Skin wound healing is a complex process involving various cellular and molecular events. However, chronic wounds, particularly in individuals with diabetes

Atrial fibrillation (AF) can occur even after the correction of mitral valve (MV) pathology in patients who have pre-operative sinus rhythm and undergo MV surgery. However, the factors associated with the occurrence of AF after MV surgery are still unclear. The aim of this retrospective study was to investigate the factors determining the occurrence of permanent AF after MV surgery in patients with preoperative sinus rhythm who underwent MV surgery. Four hundred and forty-two patients (mean age 46 ± 12, 190 men) who underwent MV surgery and sinus rhythm were investigated retrospectively. Transthoracic echocardiography was performed before and after MV surgery at the time of dismissal. Permanent post-operative AF occurred in 81 (18%) patients even after successful MV surgery and preoperative sinus rhythm. It was more common in rheumatic etiology, a presence of mitral stenosis, lower pre- and post-operative left ventricular ejection fraction, higher post-operative mean diastolic pressure gradient across mitral prosthesis, larger post-operative left atrial volume index (LAVI) and lesser degrees of reduction in LAVI after surgery. In multiple regression analysis, post-operative LAVI was found to be an independent predictor for occurrence of AF. Post-operative LAVI > 39 ml/m2 was the cut-off value for best prediction of new onset permanent AF (sensitivity: 79%, AUC: 0.762, SE: 0.051, p < 0.001). New-onset permanent post-operative AF is not uncommon, even after successful MV surgery despite pre-operative sinus rhythm. Larger post-operative LAVI was an independent predictor for the occurrence of AF.

Inorganic phosphate (Pi) is a critical determinant of calcification, and its concentration is regulated by alkaline phosphatase (ALP) and Pit1. ALP is a key regulator of osteogenic calcification and acts by modulating local inorganic phosphate (Pi) concentrations through hydrolyzing pyrophosphate in the extracellular matrix (ECM). Pit1, a sodium-dependent phosphate transporter, regulates calcification via facilitating phosphate uptake within the cells. To investigate whether zinc differentially regulates osteoblastic and vascular calcifications, we examined ALP activity and Pit1 in osteoblastic and vascular smooth muscle cells (VSMCs). Our findings demonstrate that calcification in osteoblastic MC3T3-E1 cells is decreased via diminished ALP action under zinc deficiency. In contrast, zinc-deficiency-induced calcification in VSMCs is independent of ALP action, as demonstrated by very weak ALP activity and expression in calcified VSMCs. In zinc-deficient A7r5 VSMC, P accumulation increased with increasing Na phosphate concentration (3–7 mM) but not with β-GP treatment, which requires ALP activity to generate Pi. Ca deposition also increased with Na phosphate in a dose-dependent manner; in contrast, β-GP did not affect Ca deposition. In osteoblastic cells, Pit1 expression was not affected by zinc treatments. In contrast, Pit1 expression is highly upregulated in A7r5 VSMC under zinc deficiency. Using phosphonoformic acid, a competitive inhibitor of Pit1, we showed that calcification is inhibited in both A7r5 and MC3T3-E1 cells, indicating a requirement for Pit1 in both calcifications. Moreover, the downregulation of VSMC markers under zinc deficiency was restored by blocking Pit1. Taken together, our results imply that zinc-deficiency-induced calcification in VSMC is independent of ALP action in contrast to osteoblastic calcification. Moreover, Pit1 expression in VSMCs is a target for zinc deficiency and may mediate the inhibition of VSMC marker expression under zinc deficiency.

Kang HJ, et al. Korean Circ J. 2025 Apr;55:e66. https://doi.org/10.4070/kcj.2024.0385

Sepsis-induced cardiomyopathy (SIC) is known to show cardiac dysfunction in patients with sepsis. Both a decrease or an increase in ejection fraction (EF), an indicator of cardiac function, can occur. The purpose of this study was to identify factors associated with abnormal left ventricular (LV) function measured by EF in patients with sepsis in the intensive care unit (ICU). This was a retrospective study performed from November 2016 to December 2018. Three-hundred and sixty-six patients (mean age, 73 ± 13 years; 191 [52%] men) admitted to the ICU with sepsis were included. Patients were classified into three categories according to LV EF (group 1 –[EF<50%, n = 36], group 2 –[50≤EF<70%, n = 252], and group 3 –[EF≥70%, n = 78]). Echocardiographic assessment was performed within 48 hours of diagnosis of sepsis. We analyzed clinical factors including mortality, echocardiographic findings, and laboratory parameters. Decreased LV EF occurred in 36 (10%) patients and hyper-dynamic EF developed in 78 (21%) patients. Of 366 patients, 103 (28%) patients died. Baseline characteristics were similar in the three groups, except female sex an indicator of abnormal EF. Mortality rates were also similar in the three groups; however, mortality rates were significantly higher in patients with abnormal EF (decreased or increased vs. normal). Echocardiographic parameters were significantly different in the three groups, in terms of LV systolic parameters and chamber size. Small left atrium (LA) and small LV were significantly associated with abnormal EF (especially in patients with increased EF). High brain natriuretic peptide was associated with decreased EF. Among these factors, female sex and small LA were significantly associated with abnormal EF in the multiple regression analysis. Our findings highlight that female sex and small cardiac size are associated with abnormal EF, and therefore, death. Therefore, female patients and patients with small LA should be monitored closely when they present with sepsis.