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  • Orthostatic blood pressure  (3)
  • drug interaction  (3)
  • genetic polymorphism  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Mianserin: Cardiovascular effects in elderly patients (1983)
    Springer
    Psychopharmacology 80 (1983), S. 174-177 
    Details
    ISSN: 1432-2072
    Keywords: Elderly patients ; Mianserin therapy ; Plasma level monitoring ; Orthostatic blood pressure ; 24-h Electrocardiographic recording ; Systolic time intervals
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cardiovascular effects of the tetracyclic antidepressant drug mianserin were examined in a prospective study including ten elderly depressed patients (age 60–77 years). During 1 week on placebo and 5 weeks on mianserin, 60 mg per day, orthostatic blood pressure testing, recording of standard electrocardiogram, 24-h electrocardiographic recording and systolic time intervals were carried out along with frequent monitoring of plasma levels of mianserin (13–57 μg/l) and the primary metabolite desmethylmianserin (7–27 μg/l). Mianserin caused a significant increase in orthostatic systolic blood pressure drop, and this correlated well with the plasma mianserin levels (r s=0.70). There were no significant changes in supine blood pressure or in orthostatic changes in heart rate. No cardiac conduction disturbances or arrhythmias were provoked, but mianserin caused changes in systolic time intervals indicating impairment of left ventricular contractility and performance. Like tricyclic antidepressants mianserin should thus be used with caution in patients with latent or overt cardiovascular disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00427964
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  • 2
    Electronic Resource
    Electronic Resource
    Cardiovascular effects of imipramine and nortriptyline in elderly patients (1981)
    Springer
    Psychopharmacology 74 (1981), S. 360-364 
    Details
    ISSN: 1432-2072
    Keywords: Elderly patients ; Antidepressive treatment ; Orthostatic blood pressure ; Systolic time intervals ; 24-hour ambulatory ECG
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cardiovascular effects in elderly depressed patients (age 62–78 years) treated with imipramine (N=11) or nortriptyline (N=10) were recorded by monitoring of heart rate, blood pressure, systolic time intervals, standard ECG and 24-h ECG. The two drugs exhibited distinctly different cardiovascular reactions. The use of imipramine was severely limited by orthostatic hypotension occurring at subtherapeutic plasma levels, which resulted in falls with fracture in two patients. In contrast, nortriptyline at therapeutic drug levels did not significantly influence orthostatic blood pressure regulation. Nortriptyline caused moderate changes in systolic time intervals, indicating impairment in myocardial contractility. This effect was not seen with imipramine, but a majority of the patients did not reach therapeutic plasma levels because of the blood pressure reactions. Neither imipramine nor nortriptyline induced changes in cardiac conduction time measurements or arrhythmias. In addition to the blood pressure reactions, the use of imipramine was complicated by dose dependent kinetics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00432748
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  • 3
    Electronic Resource
    Electronic Resource
    Cardiovascular effects of amitriptyline in the treatment of elderly depressed patients (1985)
    Springer
    Psychopharmacology 87 (1985), S. 212-215 
    Details
    ISSN: 1432-2072
    Keywords: Elderly patients ; Antidepressive treatment ; Orthostatic blood pressure ; Systolic time intervals
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Thirteen elderly depressed patients (age 60–82 years) were treated for 5 weeks with a fixed dose of amitriptyline 100 mg (sustained release preparation). In all patients the sum of concentrations of amitriptyline and nortriptyline exceeded 130 μg/l, which is the recommended plasma level. Cardiovascular side effects were recorded by monitoring heart rate, blood pressure, standard ECG and systolic time intervals. During treatment, a transient increase in the supine heart rate was observed without significant changes in the supine blood pressure. The orthostatic drop in blood pressure was markedly increased during treatment without a compensatory increase in heart rate, and these changes remained significant during the whole investigational period. PQ and QRS were significantly increased during treatment, and significant changes in the systolic time intervals were found indicating impairment of myocardial conduction and contractility. In three patients medication was discontinued due to cardiovascular side effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00431810
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  • 4
    Electronic Resource
    Electronic Resource
    Inhibition by paroxetine of desipramine metabolism in extensive but not in poor metabolizers of sparteine (1993)
    Springer
    European journal of clinical pharmacology 44 (1993), S. 349-355 
    Details
    ISSN: 1432-1041
    Keywords: Paroxetine ; Desipramine ; sparteine/debrisoquine ; genetic polymorphism ; drug-drug interaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Nine extensive metabolizers (EMs) and eight poor metabolizers (PMs) of sparteine took a single oral dose of 100 mg of desipramine HCI before and while taking paroxetine 20 mg per day. Before paroxetine, the median of the total desipramine clearance was 7 times higher in EMs than in PMs (102 and 15 l·h−1 respectively). This confirms that desipramine is extensively metabolized via the sparteine/debrisoquine oxidation polymorphism i.e. by CYP2D6. During paroxetine, the median clearances were 22 l·h−1 and 18 l·h−1 in EMs and PMs respectively. The 5-fold decrease in clearance in EMs when desipramine was co-administered with paroxetine confirms that paroxetine is a potent inhibitor of CYP2D6. The lack of effect on clearance in PMs shows that paroxetine is a selective inhibitor of CYP2D6, which is absent from the livers of PMs. Before paroxetine, the median of desipramine clearance via 2-hydroxylation was 40-times higher in EMs than in PMs (56 and 1.4 l·h−1 respectively), but during paroxetine, it was only 2-times higher (6 and 2.9 l·h−1 respectively). The increase in this clearance in PMs suggests that paroxetine is an inducer of the alternative, unidentified P 450(s) which catalyze(s) the formation of 2-OH-desipramine in this phenotype. Before paroxetine, the median amounts of 2-OH-desipramine glucuronide recovered in urine were 69% and 68% of the total recovery of 2-OH-desipramine in urine in EMs and PMs respectively. During paroxetine, the corresponding values were 77% and 84%. This increase in the relative recovery of the glucuronide was statistically significant in both phenotypes, suggesting that paroxetine is a weak inducer of the glucuronidation of 2-OH-desipramine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00316471
