SSRIs and adverse pregnancy outcomes.
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Clinical Trials as Topic↗
Biomedical subjects
Adriaan Honig
Publications and source records attributed to Adriaan Honig.
S100 and impact of ECT on depression and cognition.
OBJECTIVES: The main side effects of electroconvulsive therapy (ECT) are in the realm of cognition. The S100-beta is a calcium-binding protein that is expressed by astrocytes in the central nervous system during depression and has been suggested to modulate the impact of ECT on cognition. METHODS: Serum samples of S100-beta were taken before and 1 and 3 hours after each ECT session in 12 depressed patients (mean age, 54 years), treated with bilateral ECT twice weekly (mean, 6 sessions). Measures of depression (Symptom Checklist-90 depression dimension) and a neurocognitive test battery yielding 3 domains of general cognition, memory, and subjective cognitive impairment were administered 1 day before and 5 and 30 days post-ECT. RESULTS: Electroconvulsive therapy was associated with a reduction in depression and subjective cognitive impairment at 5 and 30 days post-ECT. Electroconvulsive therapy was associated with a small but significant rise in S100-beta 1 hour post-ECT (adjusted B = 0.013, P = 0.035), with a directionally similar but reduced effect size at 3 hours post-ECT (adjusted B = 0.010, P = 0.10). Higher level of S100-beta at baseline was associated with poorer memory function at 5 and 30 days of follow-up (adjusted B per tertile group increase, 0.38, P = 0.013) but also with less subjective cognitive impairment (B = -28.2, P < 0.001) and less depression at follow-up (B = -15, P = 0.009). CONCLUSION: The S100-beta at baseline may be a marker predicting and possibly mediating the differential impact of ECT on cognition and depression.
Adult↗
Recognizing increased risk of depressive comorbidity after myocardial infarction: looking for 4 symptoms of anxiety-depression.
BACKGROUND: Screening for depression in myocardial infarction (MI) patients must be improved: (1) depression often goes unrecognized and (2) anxiety has been largely overlooked as an essential feature of depression in these patients. We therefore examined the co-occurrence of anxiety and depression after MI, and the validity of a brief mixed anxiety-depression index as a simple way to identify post-MI patients at increased risk of comorbid depression. METHODS: One month after MI, 176 patients underwent a psychiatric interview and completed the Beck Depression Inventory (BDI) and the Symptoms of Anxiety-Depression index (SAD(4)) containing four symptoms of anxiety (tension, restlessness) and depression (feeling blue, hopelessness). RESULTS: Thirty-one MI patients (18%) had comorbid depression and 37 (21%) depressive or anxiety disorder. High factor loadings and item-total correlations (SAD(4), alpha = 0.86) confirmed that symptoms of anxiety and depression co-occurred after MI. Mixed anxiety-depression (SAD(4)>or=3) was present in 90% of depressed MI patients and in 100% of severely depressed patients. After adjustment for standard depression symptoms (BDI; OR = 4.4, 95% CI 1.6-12.1, p = 0.004), left ventricular ejection fraction, age and sex, mixed anxiety-depression symptomatology was associated with an increased risk of depressive comorbidity (OR = 11.2, 95% CI 3.0-42.5, p < 0.0001). Mixed anxiety-depression was also independently associated with depressive or anxiety disorder (OR = 9.2, 95% CI 3.0-27.6, p < 0.0001). CONCLUSIONS: Anxiety is underrecognized in post-MI patients; however, the present findings suggest that anxiety symptomatology should not be overlooked in these patients. Depressive comorbidity after MI is characterized by symptoms of mixed anxiety-depression, after controlling for standard depression symptoms. The SAD(4) represents an easy way to recognize the increased risk of post-MI depression.
Anxiety Disorders↗
Symptom dimensions of depression following myocardial infarction and their relationship with somatic health status and cardiovascular prognosis.
