Predictors of Adverse Left Ventricular Remodeling and Final Infarct Size After Primary Percutaneous Coronary Intervention for ST Elevation Myocardial Infarction: A Strain Analysis Study Using Echocardiography and Feature Tracking Cardiac Magnetic Resonance

ST-segment elevation myocardial infarction (STEMI) is one of the most important causes of death and disability around the world.

The main goal in the management of acute myocardial infarction (AMI) is early restoration of coronary artery flow in order to preserve viable myocardium. Primary percutaneous coronary intervention (PCI) has proven to be superior to other reperfusion strategies in terms of mortality reduction and preservation of left ventricular (LV) function. Despite improvements in the treatment of MI, 30% of patients show LV remodeling post-MI. Over time, remodeling adversely affects cardiac function and can lead to significant morbidity and mortality. Early risk stratification is essential to identify patients who will benefit from close follow-up and intense medical therapy.

The most widely investigated functional left ventricular (LV) characteristic to predict patient outcome after STEMI is LV ejection fraction (LVEF). Several structural LV characteristics have also shown to be important predictors of cardiovascular adverse events and death, including LV end diastolic volume (LVEDV), end systolic volume (LVESV) and mass (LVM).

Cardiovascular magnetic resonance (CMR) imaging is the current reference standard for assessing ventricular volumes and mass. Adverse remodeling results from an inability of the heart to maintain geometry post MI in the context of large infarcts and increased wall stresses.

The compensatory hypertrophic response of the remote non-infarcted myocardium (end diastolic wall thickness (EDWT) and end systolic wall thickness (ESWT)) might also play an important role in the remodeling after myocardial infarction but this needs to be investigated.

Infarct size -as a crucial endpoint for adverse remodeling- is influenced by several factors: - the size of the area at risk (AAR) (myocardium supplied by the culprit vessel); residual flow to the ischemic territory (e.g., collateral flow); myocardial metabolic demand; and the duration of coronary occlusion.

Assessment of the size and distribution of the infarction area after revascularization therapy can facilitate prompt and appropriate clinical intervention. Biomarkers such as troponin and creatine kinase are mainly used for AMI identification but lack myocardial specificity and may overestimate the (IS). Left ventricle ejection fraction (LVEF) fails to detect minimal and early pathological changes. The myocardial damage following STEMI can be assessed accurately by delayed gadolinium enhancement imaging using CMR imaging. In the acute phase of a STEMI, the extracellular space is increased in the infarct region due to a combination of necrosis, hemorrhage, and edema. The extent of hyper enhancement in the acute phase has been related to the outcome in patients with STEMI. However, later on the necrotic tissue is replaced by fibrotic scar tissue also with increased extracellular space. This process leads to ongoing 'infarct shrinkage' after the first week until the infarction reaches its final size after ∼30 days. - - Measurement of hyper enhancement in the acute phase of an infarction might therefore overestimate the necrotic infarct size, whereas 'final extent of hyper enhancement' is more precisely related to the amount of necrotic tissue. In STEMI patients the prognostic importance and predictors of the final infarct size are not fully elucidated.

Myocardial strain is a quantitative index based on measuring myocardial deformation during a cardiac cycle. Major tools for detecting changes in myocardial strain include CMR tagging, CMR feature tracking (FT-CMR) and speckle tracking echocardiography (STE). Previous studies have shown an advantage of strain in sensitively and accurately diagnosing and assessing IS compared to traditional functional indexes. However, the degree to which strain analysis can reflect the infarction areas quantified by CMR, adverse LV remodeling as well as the diagnostic accuracy of this analysis is still under dispute. In the past 3 years in particular, newly developed three-dimensional (3D) STE has overcome the inherent shortcomings of two-dimensional (2D) STE.