Left ventricular remodeling after acute myocardial infarction (AMI) begins as an adaptive process modifying the ventricular size, shape, structure, and mass in response of loss of viable and functional myocardium. It is mediated by intracellular signaling pathways, inflammatory reaction, neuro-hormonal activation, and genetic factors.1,2 Cardiomyocytes necrosis after an acute ischemic injury triggers an intense inflammatory response marked by neutrophils, macrophages, and monocytes migration into the infarcted zone, thereby activating an intracellular signaling cascade and stimulating the renin-angiotensin-aldosterone and sympathetic nervous systems. All these result in myocardial scar formation and ventricular cavity dilation.3, 4, 5, 6 The process of remodelling has been divided into two phases: the early remodeling phase accounting for the first 72 h post infarction and the late remodeling phase.7 Infarct expansion enhanced by the degradation of collagen scaffold by the activated matrix metalloproteinases after neutrophils infiltration is the main finding of the early remodeling phase.8 Then, regional wall thining and ventricular dilation are observed in the infarcted areas altering the systolic and diastolic function.9 The sympathetic adrenergic system, renin-angiotensin-aldosteron system and the release of natriuretic peptides are activated because of the decreased cardiac output and the variation in the circulatory hemodynamics.10 The late remodeling phase is characterized by TGF-β1 production, type I and III collagen synthesis, fibroblast transformation into myofibroblast, myocyte hypertrophy and cardiac fibrosis.5,11 It is worthy to mention that the process of post AMI remodeling is not homogeneous and depends on four determining factors: the infarction morphologic characteristics (injury size≥16–20 %, transmural infarction),12,13 healing characteristics (balance between type I and type III collagen),14 hemodynamic stress (cardiac overload state)15,16 and modulators level (angiotensin II, interleukin 1-6, catecholamine, insulin-like growth factor1, tumoral necrosis factor, endothelin 1, transforming growth factor β-1).17,18 Existing litterature has identified large, transmural, and anterior infarctions, no-reflow phenomenon, decreased ejection fraction, elevated blood pressure, early coronary reocclusion, absence or ineffective reperfusion strategy, using of non-steroidal anti- inflammatory drugs or corticosteroids during the acute phase of AMI, smoking and increased baseline glycemia as independant predictors for post-AMI cardiac remodeling.1,15,19, 20, 21 However, small, subendocardial and inferior infarctions, untouched microcirculation, functional collateral circulation, and effective reperfusion therapy prevent the onset of remodeling process.22, 23, 24 Left ventricular remodeling remains the major determinant of cardiac function and survival after recovery from AMI.25 The present review examined the different available and promissing therapeutic approches to manage and attenuate the adverse effects of post-AMI cardiac remodeling process by targeting the underlying pathophysiological mechanisms.