OBJECTIVE: The reporting of depressive symptoms following myocardial infarction may be confounded by complaints originating from the myocardial infarction. Therefore, it is difficult to estimate the effects of post-myocardial infarction depression and its treatment on cardiovascular prognosis. The authors' goal was to study the relationship between depressive symptom dimensions following myocardial infarction and both somatic health status and prospective cardiovascular prognosis. METHOD: In two studies of myocardial infarction patients (N=494 and 1,972), the Beck Depression Inventory was used to determine the dimensional structure of depressive symptoms following myocardial infarction. Three symptom dimensions-somatic/affective, cognitive/affective, and appetitive-were compared with baseline left ventricular ejection fraction, Charlson comorbidity index, Killip class, and previous myocardial infarction. The relationship between depressive symptom dimensions and prospective cardiovascular mortality and cardiac-related readmissions was also examined (mean follow-up duration=2.5 years). RESULTS: Somatic/affective symptoms were associated with poor health status (left ventricular ejection fraction, Charlson comorbidity index, Killip class, and previous myocardial infarction) and predicted cardiovascular mortality and cardiac events. Cognitive/affective symptoms were only marginally associated with somatic health status and not with cardiovascular death and cardiac events. Appetitive symptoms were related to somatic health status but did not predict cardiovascular death or cardiac events. CONCLUSIONS: Somatic/affective depressive symptoms following myocardial infarction were confounded by somatic health status yet were prospectively associated with cardiac prognosis even after somatic health status was controlled. Cognitive/affective depressive symptoms were only marginally related to health status and not to cardiac prognosis. These findings suggest that treatment of depression following myocardial infarction might improve cardiovascular prognosis when it reduces somatic/affective symptoms.
Cause of Death↗
Relationship between left ventricular dysfunction and depression following myocardial infarction: data from the MIND-IT.
AIMS: Depression in patients following myocardial infarction (MI) is associated with an increased risk of mortality, but this association may be confounded by cardiac disease severity. We explored the relationship between left ventricular ejection fraction (LVEF) and depression in MI patients. METHODS AND RESULTS: In the Myocardial Infarction and Depression-Intervention Trial (MIND-IT), 1989 MI patients were assessed for depressive symptoms [Beck Depression Inventory (BDI) t = 0, 3, 6, 9, and 12 months post-MI]. Patients with BDI score > or =10 were assessed for the presence of International Classification of Diseases, 10th revision (ICD-10) depressive disorder (t = 3, 6, 9, and 12 months post-MI). Patients were divided into categories according to their LVEF during hospitalization, i.e. LVEF <30%, LVEF 30-45%, LVEF 45-60%, and LVEF > or = 60%. During hospitalization, presence of depressive symptoms was higher in patients with LV dysfunction. A relationship was found between LVEF and ICD-10 depressive disorder, i.e. a lower LVEF was associated with a higher rate of depression from 3-12 months post-MI (P < 0.01). Levels of LVEF inversely correlated with the BDI score at 3 months post-MI. Associations persisted after adjustment for demographics, risk factors for coronary artery disease, co-morbidity, Killip class, and baseline BDI score. CONCLUSION: In MI patients, the rate of depression and the severity of depressive symptoms are significantly related to the severity of LV dysfunction. The association between depression and LV dysfunction must be acknowledged when evaluating the prognostic effects of depression in cardiac patients.
Depressive Disorder↗
Increased cerebral serotonin-2A receptor binding in depressed patients with myocardial infarction.
Serotonin (5-HT) has been implicated in the pathophysiology of depression. It is not known whether depression in post-myocardial infarction (MI) patients is also serotonin-mediated. In somatically healthy depressed persons, increased brain 5-HT(2A) receptor binding has been reported in some studies. In animal studies, decreased serotonin activity was found after induction of MI. In the present study, it was hypothesized that depressed post-MI patients would exhibit increased brain 5-HT(2A) receptor binding compared with non-depressed post-MI patients. Single photon emission computed tomography (SPECT) with the radioligand 123I-5-I-R91150, a 5-HT(2A) receptor antagonist, was used to study 5-HT(2A) receptor binding. SPECT scans were performed in nine depressed post-MI patients, 10 non-depressed post-MI patients and 10 healthy control subjects. Results were analysed using statistical parametric mapping. Depressed post-MI patients showed increased 5-HT(2A) receptor binding compared with non-depressed post-MI patients, and MI patients showed decreased 5-HT(2A) receptor binding compared with control persons. Both post-MI depression and MI seem to be associated with changes in 5-HT(2A) receptor binding.
