Prevention
Anticoagulants are drugs used to prevent the formation of blood clots, reducing the risk of stroke, heart attack and pulmonary embolism. Heparin and warfarin are used to inhibit the formation and growth of existing thrombi, with the former used for acute anticoagulation while the latter is used for long-term anticoagulation. The mechanism of action of heparin and warfarin are different as they work on different pathways of the coagulation cascade. Heparin works by binding to and activating the enzyme inhibitor antithrombin III, an enzyme that acts by inactivating thrombin and factor Xa. In contrast, warfarin works by inhibiting vitamin K epoxide reductase, an enzyme needed to synthesize vitamin K dependent clotting factors II, VII, IX, and X. Bleeding time with heparin and warfarin therapy can be measured with the partial thromboplastin time (PTT) and prothrombin time (PT), respectively. Treatment
Once clots have formed, other drugs can be used to promote thrombolysis or clot breakdown. Streptokinase, an enzyme produced by streptococcal bacteria, is one of the oldest thrombolytic drugs. This drug can be administered intravenously to dissolve blood clots in coronary vessels. However, streptokinase causes systemic fibrinolytic state and can lead to bleeding problems. Tissue plasminogen activator (tPA) is a different enzyme that promotes the degradation of fibrin in clots but not free fibrinogen. This drug is made by transgenic bacteria and converts plasminogen into the clot-dissolving enzyme, plasmin. Recent research indicates that tPA could have toxic effects in the central nervous system.
Syphilitic aortitis  is inflammation of the aorta associated with the tertiary stage of syphilis infection. SA begins as inflammation of the outermost layer of the blood vessel, including the blood vessels that supply the aorta itself with blood, the vasa vasorum. As SA worsens, the vasa vasorum undergo hyperplastic thickening of their walls thereby restricting blood flow and causing ischemia of the outer two-thirds of the aortic wall. Starved for oxygen and nutrients, elastic fibers become patchy and smooth muscle cells die. If the disease progresses, syphilitic aortitis leads to an aortic aneurysm. Overall, tertiary syphilis is a rare cause of aortic aneurysms. Syphilitic aortitis has become rare in the developed world with the advent of penicillin treatments after World War II. Signs and symptoms
The infection often has no symptoms until the patient develops an aneurysm because of the aortic dilatation. The disease is often discovered after a routine checkup of the heart and aorta. Although is easy to be overlooked, other symptoms of tertiary syphilis might appear such as gummas and symptoms of neurosyphilis (headache, stiff neck, gait abnormality, dementia etc). Additionally, in rare cases, chest pain and shortness of breath might appear as a result of the damage of the aorta and heart valve. Pathogenesis
Inflammatory involvement of tertiary syphilis begins at the adventitia of the aortic arch which progressively causes obliterative endarteritis of the vasa vasorum.