Key Words: metastatic breast cancer, pulmonary hypertension, tumor microembolism P ulmonary hypertension caused by tumor cell microembolism is a rare occurrence. Although various solid tumors such as breast (1), colon (2), gall bladder (3), stomach (4), and choriocarcinoma (5) have been reported to cause microembolism to lungs causing pulmonary hypertension, diagnosis is usually made at autopsy and antemortem diagnosis is extremely rare. Furthermore, there is little information on response to therapy of this condition (6,7). We describe a patient who had tumor microemboli to lungs from metastatic breast cancer, resulting in pulmonary hypertension. Evidence that pulmonary hypertension was caused by breast cancer tumor microemboli in this patient comes from bone marrow involvement with breast cancer, elevated pulmonary artery pressure, and complete resolution of symptoms and normalization of pulmonary artery pressure with breast cancer-specific treatment. To our knowledge, this is the first case report of complete response of this condition to anti-hormone therapy.
CASEA 66-year-old female was diagnosed with invasive ductal adenocarcinoma of the right breast and underwent right modified radical mastectomy. The tumor size was 1.6 cm and two out of four lymph nodes were involved with cancer. Estrogen receptor was positive and progesterone receptor was negative. HER 2 was not overexpressed. She did not receive adjuvant therapy.Three years after the diagnosis of breast cancer, she presented with rapidly progressive shortness of air of 1 week duration. Examination was remarkable only for respiratory distress at rest and there was no clinical evidence of breast cancer recurrence. Chest examination revealed normal percussion and auscultation and no parasternal lift. Heart examination revealed normal heart sounds, no added sounds, abnormally split sounds or murmurs. There was no cyanosis or lower extremity edema. She required oxygen by nasal cannula to maintain reasonable oxygen saturation. She was ruled out for an acute cardiac event by normal electrocardiogram (EKG) and normal cardiac enzymes. A chest x-ray was completely normal. Computed tomography (CT) of the chest showed no parenchymal abnormalities in the lungs and no evidence of pulmonary embolism, and CT of the abdomen showed no evidence of hepatic or other metastases. EKG revealed elevated pulmonary artery pressure of 77 mmHg with exercise and 60 mmHg at rest. Right heart catheterization confirmed elevated pulmonary artery pressure and there was no evidence of pulmonary thromboembolism. Her pulmonary function tests were normal. A whole body PET scan showed diffuse increased FDG uptake in the marrow and no other areas of abnormal activity. CA 27-29 was elevated 10-fold and CEA was mildly elevated. She underwent bone marrow aspiration which showed marrow replacement with adenocarcinoma that was strongly