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Electroconvulsive Therapy for Depression in a Cardiac Transplant Patient

Received August 25, 2000; revised February 13, 2001; accepted February 23, 2001. From the Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore MD. Address reprint requests to Dr. Lee, Meyer 248, Department of Psychiatry and Behavioral Science, Johns Hopkins Hospital, 600 North Wolfe Street, Baltimore, MD 21287–5371. Email: hochang{at}jhmi.edu

Key Words: Depression • Cardiac Transplant • Electroconvulsive Therapy

Lingering limitations in social, occupational, and social functioning may limit a patient's quality of life after a heart transplant. The survival rate of patients at 1 year and 3 years post—heart transplant are 85% and 75%, respectively.¹ A 1996 epidemiological study of 154 heart transplant recipients (83% men) reported lifetime prevalence rates of major depression at 23.7% and 17.3% pre- and 12 months posttransplant, respectively.² When pharmacotherapy fails, electroconvulsive therapy (ECT) is often a life-saving treatment option for the treatment of depression. There have been two case reports of the successful use of ECT in patients with major depressive disorder who had cardiac transplant surgery 13 months and 5 years before receiving ECT.^3,4 The following case report describes the successful use of ECT in a depressed patient who was treated less than 3 months after cardiac transplant surgery. To our knowledge, this is the shortest duration between heart transplant surgery and a successful course of ECT.

Case Report

Mr. P. was a 51-year-old married black man who was admitted to the Johns Hopkins Hospital psychiatric service for treatment of a major depressive episode in June 1999. He had undergone a cardiac transplant in March 1999. He had no family history of psychiatric illness. He had an unremarkable birth, development, and childhood. After graduating from high school, Mr. P. worked in a steel mill for 20 years. He then became a bartender for 7 years. During this period, Mr. P. developed alcoholism. He was married for 30 years and had three sons who are in good health. He had a 30 pack/year history of smoking cigarettes and was a heavy drinker of alcoholic beverages. He quit smoking and drinking 5 years before cardiac transplant. His medical problems before transplant included chronic obstructive pulmonary disease, pulmonary hypertension, anemia of chronic illness, and a history of paroxysmal atrial fibrillation. He was diagnosed with idiopathic dilated cardiomyopathy in 1987 and had a gradual deterioration of cardiac function. In March 1998, he had a left ventricular assist device placement, which was complicated by an embolic cerebrovascular accident in the right middle cerebral artery distribution. Subsequently, he stayed at the Johns Hopkins Hospital for the next 12 months, waiting for a cardiac transplant, which he finally received in March 1999. His transplant surgery and the postoperative course was unremarkable. He was noted to be in good spirits and was discharged home for physical therapy and outpatient follow-up with his cardiologist in April 1999.

After his discharge, Mr. P. showed little motivation in rehabilitation, despite the fact that his health was improving. He became anhedonic and anergic, remaining in bed for much of the day. His appetite decreased, as did his oral intake of both food and fluids. He expressed passive death wishes and intermittently had suicidal thoughts of electrocuting himself. Eventually, he was admitted to the psychiatric unit of a local community hospital with diagnoses of depression and dehydration. In the hospital, Mr. P. underwent a 2-week trial of citalopram (up to 60 mg/day) which was continued and venlafaxine (75 mg) was added as "augmentation" after 8 weeks, but Mr. P. remained severely depressed, and his poor oral fluid intake worsened his preexisting renal insufficiency. Therefore, in June 1999, he was transferred to the Johns Hopkins Hospital for consideration for ECT.

