Aspirin is effective in, treating patients with
unstable angina or
myocardial infarction. However, questions remain about the optimal dose of
aspirin and
aspirin-resistance in subgroups of patients.
Heparin also has beneficial effects mostly during the acute phase of
unstable angina, but thrombolytics are effective only in acute
myocardial infarction and not in
unstable angina. Recently, low molecular weight heparins have proved to be as effective (FRIC trial) or more effective (ESSENCE trial) than
unfractionated heparin in
unstable angina. Ongoing studies (TIMI 11B) are evaluating the efficacy of a prolonged administration of
low molecular weight heparin to alter the chronic process of
unstable angina. The new
antiplatelet drugs directed against
GP IIb/IIIa receptors are now available to improve the acute results of high risk percutaneous transluminal angioplasty (PTCA). This new
drug (c7E3) binds rapidly to
GP IIb/IIIa and prevents
fibrinogen binding to the receptor. This very potent and irreversible effect prevents platelet aggregation and decreases the incidence of acute occlusions following PTCA. especially in patients with
unstable angina. The counterpart is an increased risk of
hemorrhage, knowing that patients receive simultaneously
aspirin and
heparin. The first results of the EPILOG study also demonstrate a better outcome in elective angioplasty without significant increase of serious
bleeding, thanks to a low dose
heparin regimen. In contrast to thrombolytics, the
GP IIb/IIIa antagonist does not increase the risk of intracranial
bleeding. The results of the CAPTURE trial also confirm the clinical benefit obtained with this
drug in refractory
unstable angina. The reduction of death and
myocardial infarction is very consistent throughout the studies performed with c7E3. The Kaplan-Meier curves of freedom of death and
myocardial infarction diverge immediately after start of study medication. The acute benefits are preserved at 3 years in the EPIC trial. Similar trends were present during the acute phase with other compounds (
tirofiban,
integrelin), meaning that a class effect may exist but the long term results are disappointing. The results with new
direct antithrombins such as
hirudin, or
hirulog in acute
myocardial infarction or in PTCA for
unstable angina are negative. The development of new potent oral
antiplatelet drugs might change the treatment of
acute coronary syndromes in the future. The current progress made with antithrombotic drugs should improve the prognosis of
acute coronary syndromes.