In contrast to heparin, hirudin does not require antithrombin III as a cofactor, is not inactivated by antiheparin proteins, has no direct effects on platelets and may also inactivate thrombin bound to clot or the subendothelium. In humans, experience with r-hirudin in preventing or treating venous thromboembolism is very preliminary. However, r-hirudin achieved promising results in patients with unstable angina, or following coronary angioplasty. At present, the discovery of a r-hirudin regimen that is more efficacious than heparin and at least as safe needs a reappraisal of the drug in further trials. Most commonly these thrombi are found in the veins of the lower extremities, the thighs and calves.
Venous thrombosis can occur in healthy as well as sick individuals.
A pulmonary embolus is actually a clot that has broken free from a vein wall and has traveled to a lung, causing blockage in an artery of that lung. When an embolus blocks a blood vessel in the lung, breathing is compromised and death may ensue. Symptoms indicating that the blood clot has moved to the lungs may be absent, or may include shortness of breath, chest pain, sudden unexplained cough, and rapid heart beat. These symptoms may be due to other causes, so it is important to seek immediate medical attention if any of these symptoms occur. For this reason, venous thrombosis is a very serious medical condition and aggressive treatment is warranted.