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- 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
Development of left ventricular remodelling after acute myocardial infarction is a complex process influenced by many factors, some of which are yet to be elucidated
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 …
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