Cardiovascular adverse reactions during antidepressant treatment: a drug surveillance report of German-speaking countries between 1993 and 2010.

BACKGROUND: Antidepressants (ADs) are known to have the potential to cause various cardiovascular adverse drug reactions (ADRs). The tricyclic antidepressants (TCAs) were first revealed to be a possible source of cardiovascular ADRs. In recent years, newer classes of ADs were also suggested to have a higher risk of cardiovascular adverse effects. In particular, the selective serotonin reuptake inhibitors (SSRIs) were suspected to have the potential to induce QTc interval prolongation, and therefore increase the risk of ventricular arrhythmia. This descriptive study is based on the continuous pharmacovigilance program of German-speaking countries (Austria, Germany, and Switzerland), the Arzneimittelsicherheit in der Psychiatrie (AMSP), which assesses severe ADRs occurring in clinical routine situations. METHODS: Of 169,278 psychiatric inpatients treated with ADs between 1993 and 2010, 198 cases of cardiovascular ADRs (0.12%) were analyzed. RESULTS: Our study showed that the incidence rates of cardiovascular ADRs were highest during treatment with monoamine oxidase inhibitors (0.27%), TCAs (0.15%), and serotonin noradrenaline reuptake inhibitors (0.14%); the risk of occurring during treatment with SSRIs (0.08%) was significantly lower. The noradrenergic and specific serotonergic AD mirtazapine (0.07%) had a significantly lower risk of cardiovascular ADRs than all other ADs. Severe hypotension was the most frequent ADR, followed by hypertension, arrhythmia, and in some rare cases heart failure. CONCLUSIONS: Despite certain limitations due to the AMSP study design, our observations on cardiovascular ADRs can contribute to a better knowledge of the cardiovascular risk profiles of antidepressants in the clinical routine setting. However, prospective studies are needed to verify our findings.

Psychiatric comorbidity and additional abuse of drugs in maintenance treatment with L- and D,L-methadone.

Sixty D,L- or L-methadone treated patients in maintenance therapy were interviewed for additional drug abuse and psychiatric comorbidity; 51.7% of the entire population had a comorbid Axis-I disorder, with a higher prevalence in females (P=0.05). Comorbid patients tended to have higher abuse of benzodiazepines, alcohol, cannabis, and cocaine, but not of heroin. They had received a significantly lower D,L- (P<0.05) and L-methadone dose than non-comorbid subjects. The duration of maintenance treatment showed an inverse relationship to frequency of additional heroin intake (P<0.01). Patients with additional heroin intake over the past 30 days had been treated with a significantly lower L-methadone dosage (P<0.05) than patients without. Axis-I comorbidity appears to be decreased when relatively higher dosages of D,L- (and L-methadone) are administered; comorbid individuals, however, were on significantly lower dosages. Finally, L-, but not D,L-methadone seems to be more effective in reducing additional heroin abuse.

Relationship between nocturnal urinary cortisol excretion and symptom severity in subgroups of patients with depressive episodes.

INTRODUCTION: The aim of this naturalistic study was to gain more information about the elevation of basal hypothalamic-pituitary-adrenal (HPA) activity in relationship to symptom severity in specific subtypes of depressive episodes. METHOD: Hamilton Depression Rating Scale scores and aggregated nocturnal urinary cortisol excretion were measured in 4 groups of inpatients with depressive episodes (n = 48; monopolar nonpsychotic, monopolar psychotic, bipolar nonpsychotic and bipolar psychotic) at the beginning and at the end of inpatient treatment. RESULTS: The initial elevation of nocturnal urinary cortisol excretion was most pronounced in psychotic patients. At the end of treatment, the Hamilton Depression Rating Scale scores had decreased significantly in all patients to comparable levels, whereas the nocturnal cortisol excretion values were still relatively elevated in mono- and bipolar psychotic patients compared to mono- and bipolar nonpsychotic ones. CONCLUSION: The observation that the basal HPA activity remains elevated even after remission of symptoms in patients with psychotic depression supports the concept that a dysfunctional regulation of the HPA system is possibly a trait- rather than a state-related feature.