Biomedical subjects
Publications and source records attributed to Adriaan Honig.
Platelet factor 4 (PF 4) and beta-thromboglobulin (beta-TG) were studied in 12 depressed post-myocardial infarction (MI) patients and 12 matched non-depressed post-MI patients. PF4 was significantly higher in the depressed group than in the non-depressed group. beta-TG was increased in the depressed subgroup, but the difference was not statistically significant.
BACKGROUND: We evaluated the cognitive profile of 48 patients with major depression following their first myocardial infarction (MI). METHODS: The cognitive performance of the patients was compared with the performance of 48 non-depressed MI patients and 48 healthy controls. RESULTS: Depressed MI patients performed slower on a simple cognitive speed related measure compared with non-depressed MI patients and healthy controls. Attention and speed-related aspects of cognitive functioning were not affected. Surprisingly, (depressed) MI patients showed even better performances with respect to memory function. LIMITATION: No patients with non-MI-related depression were included. CONCLUSIONS: The cognitive profile of major depression after MI differs from that of non-cardiac-related depressive disorder, as described in the literature. This may reflect a different etiology of post MI depression from non-cardiac-related depression.
Central serotonergic vulnerability indicated by altered mood and neuroendocrine responses to an intravenous (i.v.) tryptophan (Trp) challenge was assessed in healthy adult unaffected first-degree relatives of bipolar disorder (BD) patients (n = 30) (family history; FH). The effects of a single dose of 7.0 g Trp on mood, cortisol and prolactin (Prl) in FH subjects were compared with healthy matched controls (n = 15) in a placebo-controlled, double blind cross-over design. Prl and cortisol responses increased following Trp. Overall, Trp lowered mood. Hormonal and mood effects did not differ between FH and controls. Results show some evidence for differences in serotonergic vulnerability between relatives of type I BD patients and relatives of type II BD patients.
BACKGROUND AND PURPOSE: Depression is a frequent sequela of stroke that negatively interferes with rehabilitation outcome. Personality traits have been neglected as potential vulnerability factors for poststroke depression (PSD). In a 1-year prospective study, the influence of the 5 main personality traits (ie, neuroticism, extraversion, openness, agreeableness, and conscientiousness) on the development of PSD was studied. METHODS: One month after stroke, 190 consecutive patients with a first-ever supratentorial infarct were asked to complete a personality inventory, the NEO-Five Factor Inventory, which is based on the Five Factor Model of personality. Depressive symptoms were assessed 1, 3, 6, 9, and 12 months after stroke with 3 self-rating questionnaires as screening instruments for depression. PSD was diagnosed as major or minor depression through the use of the Structured Clinical Interview from the Diagnostic and Statistical Manual of Mental Disorders. RESULTS: The 1-year cumulative incidence of depression was 38.7%. Cox regression analysis showed that patients with high neuroticism scores had a 4.6-times-higher risk of developing PSD than patients with low neuroticism scores (P=0.001) regardless of lesion location. Level of handicap was the only other factor that showed an independent effect on the occurrence of PSD. CONCLUSIONS: Neuroticism is an important predictor of PSD, a finding that emphasizes the need to take personality into account as a potential vulnerability factor for depression in stroke patients. Research on PSD should aim at delineating the interplay between neurological and psychological factors in the development of PSD.
BACKGROUND: Patients with a depressive disorder after myocardial infarction (MI) have a significantly increased risk of major cardiac events. The Myocardial INfarction and Depression-Intervention Trial (MIND-IT) investigates whether antidepressive treatment can improve the cardiac prognosis for these patients. The rationale and outline of the study are described. METHODS: In this multicenter randomized clinical trial, 2140 patients admitted for MI are screened for depressive symptoms with a questionnaire 0, 3, 6, 9, and 12 months after MI. Patients with symptoms undergo a standardized psychiatric interview. Those with a post-MI depressive episode are randomized to intervention (ie, antidepressive treatment; n = 190) or care-as-usual (CAU; n = 130). In the intervention arm, the research diagnosis is to be confirmed by a psychiatrist. First-choice treatment consists of placebo-controlled treatment with mirtazapine. In case of refusal or nonresponse, alternative open treatment with citalopram is offered. In the CAU arm, the patient is not informed about the research diagnosis. Psychiatric treatment outside the study is recorded, but no treatment is offered. Both arms are followed for end points (cardiac death or hospital admission for MI, unstable angina, heart failure, or ventricular tachyarrhythmia) during an average period of 27 months. Analysis is on an intention-to-treat basis. CONCLUSION: The MIND-IT study will show whether treatment of post-MI depression can improve cardiac prognosis.
OBJECTIVE: Major depressive disorder and depressive symptoms have been identified as independent risk factors for cardiac morbidity and mortality in patients with ischemic heart disease. Increased susceptibility to platelet activation has been proposed as one of the mechanisms by which depression acts as a significant risk factor for thrombotic events. In this review, data on platelet activation and platelet aggregation measures in depressed patients with or without concomitant cardiovascular disease are given. Data on the influence of antidepressants on parameters of platelet activation are summarized. METHODS: A literature search was done by checking MEDLINE Advanced and PsycInfo from 1990 to 2003 and through checking the bibliographies of these sources. The following key words were used for this search: platelet activation, platelet aggregation, depression, depressive disorder, ischemic heart disease, calcium, and serotonin. RESULTS: There is an indication of enhanced platelet activation and aggregation in depressed patients. Next, patients with a depressive disorder show signs of a hyperactive platelet 5-HT2A receptor signal transduction system as measured by increased platelet calcium mobilization after stimulation of platelets with serotonin. CONCLUSIONS: Depression appears to be associated with an increased susceptibility for serotonin-mediated platelet activation. Upregulation and/or increased sensitivity of 5-HT2A/1B receptors and downregulated 5-HT transporter receptors in the periphery may contribute to increased risk of thromboembolic events in patients with depression and cardiovascular disease. Increased platelet reactivity based on a hyperreactive 5-HT2A receptor signaling system might be influenced by antidepressive medication that antagonizes platelet 5-HT2A receptors.
Most instruments used to assess poststroke depression have never been specifically validated in stroke patients. This study evaluated the depression screening abilities of three questionnaires and one observer-rated scale in 202 consecutive patients 1 month after they experienced their first-ever ischemic stroke. At their respective optimum cutoff values, the sensitivity of the self-rated scales varied between 80% and 90%, while the specificity was about 60%. For the observer-rated scale (Hamilton Depression Rating Scale), sensitivity was 78.1%, and specificity was 74.6%. The instruments clearly performed better in men than in women. Despite this difference, it was concluded that all scales were acceptable screening instruments for poststroke depression.
Consecutive patients seen in the first-heart-aid service of a university hospital and given a diagnosis of noncardiac chest pain completed the self-report Hospital Anxiety and Depression Scale. Patients with a score >or=8 on either the anxiety or depression subscale (N=266, mean age=55.81 years, SD=13.03, 143 male patients) were compared with patients scoring <8 (N=78, mean age=60.55 years, SD=10. 84, 50 male patients) by means of the Mini International Neuropsychiatric Interview. Panic disorder and/or depression identified by the diagnostic interview were highly prevalent in the group with a score >or=8 (73.3% versus 3.9% in the comparison group). The Hospital Anxiety and Depression Scale is an adequate screening instrument for the detection of affective disorders in patients with noncardiac chest pain.