Cardiology and cardiovascular medicine最新文献

End-stage renal disease is a crippling diagnosis that generally requires dialysis to prolong life. To facilitate filtration of patient's blood in dialysis, surgical formation of an arteriovenous fistula (AVF) is commonly performed. Maturation of the AVF is required to allow for successful dialysis. However, AVFs commonly fail to mature, leading to the fistula closure, the necessity for another fistula site, and markedly increased morbidity and mortality. The current literature concerning molecular mechanisms associated with AVF maturation failure supports the role of inflammatory mediators involving immune cells and inflammatory cytokines. However, the role of oncostatin M (OSM), an inflammatory cytokine, and its downstream targets are not well investigated. Through inflammation, oxidative stress, and hypoxic conditions, the vascular tissue surrounding the AVF undergoes fibrosis, stenosis, and wall thickening, leading to complete occlusion and nonfunctional. In this report, first we critically review the existing literature on the role of OSM in the most common causes of early AVF failure - vascular inflammation, thrombosis, and stenosis. We next consider the potential of using OSM as a therapeutic target, and finally discuss therapeutic agents targeting inflammatory mediators involved in OSM signaling to potentiate successful maturation of the AVF.

Background: Left atrial (LA) volume indexing for body surface area (BSA) may underestimate LA size in obese and overweight people. Since LA volume is a risk marker for some cardiovascular events, it is suggested that indexing for height would be an alternative more appropriate method. The aims of this study were to find normal and the best cutoff values for LA volume indexed for height in our population.

Methods: Echocardiograms from 2018 to 2021 were reviewed and patients without known cardiac disease and completely normal echocardiograms that had the left atrial volume (LAvol) measured by biplane Simpson's method were included. LAvol was indexed by BSA (ml/m²), by height (LAvol/m), by height raised to exponent 2.7 (ml/ m^2.7) and by height squared (ml/h²).

Results: A total of 545 patients, 50.5 ± 13.4 y., 335 females (61,5%) were analyzed. There were 145 normal weight (26.6%), 215 overweight (39.4%), 154 obese (28.3%) and 31 low weight (5.7%) patients. To establish normal values we included only the normal weight group and considered normal values from 2SD below to 2SD above the mean. Mean and normal values were: LAvol/h 26.0 ±4.5, 17 - 35 ml/m, LAvol/ht² 16 ± 2.8, 10.4 - 21.6 ml/ ht² and LAvol/ht^2.7 11.4 ± 2.2, 7.0 - 15.8 ml/m^2.7. The normal LAvol/ht^2.7 differed between male and female (11.4 ± 2.4 and 12.8 ± 2.6, p < 0.001). LA diameter, LAvol, LAvol/h, LAvol/h² and LAvol/ht^2.7 increased progressively from low-weight, normal weight, overweight and obese patients (p< 0.0001), but not LAvol/BSA. When indexing LAvol for height, for height² and for height^2.7 20.8%, 22.7% and 21.4% of the obese patients, respectively, were reclassified as enlarged LA, and 7.4%, 8.8% and 8.4% of the overweight patients as well. Using ROC curve analysis, LAvol/h² had the highest AUC ant the best predictive value to identify LA enlargement and LAvol/BSA the worst one.

Conclusions: Normal values for LAvol indexed for height by three different methods are described in normal individuals. We reinforce that LAvol indexation for BSA underestimates LA size in obese and overweight patients and in these groups, specially, indexing for height² is probably the best method to evaluate LAvol.

Ischemic stroke (IS) is a common neurological disease in the elderly, but the relationship between neutrophil/albumin ratio (NAR) and leukocyte count/albumin ratio (LAR) and the severity of neurological function injury and early neurological deterioration (END) occurrence remain elusive in acute IS. A total of 299 patients with acute IS and 56 healthy controls were enrolled. According to the NIHSS score at admission, the disease group was divided into three groups (mild, moderate and severe IS), and the differences in five indexes NAR, LAR, neutrophil count, leukocyte count and albumin among the four groups were analyzed. Furthermore, explore the correlation between the above indicators and the severity of IS and END occurrence. The results showed that higher NAR, LAR, neutrophil count, leukocyte count levels and lower albumin levels were associated with acute IS, and the levels of NAR and LAR increased gradually in three groups of IS. NAR and LAR were positively and albumin was negatively correlated with the severity of IS. Meanwhile, NAR and LAR showed a good predictive value in identifying patients with END after acute IS. NAR and LAR may be predictors of the severity of IS and END occurrence after acute IS.

The structure of connective tissues including cartilage, tendons, and ligaments as well as many organs, like the skin, heart, liver, kidney, lungs, blood vessels, and bones, depend on collagen. The bulk of the network of structural proteins that make up the extracellular matrix of the heart is composed of collagen type I and type III, which provide structural support for the muscle cells and are crucial for cardiac function. The prognosis and progression of a disease or diseased state may be significantly impacted by the upregulation or downregulation of the collagen types, particularly Col I and Col III. For example, increasing Col I protein levels may impose increasing myocardial stiffness, impairing the diastolic and systolic function of the myocardium. Collagen I is a stiff fibrillar protein that gives tensile strength, whereas Col III produces an elastic network that stores kinetic energy as an elastic rebound. These two collagen proteins have distinct physical properties in nature. Therefore, the control of Col I and Col III as well as the potential relevance of the Col I/Col III ratio in many biological processes serve as the foundation for this comprehensive review article.