Left ventricular remodeling after primary percutaneous coronary intervention

Red cell distribution width and neutrophil-to-lymphocyte ratio predict left ventricular dysfunction in acute anterior ST-segment elevation myocardial infarction

“…It has been shown that the most important factor in mortality and morbidity after AMI was left ventricular systolic functions. Inflammation, oxidative stress, and neurohormonal activation play major roles in the pathogenesis of atherosclerosis, STEMI, and left ventricular remodeling after AMI [4], [24]. An elevated RDW may reflect underlying inflammation and oxidative stress in STEMI and left ventricular remodeling after AMI and may be proposed as a simple diagnostic marker for monitoring patients with STEMI.…”

Single Intracoronary Injection of Encapsulated Antagomir‐92a Promotes Angiogenesis and Prevents Adverse Infarct Remodeling

“…Adverse ventricular remodeling is presently still the major cause of contractile dysfunction and heart failure after an AMI . Despite advances in pharmacological treatments, reperfusion, resynchronization, and cell therapy, its occurrence has not been abolished . The thinning and expansion of the infarct area, which results in ventricular dilatation, has been associated with a worsened state of the microcirculation .…”

“…24 Despite advances in pharmacological treatments, reperfusion, resynchronization, and cell therapy, its occurrence has not been abolished. [25][26][27][28][29][30][31][32][33] The thinning and expansion of the infarct area, which results in ventricular dilatation, has been associated with a worsened state of the microcirculation. [34][35][36] Consequently, improving the vascular network by induction of neoangiogenesis has already been proposed as a way to prevent adverse ventricular remodeling.…”

Does Longitudinal Strain Predict Left Ventricular Remodeling after Myocardial Infarction?

“…Other components include the interstitium, fibroblasts, collagen, and coronary vasculature. 27,28 Morphologically, LV remodeling following AMI is a progressive process involving chamber dilation, infarcted wall thinning, and compensatory hypertrophy in the noninfarcted myocardium and is considered as an adaptive process and contributing to maintenance of the systolic function. However, this occurs only in a certain amount of AMI patients, while the other patients remain relatively stable without a significant LV cavity dilatation.…”