mets, and spent less time exercising compared with patients without MDD (all P values <.05). BDI scores were also negatively correlated with all 3 indices of exercise performance (all P values <.01). There were no differences in rates of SPECT ischemia in patients with MDD (40%) versus patients without MDD (45%; P =.23); however, rates of ECG ischemia were significantly lower (30%) in patients with MDD than in patients without MDD (48%; P <.0001). CONCLUSIONS: Results suggest that patients with CAD who have MDD, depressive symptomatology, or both exhibit poor exercise tolerance and performance and that ECG, as compared with SPECT, may not be as reliable in detecting ischemia in patients who are depressed.

Analysis of Variance↗

The association between major depression and levels of soluble intercellular adhesion molecule 1, interleukin-6, and C-reactive protein in patients with recent acute coronary syndromes.

OBJECTIVE: This study was conducted to determine whether or not depression is associated with higher levels of inflammatory markers in patients recovering from acute coronary syndromes. METHOD: Plasma levels of soluble intercellular adhesion molecule 1 (sICAM-1) and interleukin-6 (IL-6) and the serum level of C-reactive protein were measured in 481 patients 2 months after hospitalization for acute coronary syndromes. Diagnosis of major depression was based on the Structured Clinical Interview for DSM-IV. RESULTS: Depressed patients showed significantly higher sICAM-1 levels, a difference that remained significant after adjustment for potential confounders (gender, smoking, presence of metabolic syndrome). Although there was no significant association between depression and IL-6, there was an interaction between depression and statin therapy for levels of C-reactive protein. Depressed patients not taking statins had markedly higher C-reactive protein levels than did nondepressed patients. There was no relationship with depression in those receiving statins. CONCLUSIONS: These results suggest chronic endothelial activation among depressed patients after acute coronary syndromes. Further research is needed to determine whether or not higher levels of sICAM-1 may identify a subgroup of depressed patients at particularly high risk for cardiac events among patients with established coronary artery disease or among those without previous coronary artery disease.

Acute Disease↗

Depression and other psychological risks following myocardial infarction.

BACKGROUND: There is consistent evidence that depression symptoms predict long-term mortality following a myocardial infarction, and recent results show a dose-related gradient. The importance of other psychological variables remains unclear. METHODS: This study examines the relative importance of depression, anxiety, anger, and social support in predicting 5-year cardiac-related mortality following a myocardial infarction and assesses the role of any common underlying dimensions. The design of this cohort analytic study involves self-reports (Beck Depression Inventory, state scale of the State-Trait Anxiety Inventory, 20-item version of the General Health Questionnaire, Modified Somatic Perception Questionnaire, Anger Expression Scale, Perceived Social Support Scale, number of close friends and relatives, and visual analog scales of anger and stress). The study was conducted in 10 Montreal-area hospitals. The patients included 896 persons who experienced a myocardial infarction, aged 24 to 88 years (232 were women), followed up for 5 years using Medicare records; baseline data were complete for 95.0% of the patients. The intervention was usual care, and the main outcome measure was 5-year cardiac-related mortality. RESULTS: The Beck Depression Inventory (P<.001), the State-Trait Anxiety Inventory (P =.04), and the 20-item version of the General Health Questionnaire (P =.048) were related to outcome), but only depression remained significant after adjustment for cardiac disease severity (hazards ratio per SD, 1.46; 95% confidence interval, 1.18-1.79) (P<.001). Exploratory factor analysis revealed 3 underlying factors: negative affectivity, overt anger, and social support. There was also a covariate-adjusted trend between negative affectivity scores and outcome (P =.08). Furthermore, residual depression scores (P =.001) and negative affectivity scores (P =.05) were linked to cardiac-related mortality after adjustment for each other and cardiac covariates. CONCLUSIONS: Negative affectivity and some unique aspect of depression predict long-term cardiac-related mortality following a myocardial infarction independently of each other and cardiac disease severity. Additional research is needed to characterize the mechanisms involved.

Adult↗

Depression and anxiety and outcomes of coronary artery bypass surgery.

Psychological and psychiatric disorders independently increase the risk of cardiovascular disease and worsen the prognosis in patients with established cardiovascular lesions. The objective of this literature review is to discuss recent data concerning the relationships between depression and anxiety and the outcomes of coronary artery bypass grafting. Pathophysiological hypotheses are put forward to explain observed links. We suggest recommendations aimed at improving the psychological evaluation and management of heart surgery candidates, as well as postbypass patients, in the hope of improving quality of life and cardiovascular outcomes in these patients.

Anxiety↗

An open-label study of nefazodone treatment of major depression in patients with congestive heart failure.

OBJECTIVES: To evaluate the feasibility of screening and recruiting patients with major depression and congestive heart failure (CHF) in a tertiary care cardiology hospital and to obtain preliminary efficacy, tolerability, and safety data for nefazodone treatment of a major depressive episode in CHF patients. METHOD: We conducted a 12-week, open-label trial of nefazodone given in dosages up to 600 mg daily. We assessed patients at baseline, 1, 2, 4, 8, and 12 weeks. Measures used were the 17-item Hamilton Depression Rating Scale (HDRS), the Clinical Global Impression Scale, the Beck Depression Inventory, Spielberger's State-Trait Anxiety Inventory, and the Minnesota Living with Heart Failure Questionnaire. We also obtained pre- and poststudy ECGs, 24-hour Holter monitor recordings, and plasma levels of norepinephrine. RESULTS: After screening 443 CHF patients, 28 patients with major depression met study eligibility criteria. The 23 patients who completed 4 or more weeks of medication showed significant improvement on all depression scales and in quality of life. Of 19 subjects who completed the full 12-week trial, 74% experienced a decline of 50% or more on HDRS scores. The completers also showed a significant reduction in heart rate, an increase in QT intervals (but not in the QTc), and a marginally significant decrease in plasma norepinephrine. There were no changes in heart rate variability. CONCLUSIONS: It is feasible to screen and recruit CHF patients with major depression for an anti-depressant trial. Nefazodone seems sufficiently safe, tolerable, and efficacious to justify a larger, placebo-controlled trial.

Adult↗

Five-year risk of cardiac mortality in relation to initial severity and one-year changes in depression symptoms after myocardial infarction.

BACKGROUND: Although previous research demonstrated an independent link between depression symptoms and cardiac mortality after myocardial infarction (MI), depression was assessed only once, and a dose-response relationship was not evaluated. METHODS AND RESULTS: We administered the Beck Depression Inventory to 896 post-MI patients during admission and at 1 year. Five-year survival was ascertained using Medicare data. We observed a significant long-term dose-response relationship between depression symptoms during hospitalization and cardiac mortality. Results remained significant after control for multiple measures of cardiac disease severity. Although 1-year scores were also linked to cardiac mortality, most of that impact was explained by baseline scores. Improvement in depression symptoms was associated with less cardiac mortality only for patients with mild depression. Patients with higher initial scores had worse long-term prognosis regardless of symptom changes. CONCLUSIONS: The level of depression symptoms during admission for MI is more closely linked to long-term survival than the level at 1 year, particularly in patients with moderate to severe levels of depression, suggesting that the presumed cardiovascular mechanisms linking depression to cardiac mortality may be more or less permanent for them.

Canada↗