Depression Symptoms Treatment

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In 1957 Kuhn first described the effectiveness of imipramine in treating depressive states. Since then several derivatives of tricyclic antidepressants (TCA) have been synthetized and their use has become extensive during the last decade.

A few years after the introduction of TCA, minor therapeutic side effects from the cardiovascular system were reported, for example hypotension and ST-T changes in the electrocardiogram (ECG). Since then there have been numerous case reports about serious effects, with marked ECG changes and sometimes fatal outcome, as a result of poisoning with tricyclic antidepressants.

Pharmacologic Properties

The cardiovascular effects of tricyclic antidepressants are closely related to their action at the adrenergic neuron and involve either directly or indirectly the neurotransmitter, norepinephrine (NE). Tricyclic antidepressants block the reuptake of NE at the cell membrane of both central and peripheral adrenergic neurons, resulting in the presence of increased levels of NE at the receptor site and a potentiation of transmitter action. TCA have an atropine-like anticholinergic effect , and they have shown a selective affinity for cardiac muscle. The pharmacological effects of a new tetracyclic drug maprotiline (Ludiomil) reflect the pattern of activity characteristic of the tricyclic antidepressants.

Cardiovascular Effects of TCA at Usual Therapeutic Doses in Man

Sinus Tachycardia: a common finding at a therapeutic level of tricyclic antidepressants; this has been attributed to an atropine like effect of TCA.

Pitts has reported the incidence of sinus tachycardia in 2.9% of patients with doxepin HC1 (Sinequan) and 30% with amitriptyline.

Burrows et al studied cardiac function in 32 patients with normal hearts, before and two weeks after treatment with TCA drugs. The dosage was usually 150 mg/day. Increase in heart rate by 9.1 ± 14.2 beats/minute was noted in 26 patients.

Postural Hypotension: is more likely to occur in the presence of existing cardiovascular disease. In one study of 41 patients with cardiovascular disease receiving imipramine (range 75-200 mg) severe postural hypotension (20 mm Hg fall in diastolic BP with major symptoms) was noted in 24% and moderate hypotension (10-20 mm Hg fall in diastolic pressure with minor symptoms) in 14% of patients. In comparison only, seven percent of 41 patients without cardiovascular disease had moderate postural hypotension. Mild postural hypotension (five to 20 mm Hg fall in diastolic BP, no symptoms) was noted in 37% and 29% of patients in respective groups. Additional studies have shown variable results, which in part appear due to factors such as drug dosage, patient selection and methodology. For example, no significant orthostatic hypotension was noted in depressed patients when blood pressure was measured three weeks after initiation of therapy, yet when recordings were made during the first 72 hours of treatment, a postural fall of greater than 20 mm Hg systolic was noted in 23%.

The reported incidence of hypotension (2.6%) with doxepin HC1 (Sinequan) has been considerably lower than that occurring with amitriptyline (8.6%).

The cause of hypotensive action of tricyclic antidepressants is not fully known. A number of studies have implicated a drug induced decrease in myocardial contractility and cardiac output. Less certain is whether these drugs act at a more peripheral site. A central mechanism of action may also be involved, since stimulation of central alpha adrenergic receptors has been shown to cause an inhibition of peripheral sympathetic activity leading to a fall in blood pressure.

Other possible factors include low-dose imipramine potentiation of the vasodepressor effect of both acetylcholine and electrical stimulation of the peripheral vagus nerve, and depression of the carotid occlusion reflex I with subsequent hypotension, such as occurs when low doses are topically applied to the carotid sinus.

Hypertension: experimental evidence is consistent with the concept that tri-cyclic antidepressants can cause hypertensive reactions in man.

A patient taking desmethylimipramine (DMI) and thioridazine and undergoing general anesthesia experienced an increase in blood pressure. The use of clomipramine (Anafranil) has been associated with hypertension in three patients, the most convincing of whom was a woman whose initial pressure of 150/105 mm/Hg increased to 220/150 after five days on the drug and returned to a baseline following drug withdrawal.

Electrocardiographic Changes: when administered in therapeutic amounts, tricyclic antidepressants can cause electrocardiogram changes in man.

1. PR interval. In a group of 32 patients receiving TCA drugs, prolongation of PR interval by 0.015 ± 0.024 seconds was noted in all subjects, when ECG were recorded two weeks after onset of treatment.

2. T-wave changes. Kristiansen noticed T-wave changes in 15 of 23 patients receiving imipramine up to 200 mg/day. Of 36 patients receiving amitriptyline in ordinary therapeutic doses, only two patients showed reversible T-wave changes. Rasmussen has reported T-wave changes in 18% of 65 patients receiving amitriptyline 75-225 mg/day. No significant changes in serial ECGs were noted in 14 enuretic children aged five to ten receiving imipramine 25-75 mg/day.

3. ST segment changes. In a series of 65 patients receiving amitriptyline 75-225 mg/day, ST segment depression associated with T-wave changes was noted in 18% of the patients.

4. Conduction abnormdlities. A 78 year old woman with no history of cardiovascular disease developed complete heart block on nortriptyline (25 mg tid) which disappeared when the drug was stopped and recurred seven days after the drug was restarted.

A 2:1 atrioventricular block developed during treatment with imipramine 200 mg/day in a 74 year old man with a three year history of a right bundle branch block. Serial ECGs and determinations of blood imipramine concentrations showed that the heart block was directly related to the plasma concentration of the drug and occurred below the atrioventricular node.

Rasmussen has reported two patients receiving amitriptyline who developed left bundle branch block which disappeared when treatment was discontinued.

Burrows et al have studied His bundle electrocardiography in 12 ambulant depressed patients receiving TCA drugs. In five patients there was significant prolongation (10 mSec or more) of the interval between the His bundle and the ventricle (HV interval). There was also a positive correlation between prolongation of the HV interval and plasma levels of nortriptyline over 200 ng/ml.

Arrhythmias: in a group of 65 patients receiving amitriptyline 75-225 mg/day, electrocardiogram was done at least once during treatment lasting three or more weeks and ventricular extrasystoles were noted in 18% of patients.

A pulse rate exercise on a bicycle with continuous ECG monitoring was performed on 32 patients receiving TCA drugs; no arrhythmias or ventricular ectropic beats occurred with the exercise.

Myocardial Infarction: has been associated with the use of tricyclic antidepressants in a number of cases, but a direct causal relationship has not been established. Most cases either involve drug overdose with associated hypotension and arrhythmia or occur in people already at high risk for infarction.

Congestive Heart Failure: patients with pre-existing cardiovascular disease appear to be at a higher risk for developing this complication. Less directly, drug induced dry mouth might cause an increased fluid intake and overload a potentially compromised cardiovascular system.

Sudden Death: in a hospital based drug information system in Aberdeen, 13 of 119 patients with cardiac disease receiving amitriptyline died suddenly, compared with three in a matched control group. In 87 cardiac patients on imipramine, there were four sudden deaths compared with two in the control group. However, the Boston Collaborative Drug Surveillance Program found no increased risk of sudden death in 80 patients with cardiovascular disease receiving antidepressants.