Minor chest trauma can cause hemothorax when the bloods ability to clot is diminished as result either of anticoagulant medications or when there are bleeding disorders such as hemophilia. Iatrogenic
Iatrogenic hemothorax can occur as a complication of heart and lung surgery, for example the rupture of lung arteries caused by the placement of catheters, thoracotomy, thoracostomy, or thoracentesis. The most common iatrogenic causes include subclavian venous catheterizations and chest tube placements, with an occurrence rate of around 1% Sometimes, a Swan-Ganz catheter causes rupture of the pulmonary artery, causing a massive hemothorax. It can also be caused by other procedures like pleural, lung, or transbronchial biopsies, CPR, Nuss procedure, or endoscopic treatment of esophageal varices. Iatrogenic hemothorax is more common in people who have chronic kidney disease in the intensive care unit. Nontraumatic
Less frequently, hemothoraces may occur spontaneously. Nontraumatic hemothoraces most frequently occur as a complication of some forms of cancer if the tumour invades the pleural space. Cancers responsible for hemothoraces include angiosarcomas, schwannomas, mesothelioma, thymomas, germ cell tumours, and lung cancer. Significant hemothoraces can occur with spontaneous rupture of small vessels when the bloods ability to clot is diminished as result of anticoagulant medications. In cases caused by anticoagulant therapy, the hemothorax becomes noticeable 4–7 days after anticoagulant therapy is started. In cases of hemothorax complicating pulmonary embolism treatment, the hemothorax is usually on the side of the original embolism.
Patients receiving Angiomax monotherapy had similar rates of overall stent thrombosis (Academic Research Consortium (ARC) definition) at 30 days versus UFH plus a GP IIb/IIIa inhibitor (2.5% vs. 1.9%), with the exception of acute stent thrombosis (<24 hours), which was higher for the bivalirudin-treated patients at 1.3% vs 0.3% for the UFH-GP IIb/IIIa-inhibitor-treated patients.1-Year Results

At 1-year follow-up, a reduction in the incidence of net adverse clinical events (15.7% vs. 18.3%) and major bleeding (5.8% vs. 4.9%) was maintained in the bivalirudin monotherapy group versus UFH plus a GP IIb/IIIa inhibitor group, with no difference in the rate of major adverse cardiovascular events (11.9% vs. 11.9%)
A significant reduction in the rate of cardiac mortality in patients treated with bivalirudin monotherapy versus UFH plus a GP IIb/IIIa inhibitor was maintained at 1 year in the HORIZONS AMI trial (2.1% vs. 3.8%)The incidence of stent thrombosis  at 1 year was also similar between the 2 treatment groups (3.5% in the Angiomax group vs. 3.2% in the UFH plus GP IIb/IIIa inhibitor group).2-Year Results

At 2-year follow-up, a reduction in the incidence of net adverse clinical events (22.3% vs. 24.8%) and major bleeding (6.4% vs. 9.6%) was maintained in the bivalirudin monotherapy group versus UFH plus a GP IIb/IIIa inhibitor group, with no difference in the rate of major adverse cardiovascular events (18.7% vs. 18.8%)
A significant reduction in the rate of cardiac mortality in patients treated with bivalirudin monotherapy versus UFH plus a GP IIb/IIIa inhibitor was maintained at 2 year in the HORIZONS AMI trial (2.5% vs. 4.2%)
At  2-year follow-up, treatment with bivalirudin monotherapy resulted in a 25% reduction in all-cause mortality, representing 15 lives saved per 1000 patients treated (number needed to treat [NNT] = 67 to save 1 life).