Dasatinib
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Pulmonary arterial hypertension: case report A 59-year-old woman developed pulmonary arterial hypertension during treatment with dasatinib for chronic myeloid leukaemia. The woman presented to the emergency room with syncope. She had a progressive shortness of breath with minimal activity and precordial resting chest pain for 1 month before the presentation. Her medical history was significant for heart failure with preserved ejection fraction, severe obstructive sleep apnoea, deep vein thrombosis and pulmonary embolism for 10 years, for which she had been receiving warfarin. She had been receiving dasatinib 140mg daily [route not stated] for chronic myeloid leukaemia for 4.5 years before the presentation. Her family history was negative for pulmonary hypertension and heart failure. She had a history of smoking (50 pack-years), which she had quit 23 years ago. She was afebrile in the emergency room with a heart rate 82 beats/min, BP 122/77mm Hg, respiratory rate 20 breaths/min, and saturation 96% on room air. She was alert, oriented, and under mild distress due to chest discomfort. Physical examination of her lung was clear, with good chest excursions and air entry. No peripheral oedema, clubbing or cyanosis were seen. Her ECG revealed normal sinus rhythm and nonspecific ST-segment and T-wave changes. Brain natriuretic peptide levels were increased. A chest x-ray revealed an enlarged pulmonary conus. A contrast-enhanced CT scan of the chest revealed right ventricular and pulmonary artery enlargement with no evidence of pulmonary embolism. A twodimensional echocardiogram was then performed, which revealed significant pressure and volume overload of the right ventricle with compression of the left ventricle along with a dilated inferior vena cava, right ventricular hypertrophy with prominent trabeculations, a small pericardial effusion, and severe pulmonary hypertension with an estimated pulmonary artery systolic pressure 100mm Hg. The woman was provisionally started on a long-acting unspecified bronchodilator and diuretic agents, with some clinical improvement. She was then discharged the next day with a close follow-up in the pulmonary hypertension clinic. Subsequently, she underwent right heart catheterisation, which revealed normal right atrial pressure, but severely elevated pulmonary artery pressures. Her pulmonary capillary wedge pressure was 14mm Hg, with a transpulmonary pressure gradient 27mm Hg, cardiac output 4.6 L/min, and pulmonary vascular resistance 5.9 Wood units. A diagnosis of dasatinib-induced pulmonary arterial hypertension was confirmed. Her treatment with dasatinib was held and she was started on nilotinib. She was also initiated on a dual combination pulmonary artery vasodilator therapy with tadalafil and macitentan. As a result, a gradual, but significant improvement of her symptoms was noted along with clinical and echocardiographic improvement of her pulmonary hypertension. An echocardiogram after 11 months revealed near-total resolution of her right heart changes as compared to the ec
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