RESUMEN
Numerous recent studies have shown that patients with underlying cardiovascular disease (CVD) are at increased risk of more severe clinical course as well as mortality of COVID-19. Also, the available data suggests that COVID-19 is related to numerous de novo cardiovascular complications especially in the older population and those with pre-existing chronic cardiometabolic conditions. SARS-CoV-2 virus can cause acute cardiovascular injury, as well as increase the risk of chronic cardiovascular damage. As CVD seem to be the major comorbidity in critically unwell patients with COVID-19 and patients often die of cardiovascular complications, we review the literature and discuss the possible pathophysiology and molecular pathways driving these disease processes: cytokine release syndrome, RAAS system dysregulation, plaque destabilization and coagulation disorders with the aim to identify novel treatment targets. In addition, we review the pediatric population, the major cause of the cardiovascular complications is pediatric inflammatory multisystem syndrome that is believed to be associated with COVID-19 infection. Due to the increasingly recognized CVD damage in COVID-19, there is a need to establish clear clinical and follow-up protocols and to identify and treat possible comorbidities that may be risk factors for the development of cardiovascular complications.
RESUMEN
Since the outbreak of SARS-CoV-2 virus more than 12,500,000 cases have been reported worldwide. Patients suffering from diabetes and other comorbidities are particularly susceptible to severe forms of the COVID-19, which might result in chronic complications following recovery. Dipeptidyl peptidase-4 inhibitors exert beneficial effects in prevention/treatment of pulmonary fibrosis, heart, and kidney injury, and since they may be a long-term consequence caused by COVID-19, it is reasonable to expect that DPP-4 inhibitors might be beneficial in alleviating long-term consequences of COVID-19. With that in mind, we would like to voice our concerns over chronic implications following recovery from COVID-19, especially not only in diabetic but also in non-diabetic patients, and to indicate that some preventive measures could be undertaken by application of DPP-4 inhibitors.
RESUMEN
This study investigated with the effect of aminophylline on the penetration of aspirin through the blood-brain barrier (BBB) into the central nervous system (CNS) in rats. Acetylsalycylic was injected into the right axillary artery, to avoid the drug affecting the peripheral organs before it reached the CNS. The test animals received subcutaneously (s.c.) aminophylline 30 min before aspirin injection, while the control animals received an equimolar dose of physiological solution s.c. At time intervals of 30, 60, 90, 120, and 240 s after aspirin injection, the animals were decapitated and blood samples from the left jugular vein, as well as samples from the brainstem, cerebellum and left and right cerebral hemispheres, were taken to determine aspirin concentrations in all of them by a standard method. It was found that aspirin concentrations in the CNS were even 30 times lower than in the blood, with the concentrations being higher in the brainstem and cerebellum than in the left and right hemispheres. The presence of aminophylline did not alter aspirin concentrations either in the blood or the brain, and therefore did not affect significantly the aspirin penetration through the BBB into the CNS.