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Hypersensitivity Myocarditis and Necrotizing Coronary Vasculitis by Clomipramine Causing Steroid-Sensitive Cardiogenic Shock.

February 2019 1 Andrea Frustaci, MD Fabrizio Armando Ferilli, MD Cristina Chimenti, MD, PhD Cardiogenic shock is a cardiovascular emergency which appropriate management is strictly correlated to the prompt recognition of the underlying cause and pathway. Drug-related myocarditis is a rare disorder potentially responsible of acute cardiac deterioration. However, its recognition occurs usually at postmortem. A 48-year-old man, under treatment with clomipramine (75 mg bid) in the past 3 months for depression was admitted because of palpitation, progressive dyspnea, and hypotension (blood pressure 80/60 mm Hg) appeared 1 week earlier. He was an otherwise healthy subject and 6 months earlier had had normal hematochemical screening, blood pressure, ECG, and 2-dimensional echocardiogram. After admission he developed atrial fibrillation at mean heart rate of 150 bpm, a severe impairment of cardiac function (left ventricular ejection fraction 12% at 2-dimensional echocardiogram; Figure 1A and 1B; Movie I in the Data Supplement) with normal left ventricular end-diastolic diameter (55 mm), and pulmonary edema, that required orotracheal intubation and a ventricular assist device (extra corporeal membrane oxygenation) implantation. Routine serological and hematologic investigations were normal while leukocytes (11.5×103; neutrophils 75% and eosinophils 10%) and troponin I (2.8 μg/L; nv<0.030) were elevated. The patient was submitted to coronary angiography showing no coronary stenosis and then to left ventricular endomyocardial biopsy. Four tissue samples were processed for histology, immunohistochemistry, and polymerase chain reaction for the most common cardiotropic viruses, including adeno, entero, cytomegalo, herpes, hepatitis C, EpsteinBarr, Influenza A/B, paramixo-virus, and Parvovirus B19. Histology showed extensive inflammatory infiltrates represented by CD45RO+ T lymphocytes (Figure 2A) and degranulated eosinophils adherent to the adjacent myocytes and associated to cell necrosis(Figure 2B). Several intramural vessels were similarly infiltrated with necrosis of their wall (Figure 2C). Immunologic studies including determination of antinuclear antibody, anti-DNA, anti-neutrophil cytoplasmic antibodies, and anticardiolipin antibodies were negative. No viral genome was detectable at polymerase chain reaction. Clomipramine administration was stopped and the patient was treated with high dose steroids (methylprednisolone 1 g/die intravenously) for 3 days and then with 1 mg/kg die prednisone orally. He manifested a progressive and remarkable clinical improvement with recovery of sinus rhythm to 85 bpm, increase in blood pressure to 140/80 mm Hg, and after 10 days a complete recovery of left ventricular contractility (ejection fraction 50% at control 2-dimensional echocardiogram; Figure 1C and 1D; Movie II in the Data Supplement) associated to reduced left ventricular (from 122 to 90 mL) volume. Extra corporeal membrane oxygenation was removed. Hypersensitivity myocarditis is an uncommon drug-related disorder. Its incidence, however, appears underestimated having been reported in up to 0.47% of large autopsy series.1Various agents have been implicated including antibiot© 2019 American Heart Association, Inc. CARDIOVASCULAR IMAGES