Jankowski Piotr, Bryniarski Leszek, Styczkiewicz Katarzyna, Bilo Grzegorz, Curyło Adam, Kawecka-Jaszcz Kalina
I Klinika Kardiologii Instytutu Kardiologii, Collegium Medicum, Uniwersytetu Jagiellońskiego, 31-501 Kraków, ul. Kopernika 17.
Przegl Lek. 2003;60(8):527-31.
Restenosis after coronary angioplasty is still a significant problem despite the dynamic development of intervention cardiology. Homocysteine causes endothelial dysfunction and disorders of the coagulation system, increases in platelets aggregation and stimulates the proliferation of the vascular smooth cell. These were the reasons for investigating the relation between homocysteine level and the risk of restenosis. Some studies indicate that higher homocysteine levels increase the risk of restenosis after coronary angioplasty, while it has not been proven in other studies. The results of the only one randomized trial demonstrated that pharmacological lowering of the homocysteine level decreased the risk of restenosis after coronary angioplasty. At this time there are some studies which started focusing on the role of lowering homocysteine level in cardiovascular risk. These investigations may explain the importance of homocysteine level in the development of cardiovascular diseases. There is a need of a large prospective multicenter trial assessing the relationship between increased homocysteine level and the frequency of restenosis after coronary angioplasty. Using intravascular ultrasonography could be especially helpful in assessing the role of decreasing homocysteine level on neo-intima formation and arterial remodeling after intervention.
