Strategies for Reducing Myocardial Infarct Size Following STEMI

Valeria Paradies,Mervyn Huan Hao Chan,Derek J Hausenloy

doi:10.1007/978-981-13-1114-7_22

Abstract

In the context of ST-segment elevation myocardial infarction (STEMI), early and successful myocardial reperfusion by primary percutaneous coronary intervention (PPCI) is the most powerful intervention for reducing myocardial infarct (MI) size, preserving left ventricular (LV) systolic function and preventing the onset of heart failure. However, despite continual improvements in acute care, the mortality and morbidity rates following STEMI remain significant, with 7% death and 22% rehospitalisation for heart failure, at 1 year. Although timely reperfusion of the occluded vessel by PPCI is essential to minimise the acute ischaemic time (a major determinant of MI size) and salvage viable myocardium, the process of reperfusion itself, paradoxically, induces additional myocardial injury and cardiomyocyte death, a phenomenon which has been termed ‘myocardial reperfusion injury’. This has been shown to contribute to up to 50% of the final MI size, making it an important therapeutic target to reduce MI size in STEMI patients reperfused by PPCI. However, the translation of novel cardioprotective strategies for targeting myocardial reperfusion injury to reduce MI size following STEMI has been both challenging and disappointing. In this chapter, we provide an overview of myocardial reperfusion injury, discuss the challenges facing the investigation of treatment strategies for reducing MI size following STEMI and highlight future cardioprotective therapies for potentially improving clinical outcomes in STEMI patients.

Highlights

In the context of ST-segment elevation myocardial infarction (STEMI), early and successful myocardial reperfusion by primary percutaneous coronary intervention (PPCI) is the most powerful intervention for reducing myocardial infarct (MI) size, preserving left ventricular (LV) systolic function and preventing the onset of heart failure
High-dose intracoronary adenosine and nitroprusside did not reduce infarct size or Microvascular obstruction (MVO) measured by cardiac magnetic resonance imaging (CMR) Adenosine may adversely affect mid-term clinical outcome
Experimental studies have demonstrated that following a sustained coronary artery occlusion, interrupting myocardial reperfusion with short-lived episodes of alternating coronary artery occlusion and reflow in the first few minutes of reflow reduced MI size in small and large animal models of acute myocardial infarction, a phenomenon which has been termed ischaemic postconditioning (IPost)