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Cardiovascular diseases are among the leading causes of death worldwide, with well-known modifiable risk factors, such as smoking, overweight, lipid metabolism disorders, lack of physical activity and high blood pressure playing a significant role. Recent studies have now identified "clonal hematopoiesis" as a novel blood-based risk factor. Clonal hematopoiesis arises from mutations in hematopoietic stem cells, which lead to the expansion of mutated blood cells. Mutated cell clones can be detected in over 40% of individuals over 50 years old, with more than 15% of those over 90 years old harboring large clones. Surprisingly, mutated cells predispose to the development of leukemia only to a minor extent, leading to the term clonal hematopoiesis of indeterminate potential (CHIP); however, it has been shown that CHIP is associated with an increased risk of cardiovascular diseases. Individuals with CHIP-associated gene mutations have an elevated risk of atherosclerotic vascular diseases, stroke and thrombosis. Patients with heart failure with reduced ejection fraction (HFrEF), whether of ischemic or non-ischemic origin and patients with heart failure with preserved ejection fraction (HFpEF) exhibit an increased number of mutated cells in the blood. The presence of CHIP mutations is linked to a poorer prognosis in patients with existing cardiovascular diseases. Future research should aim at a better understanding of the specific effects of different mutations, clone sizes and combinations to develop personalized therapeutic approaches. Various anti-inflammatory therapeutic drugs are available, which can be tested in controlled studies.

Air pollution and traffic noise are two important environmental risk factors that endanger health in urban societies and often act together as "partners in crime". Although air pollution and noise often co-occur in urban environments, they have typically been studied separately, with numerous studies documenting consistent effects of individual exposure on blood pressure. In the following review article, we examine the epidemiology of air pollution and noise, especially regarding the cardiovascular risk factor arterial hypertension and the underlying pathophysiology. Both environmental stressors have been shown to lead to endothelial dysfunction, oxidative stress, pronounced vascular inflammation, disruption of circadian rhythms and activation of the autonomic nervous system, all of which promote the development of hypertension and cardiovascular diseases. From a societal and political perspective, there is an urgent need to point out the potential dangers of air pollution and traffic noise in the American Heart Association (AHA)/American College of Cardiology (ACC) prevention guidelines and the European Society of Cardiology (ESC) guidelines on prevention. Therefore, an essential goal for the future is to raise awareness of environmental risk factors as important and, in particular, preventable risk factors for cardiovascular diseases.

Aortic valve stenosis is one of the most frequent valvular heart diseases requiring treatment in industrialized countries. The symptom onset is associated with a significantly increased mortality, so that there is a clear indication for treatment in patients with severe, symptomatic aortic valve stenosis; however, data on the optimal treatment of patients with asymptomatic aortic valve stenosis are scarce. Smaller studies in the field of cardiac surgery suggest that early surgical valve replacement is superior to a conservative approach. For this reason, the results of additional adequately powered randomized trials are awaited with great interest. In this year numerous long-term results from randomized comparisons of the two available treatment options (surgical versus transcatheter aortic valve replacement) were published, which will further guide the heart team to find the best treatment approach for each individual.

Cardiovascular diseases and cancer have a complex relationship and show a reciprocal linkage and influence. Mutual risk factors, demographic changes and increasing multimorbidity result in an increase in the incidence of both diseases. Advances in oncological and cardiological treatment lead to a further increase in patients with cured or chronic diseases as a relevant comorbidity. The induction of cardiovascular side effects by cancer therapies leads to increased cardiovascular morbidity and mortality in cancer patients. Recent data also show that cardiovascular disease, through various factors, can also promote the development and progression of cancer. An understanding of the interrelationship between cardiovascular diseases and cancer can be seen as a major medical challenge for the future. To this end, scientific, structural, clinical and educational interfaces between cardiology and oncology are essential. This article outlines the complex relationships between cardiovascular diseases and cancer and defines current and future challenges for the best possible care of affected patients.

Cardiovascular diseases (CVD) are closely linked to protein homeostasis (proteostasis) and its failure. Beside genetic mutations that impair cardiac protein quality control, obesity is a strong risk factor for heart disease. In obesity, adipose tissue becomes dysfunctional and impacts heart function and CVD progression by releasing cytokines that contribute to systemic insulin resistance and cardiovascular dysfunction. In addition, chronic inflammation and lipotoxicity compromise endoplasmic reticulum (ER) function, eliciting stress responses that overwhelm protein quality control beyond its capacity. Impairment of proteostasis-including dysfunction of the ubiquitin-proteasome system (UPS), autophagy, and the depletion of chaperones-is intricately linked to cardiomyocyte dysfunction. Interventions targeting UPS and autophagy pathways are new potential strategies for re-establishing protein homeostasis and improving heart function. Additionally, lifestyle modifications such as dietary interventions and exercise have been shown to promote cardiac proteostasis and overall metabolic health. The pursuit of future research dedicated to proteostasis and protein quality control represents a pioneering approach for enhancing cardiac health and addressing the complexities of obesity-related cardiac dysfunction.

