Modification of re-stenosis with drugs
Scheffold, T.; Müller-Bardorff, M.; Greten, T.; von Hodenberg, E.; Katus, H.A.
Zeitschrift für Kardiologie 83(Suppl 4): 43-49
1994
ISSN/ISBN: 0300-5860 PMID: 7856279 Document Number: 430448
In the treatment of patients with symptomatic coronary artery disease using PTCA, success is limited due to restenosis rates ranging from 30-50% of the lesions treated. Medical approaches to reduce the rate of restenosis were therefore tested in a number of trials. However, in only a few randomized and controlled trials were positive effects reported. Inhibiting platelet aggregation through the use of anti-glycoprotein IIb/IIIa monoclonal antibody 7E3 and, in some studies, with 3 omega fatty acids, a significant reduction in the rate of restenosis was observed. Many trials testing less potent inhibitors of platelet aggregation, such as acetylsalicylic acid, prostacyclin, thromboxane A2 receptor antagonists, and ticlopidine as well as anticoagulants such as heparin or coumarin, calcium antagonists, ACE-inhibitors, antiproliferative agents such as colchicine, methylprednisolone, and angiopeptin were inconclusive or without a positive treatment effect. The results of a hirudin multicenter trial on the rate of restenosis (Helvetica Trial) will soon be reported. There are many possible reasons for these disappointing results, such as poor standardization of the invasive studies, in analyzing the degree of coronary artery stenoses, the inadequate sample size in many trials, and insufficient local drug concentrations as well as the lack of beneficial effects of the study medication. Thus, at present there is no effective treatment to reduce the restenosis rate following PTCA. However, it can be expected that potent antithrombins, or inhibitors of platelet aggregation, may be useful.