Cardiovascular effects of antidepressant drugs

Glassman, Alexander H.; Roose, Steven P.; Rivelli, Sarah K.; Preud’homme, Xavier

doi:10.3109/08039489309104124

Cited by 47 publications

(54 citation statements)

References 23 publications

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“…Side effects are related to direct stimulation of serotonergic receptors (Stahl, 2000). Cardiovascular effects of SSRI as a group are minimal although they may slow pulse rates, but have little or no effect on PR, QRS, or QTc interval (Glassman, 1998).…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular effects of high dose venlafaxine XL in patients with major depressive disorder

Mbaya

Alam

Ashim

et al. 2007

Human Psychopharmacology

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Section: Introductionmentioning

confidence: 99%

Cardiovascular effects of high dose venlafaxine XL in patients with major depressive disorder

Mbaya

Alam

Ashim

et al. 2007

Human Psychopharmacology

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“…Due to their unspecific mode of action, they produce many side effects, cardiotoxicity being among the most serious effects (Glassman, 1998). Tricyclic antidepressants are known to inhibit calcium currents in heart myocytes (Isenberg and Tamargo, 1985;Delpón et al, 1991) and in neurons (Ogata et al, 1989;Choi et al, 1992).…”

mentioning

confidence: 99%

Inhibition of the Cardiac L-Type Calcium Channel Current by Antidepressant Drugs

Zahradnı́k

Minarovic²,

Zahradníková³

2007

J Pharmacol Exp Ther

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Antidepressants inhibit many membrane receptors and ionic channels, including the L-type calcium channel. Here, we investigated the inhibition of calcium current (I Ca ) by antidepressants in enzymatically isolated rat ventricular myocytes using whole-cell patch clamp. The molecular mechanism of inhibition was studied by comparing the voltage and state dependence of antidepressant inhibition of I Ca to the respective properties of calcium antagonists, and by studying the effect of (Ϯ)-1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-[trifluoromethyl]phenyl)-3-pyridine carboxylic acid methyl ester (Bay K8644) or diltiazem on the inhibitory potency of the antidepressants. All selected antidepressants inhibited calcium currents reversibly and concentration-dependently. At a stimulation frequency of 0.33 Hz, the antidepressants imipramine, clomipramine, desipramine, amitriptyline, maprotiline, citalopram, and dibenzepin blocked I Ca , with IC 50 values of 8.3, 11.6, 11.7, 23.2, 31.0, 64.5, and 364 M. The antidepressant drugs shifted steady-state inactivation curves of I Ca to negative voltages. The extent of the shift was similar to that induced by diltiazem or verapamil, but it was significantly smaller than that induced by felodipine. The usedependent component of the antidepressant-induced block was similar to that of diltiazem, and it was significantly more and less, respectively, than those of felodipine and verapamil. In the presence of Bay K8644, antidepressants were more effective in inhibiting I Ca . However, the inhibitory effect of antidepressants was also augmented by diltiazem, suggesting that these drugs do not compete with diltiazem for a single binding site. These data suggest that antidepressants exert their inhibitory action on cardiac L-type calcium channels by a specific interaction at a receptor site similar to, but distinct from, the benzothiazepine site.

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“…Its pharmacology and clinical efficacy have been reviewed by Wilde et al (1993). However, the cardiovascular effects of fluvoxamine in patients with severe cardiac disease are open to question (Glassman and Preud'homme 1993).…”

Section: Introductionmentioning

confidence: 99%

Comparative electrophysiological effects of the antidepressants fluvoxamine and amitriptyline in the canine heart after myocardial infarction

Ikeda

Nishimoto

Shimazu

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

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We studied the effects of fluvoxamine and amitriptyline on epicardial activation delay of premature excitations, the effective refractory period, and the incidence of ventricular arrhythmias by programmed electrical ventricular stimulation in the canine heart after myocardial infarction. Additionally, we investigated whether the inhibition of norepinephrine reuptake by amitriptyline contributes to epicardial activation delay or arrhythmias by combination with propranolol pretreatment. Amitriptyline, at a dose of 3 mg/kg, significantly prolonged epicardial activation delay of premature excitations in the infarcted zone in a frequency-dependent manner (n = 10). Amitriptyline also prolonged epicardial activation delay of premature excitations in the normal zone (n = 10). The effective refractory period in the infarcted zone was significantly prolonged by amitriptyline at a dose of 3 mg/kg (n = 8). Amitriptyline increased the incidence of ventricular arrhythmias induced by programmed electrical ventricular stimulation (n = 8). Propranolol did not affect the epicardial activation delay caused by amitriptyline or the incidence of ventricular arrhythmias induced by programmed electrical ventricular stimulation (n = 6). Fluvoxamine, on the other hand, had no significant effect on epicardial activation delay of premature excitations (n = 10) or the effective refractory period (n = 8) in both the infarcted and normal zones. Fluvoxamine did not increase the incidence of ventricular arrhythmias induced by programmed electrical ventricular stimulation (n = 8).

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Cardiovascular effects of antidepressant drugs

Cited by 47 publications

References 23 publications

Cardiovascular effects of high dose venlafaxine XL in patients with major depressive disorder

Cardiovascular effects of high dose venlafaxine XL in patients with major depressive disorder

Inhibition of the Cardiac L-Type Calcium Channel Current by Antidepressant Drugs

Comparative electrophysiological effects of the antidepressants fluvoxamine and amitriptyline in the canine heart after myocardial infarction

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