Oxidative stress and inflammation as links in a chain in patients with chronic cerebrovascular diseases

Abstract

Cerebrovascular diseases (CVD) are the main cause of death and permanent disability. The urgency of the problem of chronic CVD is associated with an increase of the absolute number of elderly and senile age in the population, a trend towards slowly increasing, sluggish pathological processes. It is obvious that any somatic disease in such patients is comorbid to cerebrovascular diseases that suggests a unified mechanism of the pathogenesis for both the main and concomitant diseases. The article notes that microangiopathy is the most common cause of CVD. The main etiopathogenetic factor affecting cerebral vessels of small caliber is endothelial dysfunction, systemic inflammation and oxidative stress. Understanding the molecular components that underlie functional abnormalities and damage of small blood vessels gives the key to the modern strategies in therapy, forming the foundation for an adequate pathogenetically justified therapy. This impact should be gradual, complex and aimed at correcting pathochemical disorders in general and neurotransmitter imbalance in particular. The drug dipyridamole, which has pleiotropic effects, can be considered as one of the pathogenetically justified means in complex drug therapy in patients with CVD.