Neovascularization and angiogenesis are vital processes in the repair of damaged tissue, creating new blood vessel networks and increasing oxygen and nutrient supply for regeneration. The importance of Adipose-derived Mesenchymal Stem Cells (ASCs) contained in the adipose tissue surrounding blood vessel networks to these processes remains unknown and the exact mechanisms responsible for directing adipogenic cell fate remain to be discovered. As adipose tissue contains a heterogenous population of partially differentiated cells of adipocyte lineage; tissue repair, angiogenesis and neovascularization may be closely linked to the function of ASCs in a complex relationship. This review aims to investigate the link between ASCs and angiogenesis/neovascularization, with references to current studies. The molecular mechanisms of these processes, as well as ASC differentiation and proliferation are described in detail. ASCs may differentiate into endothelial cells during neovascularization; however, recent clinical trials have suggested that ASCs may also stimulate angiogenesis and neovascularization indirectly through the release of paracrine factors.

Currently, atherosclerosis, which affects the vascular bed of all vital organs and tissues, is considered as a leading cause of death. Most commonly, atherosclerosis involves coronary and peripheral arteries, which results in acute (e.g., myocardial infarction, lower extremities ischemia) or chronic (persistent ischemia leading to severe heart failure) consequences. All of them have a marked unfavorable impact on the quality of life and are associated with increased mortality and morbidity in human populations. Lower extremity artery disease (LEAD, also defined as peripheral artery disease, PAD) refers to atherosclerotic occlusive disease of the lower extremities, where partial or complete obstruction of peripheral arteries is observed. Decreased perfusion can result in ischemic pain, non-healing wounds, and ischemic ulcers, and significantly reduce the quality of life. However, the progressive atherosclerotic changes cause stimulation of tissue response processes, like vessel wall remodeling and neovascularization. These mechanisms of adapting the vascular network to pathological conditions seem to play a key role in reducing the impact of the changes limiting the flow of blood. Neovascularization as a response to ischemia induces sprouting and expansion of the endothelium to repair and grow the vessels of the circulatory system. Neovascularization consists of three different biological processes: vasculogenesis, angiogenesis, and arteriogenesis. Both molecular and environmental factors that may affect the process of development and growth of blood vessels were analyzed. Particular attention was paid to the changes taking place during LEAD. It is important to consider the molecular mechanisms underpinning vessel growth. These mechanisms will also be examined in the context of diseases commonly affecting blood vessel function, or those treatable in part by manipulation of angiogenesis. Furthermore, it may be possible to induce the process of blood vessel development and growth to treat peripheral vascular disease and wound healing. Reactive oxygen species (ROS) play an important role in regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. With regard to the repair processes taking place during diseases such as LEAD, prospective therapeutic methods have been described that could significantly improve the treatment of vessel diseases in the future. Summarizing, regenerative medicine holds the potential to transform the therapeutic methods in heart and vessel diseases treatment.

The obstructive sleep apnea (OSA) is highly associated with various significant cardiovascular outcomes such as resistant hypertension (RAH). Despite this, as of now the relationship between high night-time blood pressure (BP) and left ventricular hypertrophy (LVH) in patients with OSA and RAH is not fully understood. The aim of this study was to assess the influence of the addition of eplerenone to a standard antihypertensive therapy on parameters of 24-h ambulatory blood pressure measurement (ABPM) as well as on the results of echocardiography and polysomnography in patients with OSA and RAH. The patients were randomly assigned to one of the two study groups: the treatment group, receiving 50 mg/d eplerenone orally for 6 months (n = 51) and the control group, remaining on their standard antihypertensive therapy (n = 51). After that period, a significant reduction in the night-time BP parameters in the treatment group including an increased night blood pressure fall from 4.6 to 8.9% was noted. Additionally, the number of non-dipper patients was reduced by 45.1%. The treatment group also revealed a decrease in left ventricular hypertrophy and in the apnea–hypopnea index (AHI) with a positive correlation being observed between these two parameters. This study is the first to report the improvement of the circadian BP profile and the improvement of the left ventricle geometry in patients with OSA and RAH following the addition of selective mineralocorticoid receptor antagonists to antihypertensive therapy.

