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Influence of serotonin transporter gene polymorphism on depressive symptoms and new cardiac events after acute myocardial infarction.
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BACKGROUND
In patients with acute myocardial infarction (AMI), depressive symptoms increase the risk for cardiac events. Recently, the S allele of the serotonin transporter (5-HTT) gene-linked polymorphic region was shown to reduce transcription of this gene and thus reduce serotonin reuptake, and
Whole blood serotonin and platelet activation in depressed post-myocardial infarction patients.
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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
The effect of selective serotonin re-uptake inhibitors on the risk of myocardial infarction in a cohort of patients with depression.
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OBJECTIVE
To evaluate whether selective serotonin re-uptake inhibitor (SSRI) exposure influences the risk of myocardial infarction (MI) in patients with depression.
METHODS
This study included 693 patients with MI (cases) and 2772 controls. Conditional logistic regression was used to calculate the
Current use of selective serotonin reuptake inhibitors and risk of acute myocardial infarction.
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BACKGROUND
It has been suggested that increased platelet activation increases the risk of acute myocardial infarction (AMI) in patients with depression. Selective serotonin reuptake inhibitors (SSRIs) may attenuate platelet activation by serotonin depletion in platelets. Observational studies have
Cognitive Deficits Following a Post-Myocardial Infarct in the Rat Are Blocked by the Serotonin-Norepinephrine Reuptake Inhibitor Desvenlafaxine.
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Myocardial infarction (MI) in animal models induces cognitive deficits as well as the activation of caspase in the limbic system; both can be blocked by 2 weeks of treatment following MI using tricyclic antidepressants or selective serotonin uptake blockers. Here we used three different treatment
Psychocardiological disorder and brain serotonin after comorbid myocardial infarction and depression: an experimental study.
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Objectives We investigated whether trimetazidine pretreatment can regulate central and peripheral serotonin (5-HT) in rats of myocardial infarction (MI) combined with depression. Methods Forty rats were randomly assigned to a sham operation group (n = 10) and a disease model group (n = 30). The sham
Pretreatment with Ginseng Fruit Saponins Affects Serotonin Expression in an Experimental Comorbidity Model of Myocardial Infarction and Depression.
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We previously demonstrated that serotonin (5-HT) and 5-HT2A receptor (5-HT2AR) levels in platelets were up- or down-regulated after myocardial infarction (MI) associated with depression. In this study, we further evaluated the effects of pretreatment with ginseng fruit saponins (GFS) on the
Relationship between no-reflow phenomenon and serotonin levels in patients with acute ST-elevation myocardial infarction who underwent primary percutaneous intervention.
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OBJECTIVE
Our aim was to investigate the effects of serotonin, which is a severe vasoconstrictor agent, on the occurrence of no-reflow phenomenon.
METHODS
In this cross-sectional controlled study, 40 patients, admitted to our clinic with chest pain in the first 12 hours and underwent primary
Comparison of plasma serotonin levels in patients with variant angina pectoris versus healed myocardial infarction.
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Patients with variant angina pectoris showed greater serotonin plasma levels than did control subjects and patients with healed myocardial infarction. The levels also tended to be greater in those with >1 episode/month than in those with fewer episodes. Moreover, patients with variant angina
Failure of central nervous system serotonin blockage to influence outcome in acute cerebral infarction. A double blind randomized trial.
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To determine the effect of blocking central nervous system (CNS) serotonin reuptake in the outcome of acute cerebral infarction (ACI), 49 patients were studied in a double blind, randomized trial. All patients suffered hemispheric ACI, were seen within 24 hours of onset, and were treated with low
The role of serotonin (5HT2) receptor blockade in myocardial reperfusion injury: effects of LY53857 in a canine model of myocardial infarction.
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The potential protective effects of serotonin receptor antagonism during the process of acute myocardial infarction were studied in anesthetized male dogs, which were subjected to a 90-min left circumflex coronary artery occlusion followed by 5 h of reperfusion. Either vehicle (0.9% NaCl) or the
Serotonin transporter gene polymorphism and myocardial infarction: Etude Cas-Témoins de l'Infarctus du Myocarde (ECTIM).
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BACKGROUND
Depression is a risk factor for myocardial infarction (MI). Selective serotonin reuptake inhibitors reduce this risk. The site of action is the serotonin transporter (SLC6A4), which is expressed in brain and blood cells. A functional polymorphism in the promoter region of the SLC6A4 gene
Increased cerebral serotonin-2A receptor binding in depressed patients with myocardial infarction.
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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.
Low incidence of serotonin-induced occlusive coronary artery spasm in patients with recent myocardial infarction.
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Intracoronary infusion of serotonin has been reported to induce varying degrees of coronary vasoconstriction in different coronary syndromes, but it has never been studied in patients after myocardial infarction. In patients with recent myocardial infarction, we found a low incidence (11%) of
A follow-up study of platelet-rich plasma serotonin in clinical subtypes of cerebral infarction.
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The serotonin concentration in the platelet-rich plasma of 32 patients with single and multiple stroke type cerebral infarction was investigated at various stages. Serotonin levels were decreased in the acute period. The incidence of serotonin abnormality was higher in multiple types than in the
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