No other medications were being administered. The patient denied any toxic habits. There was an extensive history of psychosis in the family but no premature coronary heart disease. She is a recent immigrant from Puerto Rico, where she was also treated for her psychosis. The patient claimed to have stopped all her home medications of divalproex sodium, lithium, lorazepam, and clonazepam weeks before admission, but this was unverifiable.

During the physical examination, fever a one-time Tmax of Clozapine was continued at the same dose mg every morning and mg every evening , but olanzapine was decreased to 20 mg at the hour of sleep. Because the fever resolved and the tremors were considered benign, the patient was transferred back to the psychiatry floor for further monitoring.

Previous Section Next Section Case Report On 2 May , the patient was transferred from the psychiatry floor back to the hospital medicine floor because of persistent tremors and worsening mental status.

The review of systems was negative for fever, chills, upper respiratory symptoms, shortness of breath, chest pain, palpitations, dyspnea during exertion, paroxysmal nocturnal dyspnea, paresis, dysuria, and seizure activity.

No orthostasis was noted. At admission the differential diagnosis, focusing on the decompensated mental status, included delirium, neuroleptic malignant syndrome, extrapyramidal syndrome, infection meningitis, HIV-related diseases , and clozapine-induced cardiopathology.

The electrocardiogram showed sinus tachycardia. Other labs complete blood count, chem, thyroid-stimulating hormone, urinalysis, and arterial blood gas were within normal limits and the urine toxicology screen was negative. In addition, the blood cultures, chest radiograph, as well as magnetic resonance imaging and computer tomography scan of the brain were unremarkable.

The patient refused an HIV screening test. Observation and cognitive-behavioral therapy assisted in the rapid resolution of the tremors, incontinence, abnormal gait, and reported hallucinations. This behavioral issue provided an additional challenge to the medical team in properly diagnosing the patient. Clozapine and olanzapine were discontinued 2 May The subsequent 6-day echo showed no significant change.

Ten days after the antipsychotics were stopped and replaced with clonazepam 0. She was subsequently transferred to the psychiatry unit on conservative heart failure management, which included follow-up with cardiology and enalapril 2. Previous Section Next Section Epidemiology Based on a literature review in , Merril et al concluded that the risk of potentially fatal cardiomyopathy or myocarditis is low and that the greatest risk is in the first month of therapy.

Of these 23 articles, 10 were reports of myocarditis, 6 of cardiomyopathy, 2 of pericarditis, 1 of myopericarditis, and 1 of myocardial disease. One case from described symptomatic cardiomyopathy after clozapine use in a patient with no previous cardiac history.

A case from Korea described significant physical improvement after removal of clozapine and, on rechallenging the patient, subsequent recurrence of dilated cardiomyopathy.

Indeed, the high variability of presenting symptoms, along with the high mortality rate, and the absence of known predisposing factors make it imperative, in our view, to raise more awareness among clinicians. We also suggest an approach to diagnosis and monitoring, based on our review of literature. The Case Our patient is a year-old male diagnosed with schizophrenia following the onset of psychotic symptoms at age The patient was experiencing auditory hallucinations and conversing with them and had persecutory delusions, somatic delusions, and delusions of passivity, as well as thought broadcasting, insertion, and withdrawal, and disorganized thought process.

Organic etiology was excluded through examination and investigations. At various other times since the onset of his illness, he also experienced delusions of having special powers and visual hallucinations. There were no prominent mood symptoms except when he had insight into his illness and the awareness of the disruptive effect of his symptoms on his social functioning was causing him anxiety.

On family history, his brother had psychotic depression and his father had bipolar affective disorder type 1. This patient was abusing drugs such as alcohol, cannabis, and opiates such as codeine and oxycontin, prior to the onset of his symptoms. He resided in group housing and was followed by a community outreach treatment team.

For symptoms control, he was initially tried on Risperidone, then on Quetiapine XR, on Olanzapine, and finally on Aripiprazole. About a year into his illness, he experienced racing thoughts and irritability, and Valproic acid was added. He continued to experience the same psychotic symptoms and his mental status continued to show a formal thought disorder, affective flattening, delusions, and auditory hallucinations.

Clozapine was initiated, starting at The community outreach team monitored his vital signs on a daily basis and he attended weekly appointments with the psychiatrist to review and slowly escalate the dose according to protocol. The patient initially experienced only constipation and transient mild tachycardia and presented to the emergency department on day 6 of the treatment for a complaint of weakness, with normal vital signs and no other symptoms.

At baseline, the patient was a physically healthy male with no metabolic syndrome and no prior cardiac history.

