The patient, Mr. Zhang, suffered from hypertension and coronary heart disease for a long time, and had suffered from pulmonary artery thromboembolism two years ago. Mr. Zhang lived on the second floor of his house. In recent days, he felt shortness of breath and dyspnea when going upstairs, but did not develop into significant wheezing and chest pain. After completing the physical examination, the respiratory physician recommended that Mr. Zhang undergo cardiac Doppler ultrasound and pulmonary angiography (CTA), and the following day, pulmonary angiography CTA showed emboli embolism in both main pulmonary arteries. After hospitalization, he was again treated with urokinase thrombolysis and subsequently received long-term anticoagulation therapy. May I ask, (1) Is the incidence of pulmonary embolism high? Who is at high risk of developing pulmonary embolism? (2) Is acute pulmonary embolism dangerous? Is it necessary to be hospitalized? (3) Which patients with pulmonary embolism need thrombolytic therapy? Why should they receive long-term anticoagulation? (4) Is warfarin the only oral anticoagulant? Can warfarin be used in combination with enteric aspirin? Comment Pulmonary embolism is a group of diseases or clinical syndromes caused by various emboli entering the pulmonary artery and its branches and blocking the blood supply to the tissues. After embolism, if the lung tissue produces severe blood supply obstruction, necrosis may occur, which is called pulmonary infarction. The most common embolus is a thrombus, and what is commonly referred to as pulmonary embolism refers to pulmonary thromboembolism. The remaining less common ones include neoplastic cells, fat droplets, air bubbles, intravenous drug particles, and long-term deep venous indwelling catheters whose tips can also cause pulmonary vascular block. A large number of studies have shown that the thrombus causing pulmonary thromboembolism mainly originates from the lower limbs and pelvic deep vein thrombosis, and deep vein thrombosis and pulmonary thromboembolism are essentially the manifestations of a disease in different parts and stages, and they are collectively called venous thromboembolism. The incidence of venous thromboembolism in Europe and the United States is very high, and according to the information published by the IUA International Conference in 2006, venous thromboembolism has become the 3rd most common vascular disease, and its incidence is comparable to that of stroke. About 480,000 patients with acute lower extremity deep vein embolism and 210,000 patients with pulmonary embolism occur each year in the United States. Pulmonary embolism ranks as the 3rd leading cause of death from acute cardiovascular disease and is a disease with a very high rate of sudden death. The incidence of pulmonary embolism is found to be 5% to 14% at autopsy. The incidence of pulmonary embolism is up to 25% in the elderly and up to 30%-45% in heart disease patients. There is no exact epidemiological data in China, but Beijing Fu Wai Hospital has reported that among more than 900 cases of cardiopulmonary vascular disease autopsies, 100 cases (11%) of large thrombus blockage above the lung segment were found, accounting for 29% of rheumatic heart disease autopsies, 26% of cardiomyopathy and 19% of pulmonary heart disease, indicating that cardiopulmonary vascular disease is also often complicated by pulmonary embolism. There are three main reasons for the formation of pulmonary embolism: (1) blood stagnation: such as long-term limb braking, prolonged bed rest, hemiplegia and other factors that stagnate venous blood. (2) Intravascular injury: it can be secondary to local injury such as trauma, but also direct injury to blood vessels, infection and other tissue injury, etc.; (3) Blood hypercoagulation. Therefore, in clinical practice, venous thromboembolic disease is generally common in patients who have undergone major surgery (e.g., orthopedic surgery/obstetrical and gynecological surgery, neurosurgery, laparotomy), trauma patients (e.g., severe trauma, multiple fractures, pelvic fractures, spinal injuries, severe cranial injuries, etc.), and stroke patients (especially patients with severe hemiparesis in ischemic stroke). Other factors such as prolonged sitting, prolonged Internet access, long-distance travel by car and airplane are also high-risk factors for the occurrence of venous thromboembolism. The occurrence of deep vein thrombosis is related to the patient’s age, degree of trauma, surgery and postoperative braking time: the older the patient, the more severe the trauma, the longer the surgery, and the longer the postoperative bed rest, the more likely thrombosis will occur. Countermeasures For pulmonary embolism, the first step is to clarify the diagnosis. Although the clinical manifestations include dyspnea and shortness of breath, chest pain, hemoptysis and cough that appear or worsen after activity, the typical “pulmonary infarction triad” (i.e. dyspnea, chest