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From bench to practice: ST-elevation myocardial infarction

Session presentations
Acute Coronary Syndromes (ACS)

For patients presenting with an acute ST-elevation MI (STEMI), the most effective therapy for limiting myocardial infarct size, preserving left ventricular systolic function and improving clinical outcomes is early and effective myocardial reperfusion using either thrombolytic therapy or primary percutaneous coronary intervention (PPCI). Early reperfusion, which has been achieved by minimizing the time from chest pain onset to PPCI time, reduces acute myocardial ischemic injury and cell death. Furthermore, recent advances in PCI technology and anti-platelet and anti-thrombotic therapies have improved the process of myocardial reperfusion.
However, paradoxically, the process of myocardial reperfusion can itself induce myocardial injury and cell death, thereby mitigating the beneficial effects of myocardial reperfusion in terms of myocardial salvage- a phenomenon which has been termed ‘myocardial reperfusion injury’. There currently exists no effective therapy for reducing myocardial reperfusion injury in PPCI patients. Derek Hausenloy (London, UK) provided current insights on the pathophysiology of reperfusion injury and possible targets for therapeutic intervention. Proof of concept trials have shown that infarct size can be reduced almost with quarter by applying per- (during) or post-conditioning interventions/medications. Larger multicenter studies are underway.


Figure: This diagram illustrates the individual contributions of acute myocardial ischemic injury and acute myocardial reperfusion injury to final myocardial infarct (MI) size in STEMI patients undergoing primary PCI (PPCI).

Giampaolo Nicolli addressed another potential target to reduce infarct size: microvascular obstruction (MVO). MVO may occur after primary PCI in up to 50% of patients after reperfusion and is associated with worse clinical outcome at follow-up. Prevention of MVO is directed against pathogenetic mechanisms: distal embolization, ischemia and reperfusion injury and the individual predisposition to MVO. Thrombus aspiration, anti-platelet and vasodilator drugs along with conditioning strategies are the mainstay of its prevention.

Timely diagnosis of STEMI is of uppermost importance to shorten treatment delays. The presence of ST elevation on the ECG during an anginal attack unresponsive to the administration of nitrates remains the determining observation in the decision to activate the cathlab. Peter Clemmensen (Copenhagen, Denmark) provided an overview on the possibilities of modern technology to record and transmit the pre-hospital ECG of patients with acute chest pain and the possible impact on treatment delays. The impact is the greatest for STEMI patients with transport times where a shorten door to balloon time compensates for longer transport delay.

Steen D Kristensen (Aarhus, Denmark) provided an overview of the optimal antithrombotic therapy: upstream starting in the ambulance and during primary PCI. The range of antithrombotic drugs has extended considerably and a number of new agents have been tested in several clinical trials. There remain, however, gaps in the knowledge: we know little about the effect of new anti-thrombotic agents in the prehospital setting; not all new intravenous anti-platelet and anti-coagulant drugs have been tested and what is the role of local drug delivery at the site of thrombus?




From bench to practice: ST-elevation myocardial infarction

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.