Whole blood serotonin and platelet activation in depressed post-myocardial infarction patients

Schins, Annique; Hamulyák, Karly; Scharpé, Simon; Lousberg, Richel; Melle, Joost van; Crijns, Harry J.G.M.; Honig, Adriaan

doi:10.1016/j.lfs.2004.04.060

Cited by 75 publications

(66 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A mirtazapine-mediated increase of BDNF seems feasible as also animal studies suggest an increase of BDNF during chronic mirtazapine treatment, at least in the hippocampus and the prefrontal cortex of rats [ 8 , 36 ] . Diff erential eff ects of mirtazapine [ 37 ] , which decreases platelet activity and venlafaxine [ 38 ] , which increases platelet activity, might explain our current observation. In this context we might miss the BDNF redistribution between platelets and plasma, which has been described during SSRI treatment [ 39 ] as we only studied serum concentrations.…”

Section: Bdnf [Ng/ml]supporting

confidence: 57%

Changes of Serum Concentrations of Brain-Derived Neurotrophic Factor (BDNF) during Treatment with Venlafaxine and Mirtazapine: Role of Medication and Response to Treatment

et al. 2012

View full text Add to dashboard Cite

Introduction: Depression, stress and antidepressant treatment have been found to modulate the expression of brain-derived neurotrophic factor (BDNF). Recent research suggests that serum BDNF concentration is reduced in depression and that antidepressant treatment leads to an increase in serum BDNF concentration. Methods: We studied depressed patients receiving a randomized antidepressant treatment with either mirtazapine (n=29) or venlafaxine (n=27) for 28 days in a prospective design. Changes in the concentrations of serum neurotrophins in response to antidepressant treatment were assessed. Results: There was a significant ?treatment? by ?medication? interaction effect on BDNF serum concentrations that indicated a decline of BDNF in venlafaxine-treated patients (7.82?3.75?7.18?5.64?ng/mL), while there was an increase in mirtazapine-treated patients (7.64?6.23?8.50?5.37?ng/mL). There was a trend for a ?treatment? by ?remission? interaction with a favourable clinical course being related to increasing serum BDNF. Discussion: Changes in BDNF serum concentrations as a result of antidepressant therapy depend on the antidepressant and potentially on the clinical course.

show abstract

Section: Bdnf [Ng/ml]supporting

confidence: 57%

Changes of Serum Concentrations of Brain-Derived Neurotrophic Factor (BDNF) during Treatment with Venlafaxine and Mirtazapine: Role of Medication and Response to Treatment

et al. 2012

View full text Add to dashboard Cite

show abstract

“…28,41 Furthermore, increased platelet activation by serotonin could also be a mechanism in which prognosis may be affected by higher levels of serotonin in plasma. 17 It has not been studied whether the in vivo plasma concentrations of metoprolol are increased when paroxetine or fluoxetine are coadministered. Two case reports describing an interaction between metoprolol and an SSRI (fluoxetine and paroxetine) support this.…”

Section: Discussionmentioning

confidence: 99%

“…This is noteworthy because depression alone is known to worsen the prognosis in HF. [1][2][3][4][5][6][7][8][9][10][11] Various reasons for this observed increased risk of death in depressed patients with HF have been proposed: nonadherence to HF medication, 12,13 smoking and lack of exercise, 14,15 greater catecholamine levels, 16 increased serotonin and platelet activation, 17 and antidepressant toxicity. 18 -20 Polypharmaceutical treatment in patients with HF has not been studied systematically, and because depression is associated with a poorer prognosis, spontaneous observations of interactions are unlikely.…”

mentioning

confidence: 99%

Prognosis in Heart Failure and the Value of β-Blockers Are Altered by the Use of Antidepressants and Depend on the Type of Antidepressants Used

Fosbøl

Gislason

Poulsen

et al. 2009

Circ: Heart Failure

View full text Add to dashboard Cite

show abstract

“…Alterations in cardiac autonomic tone 16 Common genetic vulnerability 17 Enhanced activity of the hypothalamic pituitary-axis 18 Greater platelet activation 19 Increased catecholamine levels 20 Increased whole blood serotonin 21 Inflammatory processes 22 Lower omega-3 fatty acid levels 23 Mental-stress induced ischemia 24 Toxicity of tricyclic antidepressants 25 Potential behavioral mechanisms Dietary factors 26 Lack of exercise 27 Medication nonadherence 28 Poor social support 29 …”

Section: Potential Biological Mechanismsmentioning

confidence: 99%

Depression and Cardiovascular Disease

Whooley¹

2006

JAMA

219

163

View full text Add to dashboard Cite

Major depressive disorder is a risk factor for the development of incident coronary heart disease events in healthy patients and for adverse cardiovascular outcomes in patients with established heart disease. Depression is present in 1 of 5 outpatients with coronary heart disease and in 1 of 3 outpatients with congestive heart failure, yet the majority of cases are not recognized or appropriately treated. It is not known whether treating depression improves cardiovascular outcomes, but antidepressant treatment with selective serotonin reuptake inhibitors is generally safe, alleviates depression, and improves quality of life. This article evaluates the importance of major depression in patients with cardiovascular disease, and provides practical guidance for identifying and treating this disorder. CASE PRESENTATIONA 58-year-old man with a history of coronary heart disease (CHD), type 2 diabetes mellitus, hypertension, smoking, and alcohol dependence presented for routine medical care. He had initially sought medical attention for exertional angina 5 years previously, at which time he underwent exercise treadmill testing with thallium that was positive for reversible perfusion defects in the anterior, septal, and inferior walls. Subsequent coronary angiography revealed diffuse heavy calcifications in the left anterior descending artery with a moderate lesion prior to the first diagonal. Several major septal perforators had significant lesions at their origins. In the dominant right coronary artery, there were diffuse calcifications but no significant lesions. The left circumflex and large ramus intermedius were free of discrete lesions. Left ventricular function was normal.The patient underwent single-vessel (left internal mammary artery to left anterior descending artery) coronary artery bypass grafting (CABG) surgery. He was prescribed atenolol 100 mg/ d, lisinopril 40 mg/d, lovastatin 80 mg/d, aspirin 325 mg/d, metformin 850 mg 3 times a day, and glipizide 10 mg 2 times a day. Despite being nonadherent to his prescribed medications, he remained stable for 5 years, but then one day, while doing household chores, he suddenly developed chest pressure, shortness of breath, and diaphoresis that lasted 12 hours. On admission to the hospital his troponin I was elevated and peaked at 0.7 ng/mL (normal, <0.05 ng/mL), consistent with a myocardial infarction (MI). His electrocardiogram had not changed.

show abstract

Whole blood serotonin and platelet activation in depressed post-myocardial infarction patients

Cited by 75 publications

References 66 publications

Changes of Serum Concentrations of Brain-Derived Neurotrophic Factor (BDNF) during Treatment with Venlafaxine and Mirtazapine: Role of Medication and Response to Treatment

Changes of Serum Concentrations of Brain-Derived Neurotrophic Factor (BDNF) during Treatment with Venlafaxine and Mirtazapine: Role of Medication and Response to Treatment

Prognosis in Heart Failure and the Value of β-Blockers Are Altered by the Use of Antidepressants and Depend on the Type of Antidepressants Used

Depression and Cardiovascular Disease

Contact Info

Product

Resources

About