Smoking is known to induce a hypercoagulable state, which is largely due to the increase in thrombogenic factors. These factors can include various substances in the blood that promote clot formation and increase the risk of thrombosis. Smoking leads to several physiological changes, including increased levels of certain pro-coagulant substances and changes in the endothelial function that can enhance platelet activation and adhesion.
In smokers, there is also a notable increase in inflammatory markers and other compounds such as fibrinogen, which can provide some support for the idea that smoking influences the coagulation cascade. However, the direct impact of smoking on thrombogenic factors is particularly significant as it relates to their role in increasing clot risk. This leads to a greater likelihood of clot formation in the bloodstream, thus contributing to events such as deep vein thrombosis or pulmonary embolism.
Collectively, while various factors are influenced by smoking, the primary increase in thrombogenic factors is indicative of how smoking changes the balance of coagulation and the tendency toward clot formation, thus creating a hypercoagulable state in individuals who smoke.