• thrombolysis
• adjunctive treatment
• antiplatelet therapy
• anticoagulation

Thrombotic occlusion of an epicardial coronary artery has been implicated as a potential mechanism involved in acute myocardial infarction since as early as 1910,^w1 and became generally accepted after the landmark report by De Wood and colleagues in the early 1980s.^w2

In the search for pharmacological means to dissolve thrombi, the so called “thrombolytics” were developed. These agents target fibrin, the key element in clot formation, and are therefore more accurately referred to as “fibrinolytics”. Large clinical trials confirmed the hypothesis that timely restoration of coronary patency had a notable impact on survival after ST elevation myocardial infarction: ~20–30 lives saved per 1000 patients treated.^w3 With improvements in techniques and experience, mechanical reperfusion therapy has been proven to be even more beneficial than in-hospital initiated fibrinolytic therapy.^w4 Yet, pharmacological reperfusion therapy is more widely available, more easily applicable, and less dependent of institutional experience.

Consequently, the majority of patients with ST elevation myocardial infarction receive fibrinolytic therapy. Given the profound impact of early reperfusion,¹ preferably within the first “golden” hour, the initiation of pre-hospital fibrinolysis programmes resulted in benefits in the same order as achieved by primary angioplasty, ~18 lives saved per 1000 patients, when compared to in-hospital fibrinolysis.² New pharmacological reperfusion strategies to achieve patency rates that could more favourably compare with those achieved by primary angioplasty constitute a second initiative. In addition to further optimisation of antithrombotic treatment in the acute phase, the experience with anti-ischaemic, plaque stabilising strategies applied in the (sub)acute phase and in the long term have evolved. The current review presents the latest pharmacological developments and their implications for daily clinical practice in patients with acute ST elevation myocardial infarction (fig 1).