LETTERS TO THE ,EDITOR Low Dose Tricyclic Tachycardia To the Editor.' Although tricyclic antidepressants commonly increase heart rate , clinically significant tachycardia is unusual (Diamond, 1986). We report that two different tricyclic antidepressants used in treating an adolescent produced a sudden onset of severe tachycardia (heart rate of 170). To our knowledge, this is the first report of severe tachycardia in an adolescent as a result of treatment with tricyclic antidepressants. It is important to recognize this apparently infrequent but potentially dangerous side effect and to delineate predisposing factors. A. is a 16-year-old adopted, white female admitted to the inpatient psychiatry service because of violent and oppositional behavior. Before her hospitalization, she had become assaultive toward her parents, self-mutilative, and she had overdosed on medications . Her sleep, appetite, and concentration were poor. She denied feeling depressed but was tearful and stated she wished she would die. A.'s physical examination was notable for multiple, well-healed scars on her left upper and lower extremities from previous self-injurious episodes. Her head was small but symmetrical and measured at the 25th percentile. The inner canthus, outer canthus, and outer pupillary measurements were at the 3rd percentile for her age. All of her laboratory tests were normal, including screens for metabolic and genetic abnormalities. Magnetic resonance imaging of the head showed enlarged ventricles bilaterally. Her electroencephalogram was normal. Her full-scale IQ was 89, with a verbalIQ of 82, and a performance IQ of 100. A working diagnosis of major depression was made, and A. was started on the tricyclic antidepressant, nortriptyline. Her resting heart rate before the first dose of nortriptyline ranged from 80 to 90 beats per minute. Twenty mg of nortriptyline were given at bedtime for 2 nights then increased to 40 mg the third night. Approximately 16 hours after the third dose of nortriptyline , A.'s heart rate increased to 172 beats per mintue. She complained of dizziness and felt that her heart was racing. Nortriptyline was discontinued, and her heart rate returned to the 80s within 2 days. Desipramine was then started at 20 rng, twice daily. Within 2 hours after the fourth dose , her heart rate was 168 beats per minute, and again she complained of dizziness and palpitations. Desipramine was immediately discontinued , and her heart rate returned to the 80s within 5 days. Serum drug levels of nortriptyline and desipramine were not obtained because of the very brief duration of treatment. Electrocardiograms at the time of admission and during both episodes of tachycardia were normal, except for the increased heart rate . PR and QRS intervals did not lengthen after exposure to the medication. A pediatric cardiology consultation was obtained, and Holter monitoring was completed within 48 hours after desipramine was discontinued. Results during the 24-hour period of monitoring showed tachycardia at 140 beats per minute, associated with dizziness, dyspnea, chest pain, and nausea. This was believed to be secondary to previous doses of desipramine, and no additional evaluation was recommended. A.'s Cardiac echogram at age II was normal. Her heart rate during the remainder of her hospital stay (42 days) averaged 93 .2 beats per minute, with a range of 74 to 130. A study with children , aged 7-12 years, showed baseline heart rates between 85 to 90 beats per minute before treatment with imipramine (Preskorn et al., 1983). Serum blood levels greater than 225 ng/ml increased standing mean heart rate by 13 beats per minute. In contrast to our patient, these increases were measured after longer exposure to

l .Am.A cad . Child Adolesc. Psychiatry, 30 :1 . January 1991

the medication and at therapeutic doses. Although tricyclic blood levels were not obtained in the case reported here, they could have ruled out the unlikely possibility of toxic levels. Children are thought to be at greater risk of developing side effects from tricyclic antidepressants because of the decreased ability of their blood proteins to bind to these drugs (Winsberg et al., 1974). In summary, our patient is unusual in that she developed a symptomatic tachycardia soon after taking two different tricyclic antidepressants, both in very low doses. Children are possibly more vulnerable to cardiac side effects because of the differences in metabolism of these medications in a young population. A.'s physical anomalies suggest the possibility of an undetected genetic abnormality, which could possibly affect cardiac conduction (i.e. , aberrant nodal pathways). Although this patient did not receive additional treatment with a tricyclic antidepressant, it might be possible if a B-blocker were administered concurrently (Hillard and Vieweg , 1983). Since tachycardia because of anticholinergic effects decreases with aging (Dauchot and Gravenstein, 1970), this patient may eventually tolerate treatment with a tricyclic antidepressant alone. Janell Giesler, M.D . Elizabeth Reeve , M.D . Carrie M. Borchardt, M.D. University of Minnesota Minneapolis, Minnesota REFERENCES

Dauchot, P. & Gravenstein, J. S. (1970) , Effects of atropine on the electrocardiogram in different age groups. Clin . Pharmacol . Ther. , 12:274-280. Diamond, J . M. (1986), Sudden-onset tachycardia induced in a child by imipramine. Am . J . Psychiatry , 143:1067. Hillard, J. R. & Vieweg, W. V. R. (1983), Marked sinus tachycard ia resulting from the synergistic effects of marijuana and nortriptyline . Am. J. Psychiatry, 140:62fr627. Preskorn, S. H., Weller, E. B., Weller, R. A. & Glotzbach, E. (1983), Plasma levels of imipramine and adverse effects in children. Am. J . Psychiatry , 140:1332-1335. Winsberg, B. G. , Pevel, J. M. , Hurwic , M. J. & Klutch, A. (1974), Imipramine protein binding and pharmacokinetics in children . In: The Phenothiazines and Structurally Related Drugs, eds. 1. S. Forest, C. J. Carr & E. Usdin. New York: Raven Press, pp. 425-431.

Protective Factors: Independent or Interactive? To the Editor: Drs. Jenkins and Smith are to be congratulated on an innovative, informative study of factors serving to protect children living in disharmonious homes (Jenkins and Smith, 1990). Quite rightly , they point out that the concept of a protective factor implies a modification of the effect of the stress factor, and that this means that there must be a statistical interaction between the stress and the putative protective factor and not simply a main effect from the latter. Their analyses were well designed to investigate this important issue, and their discussion of the findings is thoughtful and clinically helpful. Their rigorous and well-conceived investigation constitutes a model for other researchers to follow. However, I was most surprised to find in their introduction that I am cited as a researcher who has argued that protective factors represent independent main effects and not interactive mechanisms. Nothing could be farther from the truth. In my 1981 paper that they cite (Rutter, 1981), I argued, "The notion here, then,

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