At the time of admission to the psychiatric floor, Mr. P.'s mental status examination revealed an alert and attentive black man who made intermittent eye contact. He was notably psychomotor-retarded. He did not have any abnormal movement. He was initially cooperative with the exam, but he became increasingly irritable. His speech was monotonous and low in volume. There was latency in his answers. He did not have formal thought disorder or loose association. He described his mood as "low," and he appeared sad and constricted in his affect. His self-attitude was diminished. He had passive death wishes and suicidal thoughts. He was anergic and complained of early morning awakenings. No delusions, hallucinations, obsessions, compulsions, or phobias were elicited. The patient's symptoms satisfied DSM-IV criteria for depression. On Mini-Mental State Exam,⁵ Mr. P. scored 25 out of 30, missing 2 points on orientation, 1 point on attention, 1 point on recall, and 1 point in language skills. His Montgomery Asberg Depression Rating Scale (MADRS)⁶ was 41 out of 60. The MADRS scores correlates significantly with the Hamilton Rating Scale for Depression.

On physical examination, Mr. P.'s vital signs were normal and he was afebrile. His cardiac, pulmonary, and abdominal exam was unremarkable except for previous surgical scars. His neurological exam was consistent with a previous cerebrovascular accident with left hemiparesis with an upper motor neuron pattern of weakness, most noticeable in his left upper extremity. His left toe was up-going on the Babinski test. He was on citalopram (20 mg po qd) and venlafaxine (37.5 mg po bid). For immunosuppression, he was on prednisone (15 mg po bid), cyclosporine (Neoral; 75 mg po), and azathioprine (Imuran; 4 tablets/day). He was on acyclovir (200 mg tid), sulfamethoxazole (Bactrim DS; 1 tablet po qweek), and nystatin (swish and swallow qid) for prophylaxis for oral thrush. Other medications included diltiazem CD (240 mg qd) for hypertension, omeprazole (Prilosec; 20 mg qd) for gastritis, pravastatin (40 mg qd) for hypercholesteremia, coated aspirin (81 mg qd) and heparin (5,000 units subcutaneously bid). His initial laboratory studies included a Heme 8, which was notable for a hematocrit of 29.7 and a platelet count of 135,000. Electrolytes revealed worsening of his renal insufficiency because of his dehydrated state. Blood uric acid was 56 and creatinine was 3.0. His malnourished state was reflected by his serum albumin level of 2.3. His hepatic function panel, TSH, PT/PTT, serum vitamin B₁₂ level, and RBC folate level were normal. Urinalysis and urine toxicology results were unremarkable.

On admission to the psychiatric unit, a cardiac team was consulted to help ascertain Mr. P.'s appropriateness for ECT. Mr. P. had had a cardiac transplant less than 3 months before admission. Given the severity of his depressed state and a stable cardiac status (with a recent echocardiogram that showed mild left ventricular hypertrophy and no other abnormality), the cardiology consultation team decided that Mr. P. was an appropriate candidate for ECT. After he consented to ECT, citalopram and venlafaxine were tapered over 3 days while he continued to take his other medications. Subsequently, Mr. P. received four right unilateral ECT treatments with brief-pulse, square-wave stimulus (pulse frequency 70 Hz; pulse width, 1 msec; stimulation duration, 2 sec) and had seizure durations of between 25 and 40 sec. Esmolol and nitroglycerin were given during the procedure for control of transient high blood pressure (systolic blood pressure between 190 and 210 mmHg and diastolic blood pressure between 90 and 105 mmHg) and tachycardia (between 100 and 140 bpm) during and immediately after the seizures. He experienced no other cardiac complications. He promptly recovered without incident after each seizure other than initial confusion. After his fourth ECT, Mr. P.'s mood was noticeably improved, and his MADRS score was 15 out of 60.

Two more ECT treatments had been planned, but Mr. P. developed acute severe thrombocytopenia (45,000 platelets) that the hematology consultation team determined was primarily because of his immunosuppressive medication. Being concerned about possible intracranial hemorrhage due to thrombocytopenia during ECT, we decided to postpone further treatments. Mr. P.'s thrombocytopenia promptly resolved after discontinuation of the immunosuppressive medications, and he remained euthymic for the rest of the 2 weeks of the hospitalization. Because his improved mood was sustained without further ECT, we decided to discharge him to outpatient management without psychotropic medications. His discharge MADRS score⁶ was 6.