Binding, Competitive↗
Prediction of depressive disorder following myocardial infarction data from the Myocardial INfarction and Depression-Intervention Trial (MIND-IT).
BACKGROUND: Depression following myocardial infarction (MI) is associated with complicated cardiac rehabilitation, non-compliance and poor prognosis. Whether depression following MI can be predicted from variables routinely assessed during hospitalization for MI is unknown. METHODS: Using data from the Myocardial INfarction and Depression-Intervention Trial (MIND-IT), we identified 2,177 MI patients (mean age 63 years; 23% female). Patients were randomly divided into a derivation and a validation sample. In the derivation sample, we analyzed variables potentially associated with the development of post-MI depressive disorder, which were tested in the validation sample. RESULTS: In the year following MI, 18.5% suffered from depressive disorder (ICD-10 criteria). In a multivariate model, factors associated with depression were younger age (OR 1.94; CI 1.38-2.74), hypercholesterolemia (OR 1.68; CI 1.08-2.61), the use of calcium channel blockers at discharge (OR 1.80; CI 1.20-2.71), and left ventricular ejection fraction (LVEF) (OR 4.14 for patients with LVEF <30%; CI (2.42-7.10). The derived predictors were tested in the validation sample. The final model yielded two clinical predictors, i.e., younger age and severe LV-dysfunction, which correctly predicted post-discharge depression status in 82.9% of the MI patients. The model yielded a high negative predictive value (89%). A positive depression questionnaire (BDI) during hospitalization increased the positive predictive value of 23% to 52%. CONCLUSIONS: During hospitalization for MI and using a two-step strategy with common clinical variables, i.e., younger age, severe LV-dysfunction and BDI score during hospitalization, it is possible to identify MI patients with a high risk for subsequent development of depression.
Adult↗
Inflammatory markers in depressed post-myocardial infarction patients.
BACKGROUND: Depressive disorder in the post-myocardial infarction (MI) period has been associated with increased cardiac morbidity and mortality. Possible pathophysiological mechanisms behind this association are not clear. Major depression in physically healthy subjects has been related to immune abnormalities including increased plasma levels of interleukin-6 (IL-6), tumor necrosis factor alfa (TNF-alpha) and C-reactive protein (CRP). In patients with MI, increased inflammatory markers, such as CRP and TNF-alpha, have been associated with increased cardiovascular events. It was the aim of this study to test the hypothesis that depression in post-MI patients is associated with increased inflammation as compared to non-depressed post-MI patients. METHODS: The cytokines IL-6 and TNF-alpha ; the soluble cytokine receptors sIL-6R, sTNF-RI and sTNF-RII; neopterin; and the inflammation-sensitive plasma proteins (ISPs) CRP and haptoglobin were assessed in a group of 57 patients with a diagnosis of depression post-MI and in a control group of 46 non-depressed post-MI patients, matched for age, gender and time elapsed since MI. RESULTS: Cytokine, neopterin and ISP levels were not statistically different in the depressed post-MI group as compared to the non-depressed post-MI group. Several inflammatory markers were however elevated in both cohorts when compared with levels reported in healthy subjects, indicating persistent inflammation several months after MI. CONCLUSIONS: There was no indication of increased inflammation in depressed post-MI patients as compared to non-depressed post-MI patients.
Adult↗
Whole blood serotonin and platelet activation in depressed post-myocardial infarction patients.
Depression is an independent risk factor for post myocardial infarction (MI) mortality. Abnormalities in platelet function have been proposed as one of the mechanisms involved in increased cardiovascular risk among patients with depression post-MI. Depression in somatically healthy patients has been associated with increased platelet activation. Some but not all studies showed changes in blood serotonin level. Increased platelet activation and blood serotonin level have been associated with increased risk of cardiac events in patients with MI. The goal of this study was to investigate whether 1) depressed post-MI patients have higher markers of platelet activation as measured by plasma levels of beta-thromboglobulin (betaTG), platelet factor 4 (PF4) and soluble CD40 ligand (sCD40L) and higher serotonin (5-HT) levels than non-depressed post-MI patients and 2) treatment with the antidepressant mirtazapine decreases platelet activation. In this study, 25 depressed post-MI patients were asked for blood collection before start as well as after 8 weeks treatment with mirtazapine or placebo. The control group (n=22) consisted of non-depressed post-MI patients, matched for age, gender and time elapsed since MI. Plasma levels of betaTG, PF4 and sCD40L were not statistically different between the groups, but 5-HT levels were significantly higher in depressed patients. Treatment with mirtazapine resulted in a non-significant decrease in betaTG and PF4 and platelet 5-HT levels. Platelet and whole blood 5-HT, but not platelet activation was significantly increased in depressed post-MI patients. Treatment with mirtazapine showed a non-significant decrease in platelet activation and platelet 5-HT.
