Arquivos brasileiros de cardiologia最新文献

Targeted temperature management (TTM) is currently the only potentially neuroprotective intervention recommended for post-cardiac arrest care. However, there are concerns among the scientific community regarding conflicting evidence supporting this recommendation. Moreover, the bulk of trials included in systematic reviews that inform guidelines and recommendations have been conducted in developed countries, with case mix and patient characteristics that significantly differ from the reality of developing countries such as Brazil. Elevated body temperatures induce changes in the blood-brain barrier integrity and increase the brain's demand for oxygen. They can cause imbalances in cerebral oxygen metabolism and blood flow, leading to inflammation and apoptosis. The primary aim of temperature control (TTM) is to control the secondary injury pathways by avoiding high temperatures. TTM, previously named therapeutic hypothermia, was first used to treat post-cardiac arrest brain injury in the 1950s. After that, we have been having relevant trials regarding TTM, with conflicting results as follows: TTM1, HACA study, TTM2, HYPERION study, and some meta-analyses kept the temperature management after a cardiac arrest in the discussion. In addition to individualizing the optimal target temperature for specific clinical scenarios and patient profiles, other aspects of high-quality TTM delivery are critical. The timing of target temperature achievement, duration of cooling, rewarming rates, and sedation practices have been evaluated in recent trials. In conclusion, it is crucial to determine the most effective TTM approach to achieve the best possible neurological outcomes while minimizing potential adverse effects.

Background: Chronic kidney disease (CKD) is associated with a higher prevalence of valvular diseases and increased mortality from cardiovascular causes. Factors that influence the genesis of cardiac valve calcification (CVC) in these patients are not well-defined.

Objective: To determine the risk factors for valvular calcification in patients with CKD.

Methods: Systematic review based on PRISMA, which included observational studies evaluating the association of clinical and laboratory data with CVC in patients with CKD, undergoing or not hemodialysis or peritoneal dialysis. Articles were retrieved from databases (MEDLINE; SCIELO; CENTRAL; EMBASE; LILACS/BVS) and selected blindly by two authors; discrepancies were resolved by a third author. Data collection and synthesis were carried out by the main author. The assessment of methodological quality and risk of bias was based on STROBE and Newcastle-Ottawa guidelines.

Results: A total of 783 studies were identified, of which 20 were included, encompassing 13,314 patients from 10 countries. The factors most strongly associated with CVC were age >55 years, glomerular filtration rate <53 mL/min/1.73m2, renal replacement therapy (RRT) >20 months, hypoalbuminemia, C-reactive protein (CRP), serum levels of IL-6, TNF-α, parathyroid hormone, hyperphosphatemia, hypercalcemia, Ca × P product, and FGF-23 resulting from secondary hyperparathyroidism. Both mitral and aortic valves were studied, and no differences were observed between hemodialysis and peritoneal dialysis.

Conclusion: Age, RRT, chronic inflammation, and secondary hyperparathyroidism promote calcium and phosphate deposition in the valves, making CKD patients more susceptible to CVC) Monitoring these parameters provides opportunities for prevention and treatment.