Despite the rapid advancement of left ventricular assist devices (LVADs), adverse events leading to deaths have been frequently reported in patients implanted with LVADs, including bleeding, infection, thromboembolism, neurological dysfunction and hemolysis. Cannulation forms an important component with regards to thrombus formation in assisted patients by varying the intraventricular flow distribution in the left ventricle (LV). To investigate the correlation between LVAD cannula placement and potential for thrombus formation, detailed analysis of the intraventricular flow field was carried out in the present study using a two way fluid structure interaction (FSI), axisymmetric model of a passive LV incorporating an inflow cannula. Three different cannula placements were simulated, with device insertion near the LV apex, penetrating one-fourth and mid-way into the LV long axis. The risk of thrombus formation is assessed by analyzing the intraventricular vorticity distribution and its associated vortex intensity, amount of stagnation flow in the ventricle as well as the level of wall shear stress. Our results show that the one-fourth placement of the cannula into the LV achieves the best performance in reducing the risk of thrombus formation. Compared to cannula placement near the apex, higher vortex intensity is achieved at the one-fourth placement, thus increasing wash out of platelets at the ventricular wall. One-fourth LV penetration produced negligible stagnation flow region near the apical wall region, helping to reduce platelet deposition on the surface of the cannula and the ventricular wall.

The circadian system in the human body responds to daily environmental changes to optimise behaviour according to the biological clock and also influences various physiological processes. The suprachiasmatic nuclei are located in the anterior hypothalamus of the brain, and they synchronise to the 24 h light/dark cycle. Human physiological functions are highly dependent on the regulation of the internal circadian clock. Skeletal muscles comprise the largest collection of peripheral clocks in the human body. Both central and peripheral clocks regulate the interaction between the musculoskeletal system and energy metabolism. The skeletal muscle circadian clock plays a vital role in lipid and glucose metabolism. The pathogenesis of osteoporosis is related to an alteration in the circadian rhythm. In the present review, we discuss the disturbance of the circadian rhythm and its resultant effect on the musculoskeletal system. We also discuss the nutritional strategies that are potentially effective in maintaining the system’s homeostasis. Active collaborations between nutritionists and physiologists in the field of chronobiological and chrononutrition will further clarify these interactions. This review may be necessary for successful interventions in reducing morbidity and mortality resulting from musculoskeletal disturbances.

Background/Objectives: Nutritional status significantly influences cardiac surgery outcomes, with malnutrition contributing to poorer results and increased complications. This study addresses the critical gap in understanding by exploring the relationship between pre-operative nutritional status and post-operative cognitive dysfunction (POCD) in adult cardiac patients. Methods: A comprehensive search across key databases investigates the prevalence of malnutrition in pre-operative cardiac surgery patients, its effects, and its association with POCD. Factors exacerbating malnutrition, such as chronic illnesses and reduced functionality, are considered. The study also examines the incidence of POCD, its primary association with CABG procedures, and the impact of malnutrition on complications like inflammation, pulmonary and cardiac failure, and renal injury. Discussions: Findings reveal that 46.4% of pre-operative cardiac surgery patients experience malnutrition, linked to chronic illnesses and reduced functionality. Malnutrition significantly contributes to inflammation and complications, including POCD, with an incidence ranging from 15 to 50%. CABG procedures are particularly associated with POCD, and malnutrition prolongs intensive care stays while increasing vulnerability to surgical stress. Conclusions: The review underscores the crucial role of nutrition in recovery and advocates for a universally recognized nutrition assessment tool tailored to diverse cardiac surgery patients. Emphasizing pre-operative enhanced nutrition as a potential strategy to mitigate inflammation and improve cognitive function, the review highlights the need for integrating nutrition screening into clinical practice to optimize outcomes for high-risk cardiac surgery patients. However, to date, most data came from observational studies; hence, there is a need for future interventional studies to test the hypothesis that pre-operative enhanced nutrition can mitigate inflammation and improve cognitive function in this patient population.