Adult↗
Reply to a reader's comment.
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Cholesterol, LDL↗
Brain- and heart-type fatty acid-binding proteins in the brain: tissue distribution and clinical utility.
BACKGROUND: Detection of brain injury by serum markers is not a standard procedure in clinical practice, although several proteins, such as S100B, neuron-specific enolase (NSE), myelin basic protein, and glial fibrillary acidic protein, show promising results. We investigated the tissue distribution of brain- and heart-type fatty acid-binding proteins (B-FABP and H-FABP) in segments of the human brain and the potential of either protein to serve as plasma marker for diagnosis of brain injury. METHODS: B-FABP and H-FABP were measured immunochemically in autopsy samples of the brain (n = 6) and in serum samples from (a) patients with mild traumatic brain injury (MTBI; n = 130) and (b) depressed patients undergoing bilateral electroconvulsive therapy (ECT; n = 14). The protein markers S100B and NSE were measured for comparison. Reference values of B-FABP and H-FABP were established in healthy individuals (n = 92). RESULTS: The frontal, temporal, and occipital lobes, the striatum, the pons, and the cerebellum had different tissue concentrations of B-FABP and of H-FABP. B-FABP ranged from 0.8 microg/g wet weight in striatum tissue to 3.1 microg/g in frontal lobe. H-FABP was markedly higher, ranging from 16.2 microg/g wet weight in cerebellum tissue to 39.5 microg/g in pons. No B-FABP was detected in serum from healthy donors. H-FABP serum reference value was 6 microg/L. In the MTBI study, serum B-FABP was increased in 68% and H-FABP in 70% of patients compared with S100B (increased in 45%) and NSE (increased in 51% of patients). In ECT, serum B-FABP was increased in 6% of all samples (2 of 14 patients), whereas H-FABP was above its upper reference limit (6 microg/L) in 17% of all samples (8 of 14 patients), and S100B was above its upper reference limit (0.3 microg/L) in 0.4% of all samples. CONCLUSIONS: B-FABP and H-FABP patterns differ among brain tissues, with the highest concentrations in the frontal lobe and pons, respectively. However, in each part of the brain, the H-FABP concentration was at least 10 times higher than that of B-FABP. Patient studies indicate that B-FABP and H-FABP are more sensitive markers for minor brain injury than the currently used markers S100B and NSE.
Adult↗
Fatty acid profile and affective dysregulation in irritable bowel syndrome.
Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder with a high co-occurrence with affective dysregulation. Affective disorders have been associated with specific changes in the PUFA and cholesterol profile. In IBS, similar changes may be present as have been reported in patients with affective disorders. This exploratory study investigates (i) the level of affective dysregulation (AD) in IBS patients and healthy controls; (ii) PUFA and cholesterol profiles in IBS patients compared with controls; and (iii) associations between PUFA and cholesterol parameters with the level of AD. Blood samples were obtained for determination of the FA composition of plasma phospholipids and serum cholesterol in 23 diarrhea-predominant IBS patients and 23 healthy matched controls. AD was scored using the Symptom Check List depression scale, the Hospital Anxiety and Depression Scale, and the Hamilton Depression Rating Scale. The level of AD was higher in IBS patients compared with controls. PUFA and cholesterol profiles did not differ significantly between groups. Total n-3 PUFA and cholesterol were significantly negatively associated and the ratio of n-6 to n-3 PUFA and the ratio of arachidonic acid to EPA were significantly positively associated with the level of AD. The findings of the present study reveal that AD was higher in IBS patients compared with healthy controls and that changes in PUFA and cholesterol profiles were significantly associated with the level of AD. These results warrant further studies regarding the role of PUFA and cholesterol status in the co-occurrence of AD and functional gastrointestinal disorders.
