Androgenic-Anabolic Steroid (Boldenone) Abuse as a Cause of Dilated Cardiomyopathy

A 34-year old, previously healthy male, presented to the ER with worsening dyspnea over a period of three weeks and the appearance of blood tinged sputum. Soon after presentation, the patient was hypoxemic and required mechanical ventilation. Chest X-ray demonstrated bilateral infiltrates and he was admitted to the ICU with the tentative diagnosis of acute respiratory distress syndrome. Investigation by PICCO, Suggested the presence of heart failure were and the patient was transferred to the ICCU. On admission, the patient maintained normal blood pressure but still needed mechanical support with high FiO2 values to maintain adequate oxygenation. Physical examination was remarkable for his muscular appearance. The heart sounds were regular. The lungs were clear to auscultation, although chest X-ray revealed signs of pulmonary edema. Blood count was remarkable for hemoglobin of 21 gr/dl with hematocrite of 65%. His blood chemistry showed creatinine level on 1.74 mg/dL, with no electrolytes imbalance. LFT were normal, total protein and albumin levels were normal, elevated CK with normal TnT. CRP 10 mg/L (normal level <10 mg/L). Blood cultures and panel of common respiratory infections were all negative. ECG showed normal sinus rhythm, with p pulmonale, signs of hypertrophy and inverted T waves in chest leads. Swan-gantz Cather measurements revealed cardiac output (CO) 3.9, capillary wedge pressure 34 mmHg, SVR 2070 and CI 2.2 consistent with cardiogenic shock. Transthoracic echocardiography demonstrated severe global dysfunction (left ventricular ejection fraction = 20%) with severely dilated left ventricle 5.1 cm (end-systolic diameter), asymmetric hypertrophy (Septum 14 mm, Posterior wall 12 mm). Minimal mitral and tricuspid regurgitation were also noted (Table 1 and Figure 1).