Introduction: Cardiovascular pathology occupies a dominant place in morbidity structure. The very rapid development of science and technology, that radically changes the level of physical activity by reducing it, the energy value of the food increment and chronic stress have a negative influence on human life. These changes in the society lead to an increase in the number of people with pathological changes in metabolism at different levels, which in turn were distributed into a group of pathologies called “metabolic”, and which originally foster the development of atherosclerosis. This article reflects aspects of neovascularisation of the atherosclerotic plaque (AP) in patients with metabolic syndrome (MS). Especially in childhood and adolescence these changes are less observed (slight hypertension, increased body weight, dyslipidemia), but afterwards they cause atherosclerotic lesions in organs and systems. Previous studies have shown that expression of CD105 (endoglin) is a sensitive marker both for endothelial cells and for activation/proliferation of microcapillary in aggressive growth of solid tumors and atherosclerotic plaque lesions, because the intimal neovascularisation contributes significantly to the further stability or instability of atherosclerotic plaque, hemorrhage and rupture. Material and methods: We used morphological and immunohistochemical analysis to investigate the expression of CD34, SMA (smooth muscle actin) and CD105-positive in the affected large-caliber (aorta, carotid, mesenteric, iliac), and medium (cerebral, coronary, renal, vertebral arteries) vessels samples taken during the necropsies of patients who died from atherosclerotic complications and/or metabolic syndrome. Results: The most dominant studied vessels were CD34 positive at the intimal level in the atherosclerotic plaque region; in the fibrous plaque – rarely; in adventitia, namely vasa vasorum, CD34 positive (small and medium vessels). Marker SMA is detected in smooth muscle cells, myoepithelial, myofibroblast cells, and, to a lesser extent, in pericytes. Internal positive control for SMA was featured by the positive reaction in myocytes from the tunica media of arterial vessels of muscular and musculo-elastic types as well as by smooth muscle cells and pericytes of blood vessels. Negative reaction was represented in the newly formed vessels (an explanation is that the newly formed vessels being immature are voided of pericytes). The CD105-positive vessels density was higher in the plaque in close proximity to the atherosclerotic plaque (at adventitial and intimal level) and significantly decreased aloof from atherosclerotic lesion. Furthemore, noncomplicate plaques (intermediate and fibrous) have shown positive vessels for endoglin, which reflects angiogenic cell proliferation. Endoglin-positive vessels were grouped near the atherosclerotic lesions and had lower density distantly, similarly to the issues identified in complicated plaques (calcified and exulcerated). An eloquent fact is that expression of neovascularisation at intimal level of fibrous and complicated plaque is highly variable. Some of these newly formed CD105-positive vessels were immature, thin walled; formation of plexuses, seams, and isolated CD105-positive cells and without smooth muscle cell actin expression serves as an argument to consider them new-formed vessels. To a high degree of atherosclerotic plaques the proliferation of CD105-positive new-formed vessels was varied in most types of arteries, videlicet a significantly increased number of adventitious vessels were associated with plaques regions in affected arteries. Another observed feature is that the neovascularisation process is expressed also from intimal part at plaque level of medium and small caliber vessels. Conclusion: Interpretation and vitality (stability and instability) of the atherosclerotic plaque depends to a large extent on the angiogenesis process of atherosclerotic plaque. Our results show that comparative immunohistochemical method with the application of specific vascular markers demonstrates important pathogenetic aspects in the atherosclerotic plaque formation. CD105 is an useful marker of angiogenesis within the adventitious and intimal vessels and suggests the existence of significant differences in the pathological development of atherosclerosis in separate vascular beds, that can have important consequences when considering the management and actual treatment, and the perspective of this disease.