Adult↗
One year cumulative incidence of depression following myocardial infarction and impact on cardiac outcome.
BACKGROUND: Major depression has been identified as an independent risk factor for increased morbidity and mortality in mixed patients populations with first and recurrent myocardial infarction (MI). The aim of this study was to evaluate whether incidence of major and minor depression is as high in a population with merely first-MI patients as in recurrent MI populations. Furthermore, it was evaluated whether in first-MI patients major and minor depression, and depressive symptoms, had an impact on cardiac mortality and morbidity up to 3 years post MI. METHODS: A consecutive cohort of 206 patients with a first MI were included in this study. One month following MI, all patients were interviewed using the Structured Clinical Interview for DSM-IV (SCID-I-R). Three, six, nine and twelve months following MI, patients filled out three psychiatric self-rating scales for depression, the Beck Depression Inventory (BDI), the Hospital Anxiety and Depression Scale (HADS), and the 90-item Symptom Checklist (SCL-90). Patients, exceeding a previously defined cut-off value on at least one of these scales, were reinterviewed using the SCID. The BDI was applied to assess depressive symptoms in relation to cardiac outcome as the SCL-90 and HADS showed similar results. Cardiac outcome was defined as major cardiac event, i.e., death or recurrent MI, and health care consumption, i.e., cardiac rehospitalisation and/or frequent visits at the cardiac outpatient clinic. Depression outcome was assessed from 1 month post MI up to 1 year post MI whereas cardiac outcome was assessed between 1 month and 3 years post MI. RESULTS: A 1-year incidence of 31% of major and minor depression was found in first-MI patients. The highest incidence rate for both major and minor depression was found in the first month after MI. Compared with nondepressed patients, depressed patients were younger (P=.001), female (P=.04) and were known with a previous depressive episode (P=.002). Neither major/minor depression nor depressive symptoms significantly predicted major cardiac events, but did predict health care consumption (P=.04 and P<.001, respectively). CONCLUSIONS: Incidence of major and minor depression is similar in this first-MI patients population as in recurrent MI populations. Major/minor depressive disorder nor depressive symptoms predicted neither mortality nor reinfarction.
Cohort Studies↗
Development and feasibility of a nurse administered strategy on depression in community-dwelling patients with a chronic physical disease.
This contribution reports on the acceptability and feasibility to nurses and patients of an intervention to ameliorate minor depression among patients with chronic physical diseases. Elderly patients with chronic obstructive pulmonary disease (COPD) and type II Diabetes Mellitus were recruited from 10 general practices. All eligible patients were screened. Twenty-nine patients with minor depression gave their informed consent to participate in this feasibility study. The nurses spent an average of 70 min per visit. Our intervention appeared feasible and acceptable to patients and nurses. For the nurses, it provided an additional tool for a well-known problem. The majority of the patients regarded the intervention as worthwhile and effective. Patients had difficulties in understanding the link between physical complaints and symptoms of depression. The intervention has been further improved on the basis of our experiences, and is now ready to be tested in an effectiveness study.
Aged↗
Comparing symptoms of depression and anxiety as predictors of cardiac events and increased health care consumption after myocardial infarction.
OBJECTIVES: We sought to compare symptoms of depression and anxiety as predictors of incomplete recovery after a first myocardial infarction (MI). BACKGROUND: Depressive symptoms have been related to post-MI mortality and health care consumption, but little is known about the effect of anxiety. We wanted to examine the effect of emotional distress on health care consumption and whether depressive symptomatology is a better predictor of prognosis than anxiety. METHODS: Subjects were 318 men (mean age 58 years) who completed the depression, anxiety, and hostility scales from the 90-item symptom check list after they survived a first MI. RESULTS: After an average follow-up of 3.4 years, there were 25 cardiac events (fatal or non-fatal MI). Symptoms of both depression (hazard ratio [HR] 2.32, 95% confidence interval [CI] 1.04 to 5.18; p = 0.039) and anxiety (HR 3.01, 95% CI 1.20 to 7.60; p = 0.019) were associated with cardiac events, adjusting for age, left ventricular ejection fraction, and use of antidepressants. However, a multivariate analysis including all three negative emotions indicated that symptoms of anxiety (HR 2.79, 95% CI 1.11 to 7.03; p = 0.029) explained away the relationship between depressive symptoms and cardiac events. Regarding health care consumption, anxiety (OR 2.00, 95% CI 1.24 to 3.22; p = 0.005), but not depression/hostility, was a predictor of cardiac rehospitalization and frequent visits at the cardiac outpatient clinic. CONCLUSIONS: Symptoms of depression and anxiety were associated with cardiac events. Anxiety was an independent predictor of both cardiac events and increased health care consumption and accounted for the relationship between depressive symptoms and prognosis. Symptoms of anxiety need to be considered in the risk stratification and treatment of post-MI patients.