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  • 5
    Electronic Resource
    Electronic Resource
    The effect of quinidine on the analgesic effect of codeine (1992)
    Springer
    European journal of clinical pharmacology 42 (1992), S. 587-591 
    Details
    ISSN: 1432-1041
    Keywords: Codeine ; Quinidine ; CYP2D6 ; hypolagesia ; drug interaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary We have studied the hypoalgesic effect of codeine (100 mg) after blocking the hepatic O-demethylation of codeine to morphine via the sparteine oxygenase (CYP2D6) by quinidine (200 mg). The study was performed in 16 extensive metabolizers of sparteine, using a double-blind, randomized, four-way, cross-over design. The treatments given at 3 h intervals during the four sessions were placebo/placebo, quinidine/placebo, placebo/codeine, and quinidine/codeine. We measured pin-prick pain and pain tolerance thresholds to high energy argon laser stimuli before and 1, 2, and 3 h after codeine or placebo. After codeine and placebo, the peak plasma concentration of morphine was 6–62 (median 18) nmol·.l−1. When quinidine pre-treatment was given, no morphine could be detected (〈4 nmol·l−1) after codeine. The pin-prick pain thresholds were significantly increased after placebo/codeine, but not after quinidine/codeine compared with placebo/placebo. Both placebo/codeine and quinidine/codeine increased pain tolerance thresholds significantly. Quinidine/codeine and quinidine/placebo did not differ significantly for either pin-prick or tolerance pain thresholds. These results are compatible with local CYP2D6 mediated formation of morphine in the brain, not being blocked by quinidine. Alternatively, a hypoalgesic effect of quinidine might have confounded the results.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00265920
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  • 6
    Electronic Resource
    Electronic Resource
    Steady-state levels of imipramine and its metabolites: Significance of dose-dependent kinetics (1986)
    Springer
    European journal of clinical pharmacology 30 (1986), S. 43-49 
    Details
    ISSN: 1432-1041
    Keywords: imipramine ; desipramine ; hydroxymetabolites ; plasma concentration monitoring ; dose-dependent kinetics ; drug interaction ; levomeprazine ; perphenazine ; therapeutic response ; sparteine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Seventeen hospitalized patients (age 39–66 years), received a loading dose of 100 mg imipramine HCl and then 50 mg b.i.d. The 12-h plasma concentration at steady-state varied between 40–637 nmol/l for imipramine, 49–1148 nmol/l for desipramine and 89–1603 nmol/l for imipramine + desipramine. Guided by plasma level monitoring, a final therapeutic plasma level between 548–910 nmol/l for imipramine + desipramine was achieved (therapeutic dose range: 50–400 mg/day). Mean time to reach the therapeutic level was 19 days. The mean 2-OH-imipramine/imipramine ratio was 0.24 and mean 2-OH-desipramine/desipramine ratio was 0.56. There was a significant intrapatient correlation between the two ratios, both during 100 mg imipramine/d and at the therapeutic dose level. A low ratio was associated with high imipramine and particularly with a high desipramine level. Well defined steady state levels were established at two different dose levels in 12 patients and at three dose levels in 5 patients. With increasing dose there was a marked and disproportionate rise in the desipramine level and to some extent in the imipramine level. Saturation of imipramine and desipramine hydroxylation appeared to be responsible for the dose-dependent kinetics. Concomitant treatment with levomepromazine and perphenazine in one patient resulted in a significant rise both in imipramine and desipramine concentration, apparently due to inhibition of the hydroxylation. Eleven out of twelve endogenously depressed patients responded completely to treatment, whereas the response was poor in the non-endogenously depressed patients despite optimal drug levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00614194
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  • 7
    Electronic Resource
    Electronic Resource
    Quinidine inhibits the 2-hydroxylation of imipramine and desipramine but not the demethylation of imipramine (1989)
    Springer
    European journal of clinical pharmacology 37 (1989), S. 155-160 
    Details
    ISSN: 1432-1041
    Keywords: imipramine ; desipramine ; quinidine ; sparteine oxidation ; cytochrome P450 isoforms ; genetic polymorphism ; drug interaction ; metabolic clearance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary On separate occasions 6 extensive metabolizers of sparteine took a single oral dose of 100 mg imipramine and desipramine before and during the intake of quinidine sulphate 200 mg/day. During quinidine the total oral clearance of imipramine on average was reduced by 35%, and that of desipramine by 85%. The clearance of imipramine via demethylation was not significantly reduced during quinidine administration, whereas its clearance by other pathways, largely 2-hydroxylation, was reduced by more than 50%. 2-OH-Imipramine and 2-OH-desipramine were detected in plasma before (maximum concentrations 30–100 nmol · l−1) but not during quinidine. It appears that quinidine is a potent inhibitor of the sparteine/debrisoquine oxygenase, P450dbl, which is responsible for the 2-hydroxylation of imipramine and desipramine, but not of the P450 isozyme responsible for the demethylation of imipramine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00558224
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