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Re: does maprotiline have cardiac conduction effects? » linkadge

Posted by saturn on May 11, 2007, at 22:47:26

In reply to does maprotiline have cardiac conduction effects?, posted by linkadge on May 11, 2007, at 19:03:56

Maprotiline (Ludiomil)

Not surprisingly the minor structural differences between maprotiline and the TCAs have not resulted in any changes in the drug's cardiovascular pharmacologic profile when compared to the TCAs. Like the TCAs, it shows conduction delays at normal therapeutic doses and, in overdose, cardiovascular deaths associated with heart block and asystole have been reported (Edwards and Goldie 1982, Ghosh 1981, Crome and Newman 1979). Maprotiline also produces orthostatic hypotension, although data on the rate of this adverse effect are not yet available (Edwards and Goldie 1982). Falls and associated fractures have been reported and there is little to suggest that the incidence of orthostatic hypotension is significantly different from older TCAs.

In studying the cardiovascular effects of tricyclic and tetracyclic antidepressants in therapeutic doses in 66 depressed patients, no differences were noted between tricyclic and tetracyclic antidepressants in the effects on parameters studied (Burckhardt et al 1978, Raeder et al 1978). Drugs studied were trimipramine, amitriptyline, imipramine, maprotiline, and mianserin. After 3 weeks of therapy all drugs were noted to increase heart rate and PR interval, but prolongation of the QRS interval or corrected QT interval was not significant. Flattening of T-waves was observed with no changes in serum potassium, but these were reversible upon discontinuation of treatment. After 13 months of therapy all ECG values returned to normal except the heart rate which continued to be increased. There was a significant prolongation of the preejection period and a slight but insignificant shortening of the left ventricular ejection time, indicating a decrease in myocardial contractility. These returned to normal after therapy was discontinued. Even with continued treatment for an additional 4 years, these same parameters returned to normal after discontinuation. No major dysrhythmias were observed.

The effect of therapeutic doses of maprotiline and imipramine on the heart was studied in 52 depressed patients (Mielke et al 1979). The drugs produced equivalent changes which were statistically significant. Both decreased standing systolic pressure, increased standing and supine pulse rates, and lengthened the corrected QT interval. There were no changes from pre- to post-treatment echocardiograms, and follow-up treadmill stress tests in 29 patients showed no arrhythmias or ischemic changes. All initial treadmill stress tests were normal. There have been no reports to date of maprotiline causing myocardial infarction. Clinically significant differences in cardiovascular effects of maprotiline and tricyclic antidepressants remain to be conclusively demonstrated

The full article: http://www.janela1.com/vh/docs/v0002502.htm

BTW Link, if not mistaken some of your old posts mentioned the need for a 5-HT1 antagonist as it stimulates hippocampal neurogenesis. Is that why you're interested in maprotiline? Peace.


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URL: http://www.dr-bob.org/babble/20070509/msgs/758016.html