RESUMO
Vascular diseases constitute a significant contributor to worldwide mortality rates, placing a substantial strain on healthcare systems and socio-economic aspects. They are closely associated with inflammatory responses, as sustained inflammation could impact endothelial function, the release of inflammatory mediators, and platelet activation, thus accelerating the progression of vascular diseases. Consequently, directing therapeutic efforts towards mitigating inflammation represents a crucial approach in the management of vascular diseases. Traditional anti-inflammatory medications may have extensive effects on multiple tissues and organs when absorbed through the bloodstream. Conversely, treatments targeting inflammatory vascular diseases, such as monoclonal antibodies, drug-eluting stents, and nano-drugs, can achieve more precise effects, including precise intervention, minimal non-specific effects, and prolonged efficacy. In addition, personalized therapy is an important development trend in targeted therapy for inflammatory vascular diseases. Leveraging advanced simulation algorithms and clinical trial data, treatment strategies are gradually being personalized based on patients' genetic, biomarker, and clinical profiles. It is expected that the application of precision medicine in the field of vascular diseases will have a broader future. In conclusion, targeting therapies offer enhanced safety and efficacy compared to conventional medications; investigating novel targeting therapies and promoting clinical transformation may be a promising direction in improving the prognosis of patients with inflammatory vascular diseases. This article reviews the pathogenesis of inflammatory vascular diseases and presents a comprehensive overview of the potential for targeted therapies in managing this condition.
RESUMO
Background: The triglyceride-glucose (TyG) index and triglyceride to high-density lipoprotein cholesterol (TG/HDL-c) ratio are both reliable surrogate indicator of insulin resistance and have been shown to be valuable in predicting various cardiovascular diseases. However, few studies have explored its association with the prognosis of type B aortic dissection (TBAD) patients receiving thoracic endovascular aortic repair (TEVAR). Methods: A total of 1,425 consecutive patients who underwent TEVAR were included. Data from 935 patients were analyzed in the study. The endpoint was defined as 30-day and 1-year aortic-related adverse events (ARAEs), all-cause mortality, and major adverse cardiovascular and cerebrovascular events (MACCEs). Results: There were 935 patients included during a mean follow-up time of 2.8 years. After adjusting for multiple confounding factors, continuous TG/HDL-c [hazard ratio (HR) =1.07; 95% confidence interval (CI): 1.00-1.15; P=0.041] was independently associated with 1-year all-cause mortality. Both a high (Quintile 5: TG/HDL-c ratio ≥4.11) (HR =4.84; 95% CI: 1.55-15.13; P=0.007) and low TG/HDL-c ratio (Quintile 1: TG/HDL-c ratio <1.44) (HR =4.67; 95% CI: 1.46-14.94; P=0.001) were still independent risk factors for 1-year all-cause mortality. Conclusions: Elevated baseline TG/HDL-c ratio and TG/HDL-c ≥4.11 were significantly related to a higher risk of 1-year all-cause mortality among TBAD patients undergoing TEVAR. At the same time, the low TG/HDL-c ratio was also independently associated with 1-year all-cause mortality. Special attention should be paid to TBAD patients with a higher or an overly low TG/HDL-c ratio.
