Mirtazapine was significantly more effective than a serotonin-noradrenaline reuptake inhibitor ( venlafaxine only , two trials , n = 415 ) at two weeks ( OR 2.29 , 95 % CI 1.45 to 3.59 ) and at the end of acute-phase treatment ( OR 1.53 , 95 % CI 1.03 to 2.25).In terms of dropouts , there was no robust evidence to detect a difference between mirtazapine and other antidepressants .
Mirtazapine was more likely to cause weight gain or increased appetite and somnolence than SSRIs but less likely to cause nausea or vomiting and sexual dysfunction .
AUTHORS ' CONCLUSIONS Some statistically significant and possibly clinical ly meaningful differences between mirtazapine and other antidepressive agents were found for the acute-phase treatment of major depression .
Mirtazapine is likely to have a faster onset of action than SSRIs during the acute-phase treatment .
Dropouts occur similarly in participants treated with mirtazapine and those treated with other antidepressants , although the adverse event profile of mirtazapine is unique
BACKGROUND Mirtazapine has a unique mechanism of antidepressive action and is one of the commonly used antidepressants in clinical practice .
OBJECTIVES The aim of the present review was to assess the evidence on the efficacy and acceptability of mirtazapine compared with other antidepressive agents in the acute-phase treatment of major depression in adults .
Cardiovascular variability in major depressive disorder and effects of imipramine or mirtazapine (Org 3770).
Spectral analysis of fluctuations in heart rate ( HR ) and blood pressure ( BP ) was applied to assess sympathetic and parasympathetic cardiovascular control mechanisms in patients with unipolar affective disorder before and after treatment with imipramine ( IMI ) or mirtazapine ( MIR ) .  In a double-blind r and omized study , 10 patients received treatment with IMI and 10 patients received treatment with MIR .  Cardiovascular parameters were studied before and after 4 weeks of treatment :  HR and BP ( Finapres ) were recorded continuously during supine rest ( SR ) and orthostatic challenge ( OC ; 60-degrees head-up tilting ) . During SR and OC , power spectra were calculated for HR and systolic BP . Spectral density was assessed for three frequency b and s : low ( 0.02 - 0.06 Hz ) , mid ( 0.07 - 0.14 Hz ) , and high ( 0.15 - 0.50 Hz ) . Before treatment , the depressed patients ( N = 20 ) differed from age-matched controls ( N = 20 ) only in their response to OC : the depressed patients showed more suppression of HR variability ( both mid- and high-frequency b and fluctuations ) , indicating stronger vagal inhibition , and a reduced increase of BP variability ( mid-frequency b and fluctuations ) , indicating reduced sympathetic activation . After 4 weeks of treatment , patients treated with either antidepressant drug showed significant changes of HR ( increase ) and HR variability ( decrease ) during SR and OC ; the suppression of mid- and high-frequency fluctuations of HR was larger for IMI than for MIR . The increase in HR and decrease in HR variability may be attributed to the anticholinergic properties of IMI ( strong ) and MIR ( weak ) , result ing in cardiac vagal inhibition . Whereas MIR had no effect on BP or BP variability , IMI specifically reduced mid-frequency b and fluctuations of BP as the result of a suppression of central sympathetic activity . Our data confirm and extend previous observations on the presence of autonomic dysfunctions in unmedicated depressed patients : spectral analysis of HR and BP fluctuations suggested that both parasympathetic and sympathetic mechanisms are involved , specifically during OC . The preexisting autonomic cardiovascular dysfunctions were not normalized by antidepressant drugs . In fact , some of the components of the cardiovascular autonomic dysfunction were further aggravated , depending on the pharmacologic profile of the drug under investigation
Mirtazapine was significantly more effective than a serotonin-noradrenaline reuptake inhibitor ( venlafaxine only , two trials , n = 415 ) at two weeks ( OR 2.29 , 95 % CI 1.45 to 3.59 ) and at the end of acute-phase treatment ( OR 1.53 , 95 % CI 1.03 to 2.25).In terms of dropouts , there was no robust evidence to detect a difference between mirtazapine and other antidepressants .
Mirtazapine was more likely to cause weight gain or increased appetite and somnolence than SSRIs but less likely to cause nausea or vomiting and sexual dysfunction .
AUTHORS ' CONCLUSIONS Some statistically significant and possibly clinical ly meaningful differences between mirtazapine and other antidepressive agents were found for the acute-phase treatment of major depression .
Mirtazapine is likely to have a faster onset of action than SSRIs during the acute-phase treatment .
Dropouts occur similarly in participants treated with mirtazapine and those treated with other antidepressants , although the adverse event profile of mirtazapine is unique
BACKGROUND Mirtazapine has a unique mechanism of antidepressive action and is one of the commonly used antidepressants in clinical practice .
OBJECTIVES The aim of the present review was to assess the evidence on the efficacy and acceptability of mirtazapine compared with other antidepressive agents in the acute-phase treatment of major depression in adults .