Aged↗
Fluvoxamine versus fluoxetine in major depressive episode: a double-blind randomised comparison.
A double-blind, multinational study was conducted to compare the efficacy and safety of fluvoxamine and fluoxetine in outpatients with major depressive episode; 184 patients were randomised to fluvoxamine (100 mg/day) or fluoxetine (20 mg/day) for 6 weeks. Both drugs were effective and there were no statistically significant differences between them in the area under the curve of change from baseline in the Hamilton depression rating scale (HAMD) total score. However, the percentage of HAMD responders (>or= 50% decrease in HAMD total score) at week 2, the clinical global improvement severity of illness score at week 2 and the depression subscale of the irritability, depression and anxiety scale at weeks 1, 2 and 4, all showed significant advantages for fluvoxamine. During the last 2 weeks, fluvoxamine was significantly more effective in improving the HAMD sleep disturbance scale. Both drugs were well tolerated and there were no marked differences in their side effect profiles which were typical of SSRIs. Fluvoxamine and fluoxetine have similar efficacy and safety profiles in the treatment of major depressive episode; the findings of this study indicate that fluvoxamine may have a faster onset of action with respect to resolution of depressive symptoms and result in a better improvement in sleep quality.
Adolescent↗
[Depression after first myocardial infarction. A prospective study on incidence, prognosis, risk factors and treatment].
In these studies patients with first myocardial infarction (MI) were selected for studies focusing on epidemiology, risk factors and treatment of depression post-MI. Two consecutive cohorts of first MI patients were included. The first cohort was selected between May 1994 and May 1997 (n = 206), and the second between May 1997 and October 1999 (n = 206). All patients were screened every 3 months for depression using the SCL-90 and the Zung (cohort 1) or SCL-90, BDI and HADS (cohort 2) until 12 months post-MI. Patients scoring above the cut-off of one of the questionnaires were interviewed using a standardised interview in order to evaluate whether DSM-IV criteria for major depression were met; patients of the second cohort were also interviewed 1 month post-MI, independently of the score of the questionnaires. Of both cohorts data concerning major cardiac events and increased health care consumption were assessed during a 1 to 6 years follow-up period. Patients with major depression were offered treatment in the double-blind placebo-controlled trial with fluoxetine (n = 54). Depression appeared to be a predictor of increased health care consumption, but not of major cardiac events such as cardiac death and recurrent infarction in first myocardial infarction (MI) patients up to 6 years post-MI. This finding is in contrast to findings in the literature indicating that in patient populations with mixed first and recurrent MI, depression is a risk factor for cardiac mortality. In contrast to depression, symptoms of anxiety do predict cardiac mortality and recurrent MI in patients following first MI independently of other risk factors of cardiac mortality. Recognition of risk factors for post-MI depression may help the cardiologist to identify patients at risk for depression. Examples of such risk factors are, according to our studies, complications during admission, such as arrhythmic disorders and recurrent angina pectoris, and prescription of benzodiazepines. Patients at risk can be screened for depression using a 4-item questionnaire, and, if scoring is positive, be referred for psychiatric evaluation. Although the effectivity of antidepressive treatment in MI patients has as yet not been proven, we found that fluoxetine is a cardiac-safe antidepressive agent, but only in mild depression more effective than placebo. The positive effect of antidepressive treatment on cardiac prognosis has as yet not been shown.
Antidepressive Agents, Second-Generation↗
Relation of levels of serum lipoproteins to depression after acute myocardial infarction.
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Body Mass Index↗