New markers of coronary heart disease
A detailed discussion of new biochemical and genetic markers of cardiovascular diseases (CVD) is presented in a separate article on the site. In general, several hemostatic and inflammatory markers, new lipid parameters, cell adhesion molecules, markers of infection and oxidative stress are associated with the stages of atherogenesis, thrombosis or cardiovascular events (SSSob).
Of these new risk factors (RF), only the level of CRP added prognostic information to general risk prediction models, such as the Framingham Risk Scale. High levels of CRP serve as a prognostic factor for cerebral stroke (MI), recurrent coronary events and cardiovascular death. The Centers for Disease Control and Prevention and American Heart Association guidelines endorse the definition of CRP as an adjunct to risk assessment, especially for those in the intermediate risk zone.
In the United States, recently obtained results for women show that 20–30% of people at risk of 5–20%, according to APT III, can be reclassified into a higher or lower group after measuring the level of CRV. Approval of the definition of SRV partially reflects the low cost of assessment, especially in comparison with other approaches to screening based on complex visualization technologies, such as CT, or the definition of calcification of spacecraft. In general, when the level of SRV is used in the general risk prediction algorithm, its values <1.1–3 and> 3 mg / l correspond to the low, intermediate, and high risk of future vascular diseases. Adding a high level of CRP to the formal definition of MS also improves predictive accuracy with respect to vascular events or diabetes. To date, other inflammatory markers, such as lipoprotein-associated phospholipase A2, fibrinogen, and ligand CD40, are of limited value if CRP levels are known.
Other new risk factors (RF) – lipoprotein (a) and homocysteine - are of limited value in general screening, but may be useful in the presence of a premature disease in families prone to atherosclerosis, when there are no clusters of traditional RF. In relation to lipoprotein (a), the availability of an assessment, regardless of apo re-screening, is a significant achievement that helps resolve the inconsistencies of previous reports.
A general restriction on the use of these new markers is the lack of data showing that reducing their level will lead to a decrease in vascular risk, therefore their use is limited to a risk assessment and a motivation for lifestyle changes. For example, although statin therapy reduces CRP, a post-hoc analysis suggests improved outcomes in individuals with elevated CRP, prospective studies testing the use of CRP to control statin treatment are only starting. Similarly, although folate decreases homocysteine, there is no evidence that this approach reduces vascular risk. The potential clinical benefits of these markers and today’s results regarding their modification are presented in a separate article on the site.
A number of common genetic polymorphisms are associated with coronary risk factors (RF). For example, carriers of a common mutation in the MTNFR gene have elevated levels of homocysteine and multiple inherited lipid metabolism abnormalities associated with HLP and an increased vascular risk. Similarly, almost 50% of variations in the level of CRP are inherited. However, there is no evidence that screening for this polymorphism adds essential information to more easily detectable levels of homocysteine, lipids or CRP. Data concerning arterial thrombosis contrasts with data from venous thrombosis, when an assessment of factor V Leiden and prothrombin mutation is clinically useful. Thus, although genetic screening is a promising way to identify individuals at risk for future events, its role in primary and secondary prevention of atherothrombotic diseases remains unproved today. However, the time will come when genetic screening will play a role in identifying individuals at increased risk for appropriate therapy to reduce the risk of subsequent events.