Pulmonary Veno-Occlusive Disease in a Patient with History of Major Depressive Disorder

A 27-year-old man was admitted to our department for the evaluation of dyspnea and syncope. The patient had begun to experience dyspnea on exertion function class II from one year ago which then progressed to function class III in the following 3 months ago. During this time, he had several syncopal episodes. Past medical history was significant for major depressive disorder and the patient was on olanzapine, lithium, clonazepam, sertraline since several years ago. On admission, vital signs included a body temperature of 36oC, respiratory rate of 28/ min, pulse rate of 98 beats per minute and a blood pressure of 95/60 mmHg. The arterial O2 saturation was 85% on room air. Jugular venous pulsation was elevated to the angle of mandible. Carotid artery pulses were brisk and equal bilaterally. No carotid, aortic, or femoral bruits were heard. Peripheral pulses were intact and symmetrical. On cardiovascular examination, the heart rate and rhythm were regular with a prominent P2 component. There was a systolic murmur of grade III/VI intensity best heard at the lower left sternal border. The lungs were clear. No peripheral edema, hepatomegaly, clubbing, or cyanosis was present. Electrocardiography revealed sinus rhythm with a heart rate of 98/min, right axis deviation and incomplete right bundle branch block (Figure 1). Chest X-ray showed enlarged pulmonary arteries, cardiomegaly and prominent interstitial marking in the lower zones (Figure 2). Echocardiography demonstrated normal left ventricular size and function, normal aortic and mitral valves, severe right ventricular enlargement and dysfunction, severe tricuspid regurgitation and pulmonary arterial pressure of 120 mmHg. Routine hematologic workup showed a normal ESR, normal rheumatologic panel (including rheumatoid factor and complement levels), and normal thyroid function tests. Computerized tomographic scan (CT) of the chest revealed multiple enlarged lymph nodes, enlarged main pulmonary artery, bilateral diffuse ground glass opacities and inter lobular septal thickening (Figure 3). Abdominal ultrasonography was normal. Perfusion ventilation scan of the chest demonstrated low probability for pulmonary embolism. The right heart catheterization (RHC) was done via the right subclavian vein and with the method of catheter tip. The RHC data are shown in Table 1. A diagnosis of PVOD was made according the imaging and catheterization data. Unfortunately, the patient did not respond to medical therapy and died after 8 months. Volume 3 Issue 4 2016