Background: This retrospective observational study investigated the relationship between heart rate variability (HRV) and atrial fibrillation (AF) recurrence after pulmonary vein isolation (PVI) by cryoballoon or radiofrequency ablation (RF).

Methods: We enrolled 497 patients who underwent PVI using first-generation cryoballoon (CB1), second-generation cryoballoon (CB2), or RF. We analyzed HRV as a surrogate for modulation of the intrinsic autonomic nervous system using 24‑h Holter recordings 1 or 2 days after the procedure and compared the recurrence and non-recurrence group with regard to ablation methods. Furthermore, we calculated recurrence-free survival (RFS) below/over HRV cut-off values for the whole study population and separately for each ablation method.

Results: All except one of the five time-based HRV parameters analyzed were significantly lower in the non-recurrence group than in the recurrence group after CB2. Only a trend toward lower HRV for the non-recurrence group was found after RF and no remarkable differences were detected after CB1. The HRV parameters below their calculated cut-off were associated with a significantly higher RFS rate 2 years after CB2. This also applied to root mean sum of squared distance (rMSSD) and the percentage of adjacent NN interval differences greater than 50 ms (pNN50) after RF. No differences were found regarding CB1. Concerning rMSSD, the sensitivity, specificity, and difference in RFS increased when using cut-offs that were calculated including only CB2 patients. Multivariate cox regression analysis showed that low rMSSD values could independently predict AF recurrence after adjusting for covariates (hazard ratio: 0.50; p < 0.001).

Conclusion: Low values of rMSSD early after a PVI could independently predict AF recurrence, especially after CB2.

Objective: The effect of miR-626 on the radiosensitivity to oral squamous cell carcinoma (OSCC) was evaluated in this study. Materials and Methods: The level of miR-626 in OSCC patients was determined by analyzing the data of miRNA microarray GSE113956. miR-626 was overexpressed by miR-626 mimics and knockdown were performed by miR-626 inhibitor. The level of miR-626 was detected by quantitative real-time polymerase chain reaction. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and colony formation assays were used to detect the effect of miR-626 on the growth of OSCC cells. Flow cytometry was used to detect the apoptosis of OSCC cells. Western blot and dual luciferase reporter assays were used to explore the underlying mechanism of miR-626 regulating the radiosensitivity to OSCC. The effect of miR-626 on the radiosensitivity to OSCC were examined in an in vivo xenograft model. Results: The serum miR-626 level of OSCC patients was significantly higher than that of healthy controls. miR-626 mimics significantly promoted the OSCC cell growth, but the miR-626 inhibitor significantly suppressed the OSCC cell growth. Radiation combined with the miR-626 inhibitor significantly suppressed the cell proliferation and promoted the apoptosis of SCC-4 and HSC4 cells. Moreover, miR-626 regulates the nuclear factor kappa-B (NF-κB) signaling mediated by TRAF-interacting protein with forkhead-associated domain B. Furthermore, inhibition of miR-626 enhances the radiosensitivity to OSCC in nude mice. Conclusions: miR-626 inhibition enhanced the radiosensitivity to OSCC through the downregulation of NF-κB signaling.

Background: Exercise-based cardiac rehabilitation has positive benefits for patients with chronic heart failure (CHF), but the choice of exercise intensity has been controversial. The aim of this systematic review and meta-analysis was to investigate the effects of different exercise intensities on cardiopulmonary function and quality of life (QoL) of patients with CHF.

Methods: Randomized controlled trials (RCTs) of different exercise intensities applied to patients with CHF were searched in PubMed, Web of Science, the Cochrane Library, and Embase databases from inception to December 2021. Study selection and data extraction were performed simultaneously by two independent reviewers, using the Physiotherapy Evidence Database Scale (PEDro) for quality assessment of the included literature. The weighted mean differences (WMD) or standardized mean difference (SMD) were calculated by employing a fixed or random effects model. Other statistical analyses included subgroup analysis and sensitivity analysis. Quality of evidence was evaluated by the Grade of Recommendation, Assessment, Development, and Evaluation (GRADE) method.

Results: Eight RCTs were included. Analyses reported no significant improvement in left ventricular ejection fractions (LVEF; WMD = 0.47, 95% CI [-4.10, 5.03], p = 0.841), peak oxygen uptake (peak VO₂) (SMD = 0.38, 95% CI [-0.03, 0.80], p = 0.069) and 6‑min walking distance (6MWD) (WMD = 14.10, 95% CI [-9.51, 37.72], p = 0.242). Exercise interventions of varying intensity produced small-to-moderate beneficial effects on QoL (WMD = -4.99, 95% CI [-8.29, -1.68], p = 0.003), which appeared to be attenuated at long-term follow-up (WMD = 2.12, 95% CI [-2.91, 7.16], p = 0.409).

Conclusion: High-intensity exercise does not have a significant advantage over moderate-intensity exercise in improving cardiopulmonary function and aerobic capacity in patients with CHF. Beneficial changes in QoL from high-intensity exercise also appeared to decrease during long-term follow-up, indicating a cumulative effect of the efficacy of high-intensity exercise.