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Background: For women presenting with stable chest pain (SCP), the appropriate risk assessment strategy to identify individuals unlikely to benefit from further cardiovascular imaging testing (CIT) is debatable. Thus, the present study intended to compare two risk assessment strategies in these individuals.Methods: 2592 women with SCP who underwent coronary computed tomography angiography (CCTA) were divided into low and high risk group according to 2016 National Institute of Health and Care Excellence guideline-determined strategy (NICE strategy) and 2019 European Society of Cardiology guideline-determined strategy (ESC strategy), respectively. The associations of coronary artery disease (CAD), major adverse cardiovascular event (MACE) and other subsequent clinical outcomes with risk groups and net reclassification improvement (NRI) were evaluated to compare different strategies.Results: Both NICE strategy which focused on symptom evaluation and ESC strategy which was based on pretest probability (PTP) determined by ESC-PTP model and coronary artery calcium score-weighted clinical likelihood (CACS-CL) model classified a proportion (34.49% and 63.97%, respectively) of individuals into the low risk group. Compared to NICE strategy, ESC strategy indicated stronger associations between risk groups and obstructive CAD (odds ratio: 27.63 versus 3.57), MACE (hazard ratios: 4.24 versus 1.91), more intensive clinical management as well as a positive NRI (27.71%, p < 0.0001).Conclusion: Compared to NICE strategy, ESC strategy which sequentially incorporated ESC-PTP model with CACS-CL model seemed to be associated with greater effectiveness in identifying individuals who may derive maximum benefit from further CIT in women presenting with SCP. [ABSTRACT FROM AUTHOR]

Background: The dilation of lymphatic vessels plays a critical role in maintaining heart function, while a lack thereof could contribute to heart failure (HF), and subsequently to an acute myocardial infarction (AMI). Macrophages participate in the induction of lymphangiogenesis by secreting vascular endothelial cell growth factor C (VEGF-C), although the precise mechanism remains unclear., Methods: Intramyocardial injections of adeno-associated viruses (AAV9) to inhibit the expression of VEGFR3 ( VEGFR3 shRNA) or promote the expression of VEGFR3 ( VEGFR3 ORF) in the heart; Myh6-mCherry B6 D2-tg mice and flow cytometry were used to evaluate the number of myocellular debris in the mediastinal lymph nodes; fluorescence staining and qPCR were used to evaluate fluorescence analysis; seahorse experiment was used to evaluate the level of glycolysis of macrophages; Lyz2𝐶𝑟𝑒 , VEGFCfl/fl , and PFKFB3fl/fl mice were used as a model to knock out the expression of VEGF-C and PFKFB3 in macrophages., Results: The escalation of VEGFR3 in cardiac tissue can facilitate the drainage of myocardial debris to the mediastinal lymph nodes, thereby improving cardiac function and reducing fibrosis after reperfusion injury. Conversely, myeloid VEGF-C deficiency displayed an increase in macrophage counts and inflammation levels following reperfusion injury. The inhibition of the critical enzyme PFKFB3 in macrophage glycolysis can stimulate the manifestation of VEGF-C in macrophages. A deficiency in myeloid PFKFB3 is associated with induced lymphangiogenesis following reperfusion injury., Conclusions: Our initial investigations suggest that the suppression of PFKFB3 expression in macrophages could potentially stimulate the production of VEGF-C in these immune cells, which in turn may facilitate lymphangiogenesis and mitigate the inflammatory effects of I/R injury., Competing Interests: The authors declare no conflict of interest., (© 2023 The Author(s). Published by IMR Press.)