The inability to accurately predict the occurrence of postoperative cognitive dysfunction (POCD) among open-heart surgery patients leads to concerning increases in POCD cases. Preoperative circulating biomarkers are important to identify as they are non-invasive and could provide an early prediction of POCD development, allowing for earlier and more strategized interventions. However, to date, no robust circulating biomarkers have proven effective for preoperative POCD prediction. This systematic review aims to synthesize current evidence on preoperative protein profiling among POCD patients following open-heart surgery. Thus, a thorough literature search employing PubMed, EBSCOhost, Scopus, and Science Direct was carried out. This combination of keywords was used as part of the search strategy: (“Postoperative cognitive decline” OR “Postoperative cognitive disorders” OR “Postoperative cognitive dysfunction” OR “Postoperative cognitive complications”) AND (“Thoracic Surgery” OR “Cardiac Surgery” OR “Heart Surgery”) AND (“Protein expression” OR proteomic OR “Protein profiling”). Eight hundred and twenty-nine studies were retrieved and only clinical studies reporting the circulating preoperative differentially expressed Proteins (DEPs) in the POCD patients were selected. Six studies were selected following the inclusion and exclusion criteria. Only one preoperative DEP and four immediate postoperative DEPs were extracted from the studies. All four proteins were selected for analysis using DAVID, STRING, and Cytoscape software. Due to the very low number of proteins, no clusters have been identified. This systematic review demonstrates the lack of POCD preoperative biomarkers for open-heart-surgery patients. Thus, it is suggested that more studies can be conducted to fill this gap.

Postoperative cognitive dysfunction (POCD) is cognitive decline after surgery. The authors hypothesized that gene-level changes could be involved in the pathogenesis of POCD. The present study evaluated the incidence of POCD and its associated differentially expressed genes. This was a prospective cohort study conducted on high-risk coronary artery bypass graft patients aged 40 to 75 years. POCD classification was based on a one standard deviation decline in the postoperative scores compared to the preoperative scores. The differentially expressed genes were identified using microarray analysis and validated using quantitative RT-PCR. Forty-six patients were recruited and completed the study. The incidence of POCD was identified using a set of neurocognitive assessments and found to be at 17% in these high-risk CABG patients. Six samples were selected for the gene expression analyses (3 non-POCD and 3 POCD samples). The findings showed five differentially expressed genes in the POCD group compared to the non-POCD group. The upregulated gene was ERFE, whereas the downregulated genes were KIR2DS2, KIR2DS3, KIR3DL2, and LIM2. According to the results, the gene expression profiles of POCD can be used to find potential proteins for POCD diagnostic and predictive biomarkers. Understanding the molecular mechanism of POCD development will further lead to early detection and intervention to reduce the severity of POCD, and hence, reduce the mortality and morbidity rate due to the condition.

Background: Infective endocarditis (IE) is a life-threatening cardiovascular infection with in-hospital mortality of 15–30% despite modern therapy. Contemporary IE demonstrates non-random valve involvement: aortic 40–60%, mitral 20–40%, tricuspid 5–10% (30–50% in intravenous drug users [IVDU]), and pulmonary < 1%. These patterns implicate valve-specific anatomy and hemodynamics as central determinants of susceptibility. Methods: Structured narrative review of English-language literature from PubMed/MEDLINE, Embase, Scopus, and Google Scholar (January 1990–March 2026). Search terms included “infective endocarditis,” “valve anatomy,” “hemodynamics,” “bicuspid aortic valve,” “prosthetic valve endocarditis,” and “TAVR endocarditis.” We included anatomical studies, clinical cohorts, surgical series, imaging research, and international guidelines. Evidence was synthesized narratively using Oxford CEBM levels. Results: IE susceptibility follows a biologically coherent gradient shaped by hemodynamic stress, endothelial injury, and structural substrate. The aortic valve (40–60% of native IE) is most vulnerable due to high shear stress, frequent congenital anomalies (bicuspid aortic valve [BAV]: 2% prevalence, 24% of aortic IE), and direct fibrous skeleton continuity—predisposing to periannular extension (30–40%). Mitral IE (20–40%) is largely conditional on structural disease (mitral valve prolapse [MVP]: 8-fold risk increase; embolic rates 30–50%). Tricuspid IE (5–10%; 30–50% in IVDU) reflects low-pressure hemodynamics with lower mortality (10–20%) but high recurrence (15–30%). Pulmonary IE (< 1%) is rare due to minimal hemodynamic stress. Prosthetic valves carry 0.3–6% annual IE risk; TAVR-specific risks include paravalvular regurgitation and residual native tissue. Conclusions: IE susceptibility is fundamentally determined by valve-specific anatomy interacting with hemodynamic forces and microbial virulence. This anatomy-informed framework guides risk stratification and identifies prevention targets.