Left ventricular (LV) aneurysm is frequently formed after acute myocardial infarction (AMI); however, its formation is not predetermined by the size of infarction zone per se. Rapid development of circulation failure in the process of post-infarction aneurysm (LVA) formation is based on two basic mechanisms: functional damage of the LV myocardium induced by its ischemia and its remodeling. The incidence rate of variously localized LVA development can also be explained by the peculiarities of morphological structure of the LV wall, its thickness, tension and deformations resulting in the course of LV activity in apex and basal sites. Involvement of epicardial and subepicardial myocardial layers results in significant distortion of architectonics of the LV walls. The normal ellipsoid form of the LV is transformed into the spheroid cavity where fiber contractility vector becomes more transversally oriented. This results in decrease of LV ejection fraction based on the transversal contraction of obliquely oriented cardiomyocyte fibers. Change of geometrical proportions of the LV cavity also impairs the process of transformation of myocardium created tension into the intracavitary pressure. This naturally is accompanied by the decrease of kinetic energy in the phase of blood ejection, which leads to the impairment of the blood flow from the LV cavity into systole thus transforming a “normal” spiral-wise blood flow into turbulent one. Introduction of new methods of treatment of ischemic heart disease and AMI as well as the results of the studies allowing estimating the degree of myocardial remodeling resulted in certain revision of definition and classification of LVA.