The influence of pressure injury risk on the association between left ventricular ejection fraction and all-cause mortality in patients with acute myocardial infarction 80 years or older.

BACKGROUND: We aimed to investigate whether the pressure injury risk mediates the association of left ventricular ejection fraction (LVEF) with all-cause death in patients with acute myocardial infarction (AMI) aged 80 years or older. METHODS: This retrospective cohort study included 677 patients with AMI aged 80 years or older from a tertiary-level hospital. Pressure injury risk was assessed using the Braden scale at admission, and three risk groups (low/minimal, intermediate, high) were defined according to the overall score of six different variables. LVEF was measured during the index hospitalization for AMI. All-cause death after hospital discharge was the primary outcome. RESULTS: Over a median follow-up period of 1,176 d (interquartile range [IQR], 722-1,900 d), 226 (33.4%) patients died. Multivariate Cox regression analysis showed that reduced LVEF was associated with an increased risk of all-cause death only in the high-risk group of pressure injury (adjusted hazard ratios [HR]=1.81, 95% confidence interval [CI]: 1.03-3.20; P=0.040), but not in the low/minimal- (adjusted HR=1.29, 95%CI: 0.80-2.11; P=0.299) or intermediate-risk groups (adjusted HR=1.14, 95%CI: 0.65-2.02; P=0.651). Significant interactions were detected between pressure injury risk and LVEF (adjusted P=0.003). The cubic spline with hazard ratio plot revealed a distinct shaped curve relation between LVEF and all-cause death among different pressure injury risk groups. CONCLUSIONS: In older patients with AMI, the risk of pressure injury mediated the association between LVEF and all-cause death. The classification of older patients for both therapy and prognosis assessment appears to be improved by the incorporation of pressure injury risk assessment into AMI care management.

Risk factors, clinical features, and outcomes of premature acute myocardial infarction.

Aims: To investigate the risk factors, clinical features, and prognostic factors of patients with premature acute myocardial infarction (AMI). Materials and methods: A retrospective cohort study of patients with AMI included in data from the West China Hospital of Sichuan University from 2011 to 2019 was divided into premature AMI (aged < 55 years in men and < 65 years in women) and non-premature AMI. Patients' demographics, laboratory tests, Electrocardiography (ECG), cardiac ultrasound, and coronary angiography reports were collected. All-cause death after incident premature MI was enumerated as the primary endpoint. Results: Among all 8,942 AMI cases, 2,513 were premature AMI (79.8% men). Compared to the non-premature AMI group, risk factors such as smoking, dyslipidemia, overweight, obesity, and a family history of coronary heart disease (CHD) were more prevalent in the premature AMI group. The cumulative survival rate of patients in the premature AMI group was significantly better than the non-premature AMI group during a mean follow-up of 4.6 years (HR = 0.27, 95% CI 0.22-0.32, p < 0.001). Low left ventricular ejection fraction (LVEF) (Adjusted HR 3.00, 95% CI 1.85-4.88, P < 0.001), peak N-terminal pro-B-type natriuretic peptide (NT-proBNP) level (Adjusted HR 1.34, 95% CI 1.18-1.52, P < 0.001) and the occurrence of in-hospital major adverse cardiovascular and cerebrovascular events (MACCEs) (Adjusted HR 2.36, 95% CI 1.45-3.85, P = 0.001) were predictors of poor prognosis in premature AMI patients. Conclusion: AMI in young patients is associated with unhealthy lifestyles such as smoking, dyslipidemia, and obesity. Low LVEF, elevated NT-proBNP peak level, and the occurrence of in-hospital MACCEs were predictors of poor prognosis in premature AMI patients.

Relationship of body fat and left ventricular hypertrophy with the risk of all-cause death in patients with coronary artery disease.