AKI is one of the most common yet underdiagnosed postoperative complications that can occur after any type of surgery. Contrast-induced nephropathy (CIN) is still poorly defined and due to a wide range of confounding individual variables, its risk is difficult to determine. CIN mainly affects patients with underlying chronic kidney disease, diabetes, sepsis, heart failure, acute coronary syndrome and cardiogenic shock. Further research is necessary to better understand pathophysiology of contrast-induced AKI and consequent implementation of effective prevention and therapeutic strategies. Although many therapies have been tested to avoid CIN, the only potent preventative strategy involves aggressive fluid administration and reduction of contrast volume. Regardless of surgical technique—open or endovascular—perioperative AKI is associated with significant morbidity, mortality and cost. Endovascular procedures always require administration of a contrast media, which may cause acute tubular necrosis or renal vascular embolization leading to renal ischemia and as a consequence, contribute to increased number of post-operative AKIs.

Introduction. The aim of this study was to assess blood flow in the vessels of the eyeball and changes in the optic nerve in patients with arterial hypertension and primary open-angle glaucoma. Material and Methods. The patients were divided into groups: 1 (night blood pressure, BP, fall, NBPF, not more than 10%; non-dippers); 2 (NBPF 10–15%, dippers) and 3 (NBPF>15%; extreme dippers). Results. In the group of dippers and extreme dippers, perfusion pressure was significantly lower than that in the non-dippers group, there was reduced thickness of the nerve fibers and a greater decrease in the visual field. Significant relationships between peak systolic, end-diastolic flow in the ophthalmic and central retinal arteries and night perfusion pressure, thickness of nerve fibers, and a loss of visual field were observed. Conclusion. In patients with glaucoma and well-controlled hypertension, a nocturnal BP fall of more than 10% is associated with a greater visual field defect and greater degeneration of the optic nerve fibers. Low minimum diastolic pressure and the level of nocturnal BP fall, but not the absolute value of average arterial BP at night, should be included in the group of specific risk factors in patients with hypertension and open-angle glaucoma. These findings also suggest avoiding excessive lowering of BP at night in this group.

(1) Background: The increase in cardiovascular risk related to air pollution has been a matter of interest in recent years. The role of particulate matter 2.5 (PM2.5) has been postulated as a possible factor for premature death, including cardiovascular death. The role of long-term exposure to PM10 is less known. The aim of the study was to assess the individual relationship between air pollution in habitation and the development of coronary artery disease. (2) Methods: Out of 227 patients who underwent coronary angiography, 63 (38 men and 25 women) with a mean age of 69 (63–74) years, with nonsignificant atherosclerotic changes at the initial examination, were included in the study. The baseline and repeated coronary angiography were compared to reveal patients with atherosclerotic progression and its relation to demographic and clinical factors and exposure to air pollution in the habitation place. (3) Results: In the performed analysis, we found a significant correlation between Syntax score in de novo lesions and BMI (Spearman’s rho −0.334, p = 0.008). The significant and strong correlation between median annual PM10 values of 20 µg/m³ and at least 25 µg/m³ in air pollution and the risk of de novo coronary disease was noticed (Spearman’s rho = 0.319, p = 0.011 and Spearman’s rho = 0.809, p < 0.001, respectively). (4) Conclusions: There is a positive correlation between long-term exposure to PM10 air pollution and coronary artery disease progression, demonstrated by the increase in Syntax score. The presented analysis revealed increased morbidity at lower PM10 concentrations than generally recommended thresholds. Therefore, further investigations concerning air pollution’s influence on cardiovascular risk should be accompanied by promoting lifestyle changes in the population and revisiting the needs for environmental guidelines.