Five months after being discharged from the psychiatric service, Mr. P. has continued to do well mentally and physically. He is actively participating in his rehabilitation, and neither Mr. P. nor his family have reported any depressive symptoms during his outpatient visits.

Discussion

ECT treatment for post—cardiac transplant patients is notable for inducing acute hemodynamic perturbations on a denervated heart. Transient tachyarrhythmias during and after the seizure are mediated by the major catecholamine surge induced by ECT. The termination of catecholamine action is determined primarily by neuronal norepinephrine uptake. The greatest proportion of endogenously released norepinephrine is removed locally within the heart, but the mechanism for norepinephrine removal disappears after cardiac denervation.⁴ For this reason, Pargger et al.⁴ suggest that there might be "cardiac supersensitivity" to catecholamines in a transplanted heart.

Indeed, our patient did have brief episodes of an increase in pulse rate and blood pressure during ECT treatment. However, his pulse rate and blood pressure were easily managed with a combination of a beta-blocker and nitroglycerin. Conversely, because a transplanted heart is denervated, the risk of bradyarrhythmias during ECT may actually be decreased because of lack of vagal innervation.³

The vulnerability of post—cardiac transplant patients to depression is of major concern as several studies have indicated that depression is associated with physical morbidity and mortality after heart transplantation.^8,9 Dew et al.² report that the 1-year rate of incidence of new onset post—transplant major depression among persons with no prior history is 11%. The incidence of major depression in a community sample, not selected on the basis of physical health status, is 1.3%, and a community sample of chronically physically ill persons is 2.2%.⁷ Early detection and treatment of depression may benefit cardiac transplant patients significantly in their recovery and quality of life. In this case report, we describe successful treatment of a depressed patient with ECT who had cardiac transplant surgery less than 3 months before ECT treatment. ECT should remain a treatment option for depressed cardiac transplant patients because it appears to be both safe and effective for depression in this special patient population.

REFERENCES

1. Hosenpud JD: Cardiac transplantation, in Congestive Heart Failure: Pathophysiology, Diagnosis, and Comprehensive Approach to Management, edited by Hosenpud JD, Greenberg BH. New York, Springer-Verlag, 1994, pp. 717-738
2. Dew MA, Roth LH, Schulberg HC, et al: Prevalence and predictors of depression and anxiety-related disorders during the year after heart transplantation. Gen Hosp Psychiatry 1996; 18(6 suppl):48S-61S
3. Kellner CH, Monroe RR, Burns C, et al: Electroconvulsive therapy in a patient with a heart transplant. N Engl J Med 1991; 29:663
4. Pargger H, Kaufman MA, Schouten R, et al: Hemodynamic responses to electroconvulsive therapy in a patient 5 years after cardiac transplantation. Anesthesiology 1995; 83:625-627[Medline]
5. Folstein MF, Folstein SE, McHugh PR: "Mini-mental state." A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975; 12:189-198[CrossRef][Medline]
6. Montgomery SA, Asberg M: A new depression scale designed to be sensitive to change. Br J Psychiatry 1979; 134:382-389[Abstract/Free Full Text]
7. Eaton WW, Kramer M, Anthony JC, et al: The incidence of specific DIS/DSM-III mental disorders: data from the NIMH Epidemiologic Catchment Area Program. Acta Psychiatr Scand 1989; 79:163-179[Medline]
8. Dew MA, Kormos RL, Roth LH, et al: Early post transplant medical compliance and mental health predict physical morbidity and mortality one to three years after heart transplantation. J Heart Lung Transplant 1999; 18:549-562[CrossRef][Medline]
9. Deshields TL, McDough EM, Mannen RK, et al: Psychological and cognitive status before and after heart transplantation. Gen Hosp Psychiatry 1996; 18(6S):62S-69S

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