• left ventricular remodelling
• myocardial infarction
• myocardial viability
• ischaemia

• AMI, acute myocardial infarction
• APRICOT, anti-thrombotics in the prevention of reocclusion in coronary thrombolysis
• IRA, infarct related artery
• LV, left ventricle
• TIMI, thrombolysis in myocardial infarction

During the past two decades, it has become increasingly well acknowledged that a large, transmural acute myocardial infarction (AMI) may result in complex alterations in the architecture and function of the left ventricle (LV), involving both the infarcted and non-infarcted zone. These alterations, usually referred to as “LV remodelling”, can profoundly affect the patient’s prognosis.

From the clinical viewpoint LV remodelling is a dynamic process, starting in the acute phase with infarct expansion—that is, rearrangement of wall structure—leading to myocardial thinning and lengthening, and progressing to LV dilatation and hypertrophy.¹ The remodelling process has regional and global effects on wall thickness and chamber size, as well as on shape and function.² Patients who develop LV dilatation following AMI have significantly reduced survival. In fact, LV volume is the single most important predictor of survival in patients with coronary heart disease.³ Furthermore, Gaudron and colleagues demonstrated that LV dilatation following AMI precedes deterioration of exercise performance and plays an active role in the development of chronic heart failure.⁴ They also showed that predictors of progressive LV dilatation and chronic LV dysfunction include ventriculographic LV size, LV ejection fraction at day 4 after AMI, infarct location (especially anterior), stroke index on day 4 …