Summary: Objectives: To evaluate the in vitro anti -bacterial activity of a silver-impregnated coating against a biofilm-forming strain of methicillin-resistant Staphylococcus pseud -intermedius (MRSP).Methods: A clinical MRSP isolate sourced from a failed canine knee implant was evaluated for biofilm production and used in the present study. Using a standard test method and a clinically approved titanium substrate, the antimicrobial activity of a novel silver plasma coating was determined at two times: five minutes after inoculation of the specimens (T0) and after 24 hours of incubation (T24). Scanning electron microscopy was used to evaluate the biofilm formation on specimens.Results: The tested clinical MRSP isolate was classified as a strong biofilm producer. The silver coating significantly reduced the MRSP growth more than four log steps compared to the non-coated specimens and showed more than 99.98% reduction in the number of colony forming units after 24 hours. Scanning electron microscopy images revealed that silver-coated surfaces did not manifest detectable biofilm, while biofilm formation was readily observed on the control specimens.Clinical significance: The silver coating exhibited excellent activity against the multi-drug resistant biofilm-forming MRSP isolate. The next stage of this work will involve testing in an animal model of orthopaedic infection. Positive results from animal studies would support the introduction of the silver plasma coating as a new strategy for preventing implant contamination, biofilm formation, and surgical infection in dogs undergoing orthopaedic surgery.Supplementary Material for this paper is available online at: http://dx.doi.org/10.3415/VCOT-15-08-0134

Heart failure (HF) presents a significant clinical challenge, with current treatments mainly easing symptoms without stopping disease progression. The targeting of calcium (Ca²⁺) regulation is emerging as a key area for innovative HF treatments that could significantly alter disease outcomes and enhance cardiac function. In this review, we aim to explore the implications of altered Ca²⁺ sensitivity, a key determinant of cardiac muscle force, in HF, including its roles during systole and diastole and its association with different HF types—HF with preserved and reduced ejection fraction (HFpEF and HFrEF, respectively). We further highlight the role of the two rate constants k_on (Ca²⁺ binding to Troponin C) and k_off (its dissociation) to fully comprehend how changes in Ca²⁺ sensitivity impact heart function. Additionally, we examine how increased Ca²⁺ sensitivity, while boosting systolic function, also presents diastolic risks, potentially leading to arrhythmias and sudden cardiac death. This suggests that strategies aimed at moderating myofilament Ca²⁺ sensitivity could revolutionize anti-arrhythmic approaches, reshaping the HF treatment landscape. In conclusion, we emphasize the need for precision in therapeutic approaches targeting Ca²⁺ sensitivity and call for comprehensive research into the complex interactions between Ca²⁺ regulation, myofilament sensitivity, and their clinical manifestations in HF.

Congenital heart disease (CHD), the most common congenital anomaly, remains a significant lifelong burden despite advancements in medical and surgical interventions. Induced pluripotent stem cells (iPSCs) have emerged as a groundbreaking platform in CHD research, offering patient-specific models to investigate the genetic, epigenetic, and molecular mechanisms driving the disease. Utilizing technologies such as CRISPR/Cas9 gene editing, cardiac organoids, and high-throughput screening, iPSCs enable innovative strategies in disease modeling, precision drug discovery, and regenerative therapies. However, clinical translation faces challenges related to immaturity, differentiation variability, large-scale feasibility, and tumorigenicity. Addressing these barriers will require standardized protocols, bioengineering solutions, and interdisciplinary collaboration. This review examines the critical role of iPSCs in advancing CHD research and care, demonstrating their potential to revolutionize treatment through patient-specific, regenerative approaches. By addressing current limitations and advancing iPSC technology, the field is positioned to pave the way for precision-based CHD therapies for this lifelong condition.

Background: Because body mass index (BMI) is generally used clinically to define obesity and to estimate body adiposity, BMI likely is positively correlated with epicardial adipose tissue (EAT) level. Based on echocardiography, previous outcomes on this matter have varied from almost absent to rather strong correlations between BMI and EAT. The purpose of our study was to unambiguously examine EAT content and determine if correlations exist between EAT content and BMI, cause of heart failure, or contractile force. Methods and Results: We qualitatively scored 150 human hearts ex vivo on EAT distribution. From each heart, multiple photographs of the heart were taken, and both atrial and ventricular adipose tissue levels were semiquantitatively scored. Main findings include a generally higher EAT content on nonfailing hearts compared with end‐stage failing hearts (atrial adipose tissue level 5.70±0.13 vs. 5.00±0.12, P <0.001; ventricular adipose tissue level 5.14±0.16 vs. 4.57±0.12, P =0.0048). The results also suggest that EAT quantity is not strongly correlated with BMI in nonfailing (atrial adipose tissue level r =0.069, ventricular adipose tissue level r =0.14) or failing (atrial adipose tissue level r =−0.022, ventricular adipose tissue level r =0.051) hearts. Atrial EAT is closely correlated with ventricular EAT in both nonfailing ( r =0.92, P <0.001) and failing ( r =0.87, P <0.001) hearts. Conclusions: EAT volume appears to be inversely proportional to severity of or length of time with heart failure based on our findings. Based on a lack of correlation with BMI, it is incorrect to assume high EAT volume given high body fat percentage.