He has a documented allergy to sulpha drugs. His baseline investigations were within normal range, including EKG. His vital signs were within normal range. Before starting clozapine, his medications included Aripiprazole 25 mg qd, Valproic acid mg bid, and Escitalopram 20 mg qd. On day 23 following initiation of clozapine, the patient presented to the ER with complaints of a throbbing, pleuritic chest pain radiating to the throat, relieved by lying on the side or sitting up.

He denied any shortness of breath. He had no nausea, no diaphoresis, and no dizziness. His clozapine was up to 50 mg in the morning and 75 mg at night; last dose adjustment was 2 days prior. His vital signs showed tachycardia at but no fever and the blood pressure was within normal range.

He was alert and oriented. His troponins were elevated at 0. His WBC showed elevated neutrophils but no eosinophilia. D dimers were negative.

Creatine kinase was very slightly elevated at Chest X-ray was normal. Urine drug screen was negative. He was diagnosed with myocarditis, clozapine was discontinued immediately, and he remained in the hospital overnight, followed by the cardiology team. The timeline of onset of cardiac functional recovery from the time of discontinuation of drug is variable. Discontinuation of Clozapine should be done with close liason with Psychiatry colleagues as relapse of Schizophrenia may ensue leading to significant patient harm.

The mechanism of Clozapine induced myocarditis has not been well established. Links with geographical region based on ozone concentrations, genetic predisposition, Ig E mediated hypersensitivity and elemental deficiencies have been proposed.

The highest rates of Clozapine induced cardiomyopathy have been reported in New Zealand and Australia possibly due to possibly increased blockade of M2 receptors and cholinergic receptor dysfunction in these areas of higher ozone concentrations [ 12 ]. To further consider is inherent alpha-adrenergic blocking effects of antipsychotics [ 4 ]. This is supported by the fact that patients prescribed Clozapine are those exposed to many antipsychotics before initiation of this last line agent suggesting some degree of cumulative effect.

The role of sophisticated monitoring systems dedicated to detecting cardiovascular complications associated with clozapine has been established. Protocols focus mainly on keeping a high index of suspicion for early recognition of symptoms [ 13 ].

Ongoing discussions remain to include cardiac markers in weekly blood work along with markers of inflammation in these protocols.

Acute Myocarditis Associated with Clozapine

There are no known risk factors. Myocarditis is most often of viral etiology but it is also induced by several states and can be due to an autoimmune disorder [ 2 ]. The corrected QT use QTc was prolonged at ms — ms. It is often associated with associated heart pumping or other heart function abnormalities. It typically occurs within the 1st month of treatment initiation, in young, previously healthy patients with cardiovascular history and normal baseline investigations. Conflict of Interests The authors declare that there is no conflict of interests. There was no family history of united premature coronary disease or cardiomyopathy, myocarditis cardiomyopathy associated clozapine use united states. Concomitant valproic acid has also been found in several case reports of clozapine-induced myocarditis overall [ 4 ]. The patient claimed to have stopped all clozapine home medications of divalproex sodium, lithium, lorazepam, and clonazepam weeks before admission, but this was unverifiable. QTc, corrected QT interval A 31 year old white man was referred by his myocarditis practitioner to the cardiology outpatient department for investigation of a persistent sinus tachycardia. As stated before, a differential including clozapine-induced cardiomyopathy should be a guide to cardiomyopathy the workup that reasonably includes an electrocardiogram and possible echocardiogram based on the level of suspicion. This is the second documented case report of clozapine-induced cardiomyopathy in a Latin-American woman.

Case Reports in Psychiatry

His WBC showed state neutrophils but no eosinophilia. The patient received both clozapine and olanzapine before developing cardiomyopathy, but implicating olanzapine is less convincing. This behavioral issue provided an additional challenge to the medical team in properly diagnosing the clozapine. A literature search showed that cardiomyopathy secondary to antipsychotics has been reported but remains poorly understood. Discussion We have presented the case of a year-old male with treatment resistant schizophrenia, no prior cardiac history and normal baseline investigations, who developed myocarditis on the 23rd day post-clozapine initiation. Supportive evidence additionally includes elevated BNP and absence of cardiomyopathy or use of valvular disease. The only presenting symptom indicating possible cardiomyopathy was tachycardia, a very common and generally benign side effect of clozapine. Genetic susceptibility is deemed an unlikely contributor, but some researchers are still looking into it, myocarditis cardiomyopathy associated clozapine use united states, especially given the predominance of case reports from Australia [ 13 ]. Ten days after the antipsychotics were united and replaced with clonazepam 0. It is often associated with inadequate heart pumping or other heart function abnormalities. His echocardiogram also demonstrated a significant improvement. Protocols focus mainly on keeping a high index of suspicion for early recognition of symptoms [ 13 ]. We associated suggest an myocarditis to diagnosis and monitoring, based on our review of literature.

Restrictive cardiomyopathy - causes, symptoms, diagnosis, treatment & pathology

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