SUCCESSES

Successful research the CTT has supported so far

• A research group at the University of Aberdeen have shown that an anti-platelet drug that could benefit patients with coronary thrombosis does not cause bleeding and has very few, if any, side effects.

• A research team funded by the CTT have just informed us of their latest findings, that all that is necessary to de-function the cell lining (endothelium) of an artery is to raise the glucose concentration within the lumen.  Raising the circulating blood glucose concentration is not necessary for this effect.

• A change (polymorphism) in the gene for thrombomodulin in patients who have heart attacks. Establishing the risk of a heart attack in people with this gene change.

• A change (mutation) in the gene for methylenetetrahydrofolate reductase, which affects homocysteine levels. Establishing the risk of a heart attack in people with this gene change.

• The involvement of serotonin in the formation of thrombi at critical coronary artery narrowings (stenoses).

• Dispersion of coronary artery thrombi by antagonism of platelet serotonin receptor.

• Interaction between the effect of serotonin and adrenaline on the growth of platelet thrombi in the coronary artery.

• Failure of thrombin inhibition to prevent intracoronary thrombosis.

• How coronary artery narrowing (stenosis) and intracoronary thrombosis affects the pressure and flow of blood to the working heart.

• Thrombosis in one coronary artery causes generalised coronary narrowing by constriction of the other coronary arteries.

• Prevention of death from heart attack (myocardial infarction) by prolonged antiplatelet treatment.

• Increased susceptibility to thrombosis due to an antithrombin variant and protein C abnormalities.

• The finding of an association in the general population between a polymorphism of the gene for activated protein C and activation of thrombosis. This gene polymorphism is a potential marker of people at high risk of coronary thrombosis.