pain and hemoptysis at the same time) is only seen in about 30% of patients. The gold standard for the diagnosis of pulmonary embolism is pulmonary angiography, but this test is an invasive operation with certain risks and needs to be performed in a lying position, which is not suitable for patients who have significant respiratory distress and cannot lie down. Spiral CT angiography and MRI ultra-fast imaging/angiography techniques, which can rapidly complete three-dimensional angiography of the pulmonary artery, have become common methods for diagnosing pulmonary embolism. Among them, spiral CT allows the patient to complete a CT scan in a short period of time with a single breath-hold, which can clearly show emboli in the main and lobar pulmonary arteries and better visualization of a portion of segmental or subsegmental pulmonary arteries. Other diagnostic techniques include radionuclide imaging, electrocardiography, and vascular Doppler ultrasound, but these tests are mostly used as supplemental diagnostic tools. Plasma D-dimer, a cross-linked fibrin degradation product, appears only when fibrinogen formation and breakdown are in a stable state. If plasma D-dimer concentration >500µg/L is used as a positive cut-off value for the diagnosis of vascular embolism, it has good sensitivity (98%) for determining pulmonary embolism and remains high after 3 and 7 days (96% and 93%), but its specificity is not high, and many diseases related to fibrin formation and degradation (such as malignant tumors, infections or inflammatory diseases) can also cause D-dimer is increased. Currently, the main pharmacological treatment strategies in the acute phase of pulmonary embolism are anticoagulation and thrombolysis, with minimally invasive interventional or surgical treatment used only for a small number of patients who are acutely ill and not suitable for pharmacological treatment. Thrombolytic therapy is the most important treatment for severe pulmonary embolism because it can rapidly dissolve some or all of the thrombi in the branches of the pulmonary arteries, restore the blood supply to the lung tissue, reduce the pressure in the pulmonary arteries, and reduce the death and recurrence rates in patients with severe pulmonary embolism. The time window for thrombolytic therapy is generally defined as within 14 days after the onset of disease, and should be implemented as early and carefully as possible with a confirmed diagnosis. Thrombolytic drugs (FDA approved) include: streptokinase, urokinase and rt-PA. However, there are some risks associated with thrombolytic therapy, especially the risk of intracranial hemorrhage. Therefore, thrombolytic therapy should be administered with caution to patients with pulmonary embolism with the following conditions: active internal bleeding, recent spontaneous cerebral hemorrhage, advanced age, severe hypertension that is difficult to control, recent surgery or trauma or gastrointestinal bleeding, and pregnancy. Anticoagulation therapy is the basic treatment for pulmonary embolism, which can significantly reduce the mortality and recurrence rate of patients with pulmonary embolism. Although anticoagulant drugs cannot dissolve thrombus, they can prevent further formation of thrombus. Analysis of several foreign clinical trials on acute pulmonary embolism in recent years has shown that although thrombolytic therapy improves imaging and hemodynamic abnormalities more rapidly than anticoagulation, these benefits are short-lived, with significant advantages only in the first 24 hours, and the difference in thrombus lysis in patients after 24 hours is significantly reduced, and the difference disappears after 7 days until 1 year, with no significant difference in mortality and recurrence rates . There was no difference in clinical prognosis such as mortality or symptom relief between patients treated with thrombolysis and anticoagulation. The duration of anticoagulation therapy depends mainly on the likelihood of recurrence of venous thrombosis. In patients with transient risk factors (e.g., trauma and surgery), anticoagulation therapy is recommended for 3 to 6 months, whereas in patients with recurrent DVT, most clinicians will recommend continued anticoagulation therapy for >12 months or even for life. Tips Traditional oral anticoagulants, mainly warfarin, are prone to bleeding complications and thus require regular monitoring of coagulation during long-term use; many commonly used drugs also enhance or diminish the efficacy of warfarin. This may change in recent years with the introduction of two classes of oral anticoagulants, thrombin inhibitors (e.g., dabigatranate) and factor Xa inhibitors [e.g., rivaroxaban and abixaban]. Currently, dabigatran and rivaroxaban are widely used in Europe and the United States for the prevention of DVT events after orthopedic surgery in adults, with satisfactory safety and efficacy, and without regular monitoring of coagulation parameters.