A young man with psychosis whose heart is racing

The etiology of secondary cardiomyopathy includes all of the following except:
a) tachycardia-induced
b) autoimmune
c) radiation-induced
d) infiltrative
e) endomyocardial

The authors’ observations
Cardiomyopathies are diseases of the heart muscle causing mechanical and electrical dysfunction. This group of diseases has a range of symptoms, causes, and treatments. Disease manifests typically as arrhythmia, systolic dysfunction, or diastolic dysfunc­tion. Classification systems are based on origin, anatomy, physiology, primary treat­ments, method of diagnosis, biopsy, histopa­thology, and symptomatic state.

The American Heart Association Scientific Statement5 distinguishes cardiomyopathies by degree of organ involvement. Diseases confined to the heart are defined as primary cardiomyopathy, which may have a genetic, acquired, or mixed cause. Acquired causes include inflammatory (myocarditis), stress (Takotsubo), peripartum, and tachycardia. Cardiomyopathies that are part of general­ized systemic disorders are defined as sec­ondary cardiomyopathy (Table 1).

Secondary cardiomyopathies have many causes. These include toxicity (medica­tions or alcohol), cancer therapy, infiltra­tive, storage disease, and endomyocardial, inflammatory, autoimmune, endocrine, and neurologic diseases.⁵

Evaluation of suspected cardiomyopathy begins with a history and physical focused on identifying causative factors. Selective testing, based on pretest probabilities, might include lab testing, ECG, and echocardiogra­phy, and can narrow the differential diagno­sis. When toxin-induced cardiomyopathy is suspected, withdrawing the toxin and moni­toring for improvement is recommended. The treatment and prognosis for cardiomy­opathies vary, based on the cause.⁶

Review of the literature
After 23 cases of fatal and non-fatal myo­carditis were found in a study of 8,000 patients starting clozapine,⁷ manufacturers in Australia introduced clinical guidelines. Before initiating clozapine, they recom­mended, clinicians should:
• screen for cardiac symptoms
• screen for a family history of heart disease
• obtain baseline ECG
• obtain baseline markers of myocardial damage (troponin assay and serum creatinine)
• obtain baseline echocardiogram
• repeat cardiac monitoring after the first and second week and then repeat in 6 months
• maintain a high degree of vigilance for signs and symptoms of cardiac toxicity throughout clozapine treatment.^8,9

After studying 38 cases of clozap­ine-induced myocarditis—3 fatal— Ronaldson et al¹⁰ listed primary diag­nostic features as:
• tachycardia (heart rate >100 beats per minute)
• heart rate >120 beats per minute
• temperature >37°C
• chest pain
• troponin I/T level >2 ng/mL
• C-reactive protein (CRP) > 100 mg/L
• erythrocyte sedimentation rate >50 mm/h.

Among non-fatal cases, symptoms abated after clozapine was discontinued. In 36 of the 38 cases, symptoms emerged 14 to 22 days after clozapine was started. For tachycardia to be considered a diagnostic feature, it must persist for at least 24 hours; if the heart rate is ≥120 beats per minute, however, persistence is not a criterion. It was thought that elevated CRP might herald disease onset; the authors suggest that CRP >50 mg/L should warrant increased monitoring with daily ECG and troponin levels.

Authors’ recommendations include:
• measuring troponin and CRP and order an ECG at baseline and at 7, 14, 21, and 28 days
• examining patient for signs and symp­toms of illness at these same intervals
• considering chest pain or fever as an indicator of cardiomyopathy
• asking patients to report any illness during this 4-week period
• if ECG is abnormal or troponin ele­vated, decreasing clozapine pending further investigation.¹⁰

When medications fail
We had to discontinue Mr. C’s clozapine, which meant that the therapeutic relation­ship established between him and the psy­chology fellow became an important and, at times, the only bond between him and the medical team while olanzapine was initiated. The alliance between patient and clinician is an important factor for positive prognosis in mental health treatment.^11-13 Priebe and McCabe¹⁴ asked if the therapeu­tic relationship in psychiatry is “the basis of therapy or therapy itself?” In a review of studies that used an operationalized mea­surement of the therapeutic relationship in treating severe mental illness, the authors concluded that the therapeutic relation­ship is a reliable predictor of outcome.¹⁵

In Mr. C’s case, the psychology fellow, who also works with the Partial Hospitalization Program/Intensive Outpatient Program (PHP/IOP), joined the treatment team on the inpatient unit a few days into hospitalization. Eleven meetings, includ­ing a discharge session, were held between the psychology fellow and the patient during the inpatient hospitaliza­tion. Mr. C also participated in a daily group session, facilitated by the psychol­ogy fellow.

Maintaining recognition of the bound­ary disturbance that characterizes schizo­phrenic psychoses was important for Mr. C. As Auerhahn and Moskowitz¹⁶ wrote, the inpatient therapist can be transformed by the schizophrenia patient into the all-knowing, all-powerful early mother, which could contribute to substantial improvement in the patient’s functioning and report of symptoms, only to have the patient’s symp­toms return after discharge.