Dynamic changes in myocardial architecture after reperfused acute myocardial infarction (AMI): insights from the prospective REMI study (REmodeling after Myocardial Infarction)

Dynamic changes in myocardial architecture after reperfused acute myocardial infarction (AMI): insights from the prospective REMI study (REmodeling after Myocardial Infarction)

Methods 66 consecutive patients who fulfilled inclusion criteria underwent two CMRs: 2-4 days (baseline) and 6 months (follow-up) after the AMI, comprising SSFP images for analysis of left ventricular functions and late gadolinium enhancement (LGE) MRI (0.1 mmol/Kg; DOTAREM, GUERBET, Roissy, France) for infarct analysis using a threshold method. Of 132 CMRs, 6 (4 from baseline) were non-diagnos...

Myocardial Hemorrhage After Acute Reperfused ST-Segment–Elevation Myocardial Infarction

Left ventricular remodeling after reperfused acute myocardial infarction: insights from automated ECV mapping

Background In reperfused acute ST-segment elevation myocardial infarction (STEMI), infarct size and microvascular obstruction (MVO) are strong predictors of adverse LV remodeling and poor outcome. However, the role of remote myocardium is less clear. Remote native T1 changes have been linked with adverse LV remodeling and is thought to be associated with inflammation. We used automated ECV mapp...

Ventricular Remodeling After Canine Acute Myocardial Infarction

Background Prolonged nitrate therapy during healing between 2 days and 6 weeks after anterior myocardial infarction has the potential for limiting further left ventricular remodeling (or changes in topography) and preserving function. Longterm therapy throughout healing over 6 weeks might be more beneficial than short-term therapy over the first 2 weeks after infarction. Methods and Results The...

Ventricular remodeling after acute myocardial infarction.

The term ventricular remodeling has been coined to describe the geometrical changes in size and shape of the left ventricle occurring after large myocardial infarcts. We do not exactly know what initiates this process. Slipping of myofilaments following destruction of connective tissue--probably due to metalloproteinase activation--could be the initial event. As a consequence, wall stress is in...