23 Myocarditis and cardiomyopathy were also associated with chlorpromazine, lithium, fluphenazine, risperidone, and haloperidol, but these associations need to be further investigated in order to establish whether they are causal. Figure 4. Acute myocarditis 8 days after clozapine treatment initiation: histopathological pattern. Cardiac tissue of a 18-year-old woman
with myocytolysis, diffuse eosinophilic and lymphocytic infiltrates. The etiology seems to be clearly of immunological or hypersensitivity … Discussion The above information indicates that Inhibitors,research,lifescience,medical ECG monitoring should be performed during hospitalization and ambulatory treatment, at least when multiple psychotropic drug regimens, methadone maintenance treatment, and other predisposing factors for QT prolongation are present at admission. We particularly recommend Inhibitors,research,lifescience,medical regular cardiac and ECG monitoring in patients receiving clozapine, high-dosage antipsychotics, tricyclic antidepressants, drug regimens with potential interactions, or in clinical situations recognized as promoters of QT prolongation. Further electrocardiographic studies in psychiatric patients, systematic recording of case reports, and data mining in pharmaco
vigilance systems will help establish the magnitude of cardiac adverse Inhibitors,research,lifescience,medical reactions to psychotropic drugs.
Depression is considered to be an Independent risk factor for cardiovascular
mortality and morbidity in patients with Ischemic heart disease (IHD).1,2The risk of cardiovascular disease is higher in Individuals suffering from depression,3 as is the risk of ischemic stroke.4 Among newly Inhibitors,research,lifescience,medical diagnosed patients with coronary heart disease, approximately one in five patients suffers from major depression, with a similar prevalence in patients recovering from acute myocardial infarction.5,6 The proposed mechanisms are either spurious, le, that depression predicts, but is not causally related to, cardiovascular heart disease morbidity and mortality Inhibitors,research,lifescience,medical (antidepressant cardiotoxicity, association with cardiac risk factors, sedentary lifestyle), or imply that depression may inhibitors directly influence the course of cardiac heart disease (nonadherence to cardiac treatment and regimens, dysregulation of autonomic, neuroendocrine, and serotonergic systems).7 Serotonergic neurotransmission dysfunction has been investigated and observed in major depression.8,9 Various Thymidine kinase findings support the hypothesis that alterations in serotonergic neurons play a role in the pathophysiology of depression,10 and most antidepressants have a direct influence on serotonin (5-HT) transmission and levels. 5-HT is usually a vasodilator, becoming a vasoconstrictor when the endothelium is damaged.11 It is also involved in platelet aggregation. It is taken up from plasma and stored in platelet granules.