BACKGROUND: Left ventricular hypertrophy (LVH) is prevalent in obese individuals. Besides, both of LVH and obesity is associated with subclinical LV dysfunction. The study aims to investigate the interplay between body fat and LVH in relation to all-cause death in patients with coronary artery disease (CAD). METHODS: In this retrospective cohort study, a total of 2243 patients with angiographically proven CAD were included. Body fat and LV mass were calculated using established formulas. Patients were grouped according to body fat percentage and presence or absence of LVH. Cox-proportional hazard models were used to observe the interaction effect of body fat and LVH on all-cause death. RESULTS: Of 2243 patients enrolled, 560 (25%) had a higher body fat percentage, and 1045 (46.6%) had LVH. After a median follow-up of 2.2 years, the cumulative mortality rate was 8.2% in the group with higher body fat and LVH, 2.5% in those with lower body fat and no LVH, 5.4% in those with higher body fat and no LVH, and 7.8% in those with lower body fat and LVH (log-rank P < 0.001). There was a statistically significant interaction between body fat percentage and LVH ( P interaction was 0.003). After correcting for confounding factors, patients with higher body fat and LVH had the highest risk of all-cause death (HR = 3.49, 95% CI: 1.40-8.69, P = 0.007) compared with those with lower body fat and no LVH; in contrast, patients with higher body fat and no LVH had no statistically significant difference in risk of death compared with those with lower body fat and no LVH (HR = 2.03, 95% CI: 0.70-5.92, P = 0.195). CONCLUSION: A higher body fat percentage was associated with a different risk of all-cause death in patients with CAD, stratified by coexistence of LVH or not. Higher body fat was significantly associated with a greater risk of mortality among patients with LVH but not among those without LVH.

Rhizobiales-Specific RirA Represses a Naturally "Synthetic" Foreign Siderophore Gene Cluster To Maintain Sinorhizobium-Legume Mutualism.

Iron homeostasis is strictly regulated in cellular organisms. The Rhizobiales order enriched with symbiotic and pathogenic bacteria has evolved a lineage-specific regulator, RirA, responding to iron fluctuations. However, the regulatory role of RirA in bacterium-host interactions remains largely unknown. Here, we report that RirA is essential for mutualistic interactions of Sinorhizobium fredii with its legume hosts by repressing a gene cluster directing biosynthesis and transport of petrobactin siderophore. Genes encoding an inner membrane ABC transporter (fat) and the biosynthetic machinery (asb) of petrobactin siderophore are sporadically distributed in Gram-positive and Gram-negative bacteria. An outer membrane siderophore receptor gene (fprA) was naturally assembled with asb and fat, forming a long polycistron in S. fredii. An indigenous regulation cascade harboring an inner membrane protease (RseP), a sigma factor (FecI), and its anti-sigma protein (FecR) were involved in direct activation of the fprA-asb-fat polycistron. Operons harboring fecI and fprA-asb-fat, and those encoding the indigenous TonB-ExbB-ExbD complex delivering energy to the outer membrane transport activity, were directly repressed by RirA under iron-replete conditions. The rirA deletion led to upregulation of these operons and iron overload in nodules, impaired intracellular persistence, and symbiotic nitrogen fixation of rhizobia. Mutualistic defects of the rirA mutant can be rescued by blocking activities of this naturally "synthetic" circuit for siderophore biosynthesis and transport. These findings not only are significant for understanding iron homeostasis of mutualistic interactions but also provide insights into assembly and integration of foreign machineries for biosynthesis and transport of siderophores, horizontal transfer of which is selected in microbiota. IMPORTANCE Iron is a public good explored by both eukaryotes and prokaryotes. The abundant ferric form is insoluble under neutral and basic pH conditions, and many bacteria secrete siderophores forming soluble ferric siderophore complexes, which can be then taken up by specific receptors and transporters. Siderophore biosynthesis and uptake machineries can be horizontally transferred among bacteria in nature. Despite increasing attention on the importance of siderophores in host-microbiota interactions, the regulatory integration process of transferred siderophore biosynthesis and transport genes is poorly understood in an evolutionary context. By focusing on the mutualistic rhizobium-legume symbiosis, here, we report how a naturally synthetic foreign siderophore gene cluster was integrated with the rhizobial indigenous regulation cascade, which is essential for maintaining mutualistic interactions.