The Hepatic Steatosis Index (HSI) serves as a non-invasive indicator for assessing liver fat accumulation. Its potential association with hypertension has garnered increasing attention, as metabolic dysfunctions, including hepatic steatosis, may contribute to elevated blood pressure via mechanisms such as insulin resistance and chronic inflammation.

Utilizing data from the NHANES database (2011-2018), the HSI was calculated on the basis of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and BMI.The association between HSI and hypertension was assessed by univariate analysis, weighted multivariate Logistic regression, and restricted cubic spline (RCS) models. Subgroup analyses were performed to increase the reliability of the data.

This cross-sectional study analysed data from 17,501 adults (NHANES 2011-2018) to assess the association between HSI and hypertension. Of these, 9,890 (56.51%) were diagnosed with hypertension.In the unadjusted model, HSI demonstrated a statistically significant correlation with hypertension, showing an odds ratio (OR) of 1.05 (95% confidence interval: 1.04-1.06).After adjustment for potential confounders, a higher prevalence of hypertension was observed in participants in the upper HSI quartiles (Q3 and Q4), with corresponding ORs of 2.29 (95% CI: 2.29-2.63) and 4.03 (95% CI: 3.42-4.74), respectively. RCS analysis revealed a U-shaped non-linear relationship between HSI and hypertension (P < 0.001), indicating that while hypertension risk primarily escalated with increasing HSI, a modest risk elevation was also detected at lower HSI levels. This suggests that both excessive liver fat accumulation (indicated by a high HSI) and underlying metabolic disorders (such as malnutrition or sarcopenia) may contribute to hypertension risk in individuals with unexpectedly low HSI. Subgroup analyses identified significant interactions in relation to education, cancer, and diabetes mellitus (p for interaction < 0.05), whereas no significant interactions were observed in other stratifications.

This study found a U-shaped relationship between the hepatic steatosis index (HSI) and the risk of hypertension. Although the HSI shows potential as a practical screening tool in primary care, further longitudinal studies are needed to establish causality and explore the complex bidirectional pathways involved.

Not applicable.

Heart failure (HF) is a major global public health concern, and one of the less commonly known risk factors for HF development is metabolic dysfunction-associated steatotic liver disease (MASLD), as they share a similar pathophysiological background. In this article, we evaluated a recently published review article by Arriola-Montenegro et al. This article briefly summarizes the common pathophysiology of HF and MASLD development and evaluates the available therapeutic options to treat both conditions. Clinical practice guidelines highlight the importance of initiating and titrating guideline-directed medication therapy (GDMT) for patients with HF with reduced ejection fraction. GDMT is comprised of the four pillars currently proposed in most clinical practice guidelines, namely angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), angiotensin receptor-neprilysin inhibitors, beta-blockers, mineralocorticoid receptor antagonists, and sodium-glucose co-transporter 2 inhibitors (SGLT-2i). Given the similarity of pathophysiology and risk factors, recent studies for GDMT regarding ACEIs, ARBs, mineralocorticoid receptor antagonists, and SGLT-2i have shown beneficial effects on MASLD. Nonetheless, other medications for both conditions and novel therapies require more robust data and well-designed clinical studies to demonstrate their efficacies in both conditions.

Dietary salt (sodium chloride, NaCl) is necessary for processed meat products, but intake of a high-sodium diet carries serious health risks. Considerable studies indicate that the partial substitution of NaCl with potassium chloride (KCl) can produce sodium-reduced cooked meat. However, most studies of sodium-reduced cooked meat focus on the production process in vitro, and the effect of cooked meat on health has not been well clarified in vivo.

This study finds that compared to the high-sodium group (HS), serum renin, angiotensin-converting enzyme (ACE), angiotensin (Ang) II, and the levels of some indicators of dyslipidemia are decreased in the reduced salt by partial substitution of NaCl with KCl group (RS + K). Furthermore, RS + K increases the antioxidation abilities, inhibits the renin-angiotensin system (RAS) through ACE/Ang II/Ang II type 1 receptor axis pathway, reduces synthesis of triglyceride and cholesterol and protein expressions of inflammatory factors interleukin-17A and nuclear factor-kappa B in the liver.

Partial substitution of NaCl with KCl in cooked meat can be a feasible approach for improving the health benefits and developing novel functional meat products for nutritional health interventions.

Heart failure with reduced ejection fraction (HFrEF) and nonalcoholic fatty liver disease (NAFLD) are two common comorbidities that share similar pathophysiological mechanisms. There is a growing interest in the potential of targeted therapies to improve outcomes in patients with coexisting HFrEF and NAFLD. This manuscript reviews current and potential therapies for patients with coexisting HFrEF and NAFLD. Pharmacological therapies, including angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, mineralocorticoids receptor antagonist, and sodium-glucose cotransporter-2 inhibitors, have been shown to reduce fibrosis and fat deposits in the liver. However, there are currently no data showing the beneficial effects of sacubitril/valsartan, ivabradine, hydralazine, isosorbide nitrates, digoxin, or beta blockers on NAFLD in patients with HFrEF. This study highlights the importance of considering HFrEF and NAFLD when developing treatment plans for patients with these comorbidities. Further research is needed in patients with coexisting HFrEF and NAFLD, with an emphasis on novel therapies and the importance of a multidisciplinary approach for managing these complex comorbidities.