Managing Cardiovascular Risk in Patients with Autoimmune Diseases: Insights from a Nutritional Perspective.

PURPOSE OF REVIEW: Autoimmune diseases manifest as an immune system response directed against endogenous antigens, exerting a significant influence on a substantial portion of the population. Notably, a leading contributor to morbidity and mortality in this context is cardiovascular disease (CVD). Intriguingly, individuals with autoimmune disorders exhibit a heightened prevalence of CVD compared to the general population. The meticulous management of CV risk factors assumes paramount importance, given the current absence of a standardized solution to this perplexity. This review endeavors to address this challenge from a nutritional perspective. RECENT FINDINGS: Emerging evidence suggests that inflammation, a common thread in autoimmune diseases, also plays a pivotal role in the pathogenesis of CVD. Nutritional interventions aimed at reducing inflammation have shown promise in mitigating cardiovascular risk. The integration of nutritional strategies into the management plans for patients with autoimmune diseases offers a holistic approach to reducing cardiovascular risk. While conventional pharmacological treatments remain foundational, the addition of targeted dietary interventions can provide a complementary pathway to improve cardiovascular outcomes.

A new risk factor associated with cardiovascular disease: clonal hematopoiesis of indeterminate potential.

Clonal hematopoiesis is a prevalent disease associated with all-cause death. Not only because it can be a precancerous lesion of blood system diseases but also has a strong association with cardiovascular disease. A narrow term, clonal hematopoiesis of indeterminate potential (CHIP), was proposed by Steensma et al. [1] to describe individuals with detectable somatic clonal mutations in their genes in blood or bone marrow but without a diagnosis of hematological disease or unexplained cytopenia. Recently, studies have suggested that CHIP is associated with adverse cardiovascular disease progression, particularly in patients with ten-eleven translocation 2 (TET2) mutations or DNA methyltransferase 3 alpha (DNMT3A) mutations. Age is the most crucial factor which is associated with increased CHIP prevalence. The underlying mechanisms appear to be related to inflammatory status. However, new evidence suggests that genetic factors, lifestyle and environmental factors such as smoking, obesity, and diet also play essential roles in developing CHIP. More research needs to be done on the potential genetic mechanisms driving CHIP and the environmental factors that modulate CHIP risk. This review summarizes the latest research on CHIP, discusses in detail the strong association between clonal hematopoiesis and accelerated cardiovascular disease, and rationalizes the intervention of CHIP in combination with existing evidence, which may be beneficial for future treatment.

A multimodal parallel method for left ventricular dysfunction identification based on phonocardiogram and electrocardiogram signals synchronous analysis.

Heart failure (HF) is widely acknowledged as the terminal stage of cardiac disease and represents a global clinical and public health problem. Left ventricular ejection fraction (LVEF) measured by echocardiography is an important indicator of HF diagnosis and treatment. Early identification of LVEF reduction and early treatment is of great significance to improve LVEF and the prognosis of HF. This research aims to introduce a new method for left ventricular dysfunction (LVD) identification based on phonocardiogram (ECG) and electrocardiogram (PCG) signals synchronous analysis. In the present study, we established a database called Synchronized ECG and PCG Database for Patients with Left Ventricular Dysfunction (SEP-LVDb) consisting of 1046 synchronous ECG and PCG recordings from patients with reduced (n = 107) and normal (n = 699) LVEF. 173 and 873 recordings were available from the reduced and normal LVEF group, respectively. Then, we proposed a parallel multimodal method for LVD identification based on synchronous analysis of PCG and ECG signals. Two-layer bidirectional gate recurrent unit (Bi-GRU) was used to extract features in the time domain, and the data were classified using residual network 18 (ResNet-18). This research confirmed that fused ECG and PCG signals yielded better performance than ECG or PCG signals alone, with an accuracy of 93.27%, precision of 93.34%, recall of 93.27%, and F1-score of 93.27%. Verification of the model's performance with an independent dataset achieved an accuracy of 80.00%, precision of 79.38%, recall of 80.00% and F1-score of 78.67%. The Bi-GRU model outperformed Bi-directional long short-term memory (Bi-LSTM) and recurrent neural network (RNN) models with a best selection frame length of 3.2 s. The Saliency Maps showed that SEP-LVDPN could effectively learn features from the data.

Bifidobacterium lactis BB-12 Attenuates Macrophage Aging Induced by D-Galactose and Promotes M2 Macrophage Polarization.

Immunosenescence comprises a set of dynamic changes occurring in innate and adaptive immune systems, and macrophage aging plays an important role in innate and adaptive immunosenescence. However, function and polarization changes in aging macrophages have not been fully evaluated, and no effective method for delaying macrophage senescence is currently available. The results of this study reveal that D-galactose (D-gal) can promote J774A.1 macrophage senescence and induce macrophage M1 polarization differentiation. Bifidobacterium lactis BB-12 can significantly inhibit J774A.1 macrophage senescence induced by D-gal. IL-6 and IL-12 levels in the BB-12 groups remarkably decreased compared with that in the D-gal group, and the M2 marker, IL-10, and Arg-1 mRNA levels increased in the BB-12 group. BB-12 inhibited the expression of p-signal transducer and activator of transcription 1 (STAT1) and promoted p-STAT6 expression. In summary, the present study indicates that BB-12 can attenuate the J774A.1 macrophage senescence and induce M2 macrophage polarization, thereby indicating the potential of BB-12 to slow down immunosenescence and inflamm-aging.