Background: Biomarkers, electrocardiogram (ECG) and Holter ECG are basic, accessible and feasible cardiac investigations. The combination of their results may lead to a more complex predictive model that may improve the clinical approach in acute heart failure (AHF). The main objective was to investigate which ECG parameters are correlated with the usual cardiac biomarkers (prohormone N-terminal proBNP, high-sensitive cardiac troponin I) in patients with acute heart failure, in a population from Romania. The relationship between certain ECG parameters and cardiac biomarkers may support future research on their combined prognostic value. Methods: In this prospective case-control study were included 49 patients with acute heart failure and 31 participants in the control group. For all patients we measured levels of prohormone N-terminal proBNP (NT-proBNP), high-sensitive cardiac troponin I (hs-cTnI) and MB isoenzyme of creatine phosphokinase (CK-MB) and evaluated the 12-lead ECG and 24 h Holter monitoring. Complete clinical and paraclinical evaluation was performed. Results: NT-proBNP level was significantly higher in patients with AHF (p < 0.001). In patients with AHF, NT-proBNP correlated with cQTi (p = 0.027), pathological Q wave (p = 0.029), complex premature ventricular contractions (PVCs) (p = 0.034) and ventricular tachycardia (p = 0.048). Hs-cTnI and CK-MB were correlated with ST-segment modification (p = 0.038; p = 0.018) and hs-cTnI alone with complex PVCs (p = 0.031). Conclusions: The statistical relationships found between cardiac biomarkers and ECG patterns support the added value of ECG in the diagnosis of AHF. We emphasize the importance of proper ECG analysis of more subtle parameters that can easily be missed. As a non-invasive technique, ECG can be used in the outpatient setting as a warning signal, announcing the acute decompensation of HF. In addition, the information provided by the ECG complements the biomarker results, supporting the diagnosis of AHF in cases of dyspnea of uncertain etiology. Further studies are needed to confirm long-term prognosis in a multi-marker approach.

Carbapenems are essential for the treatment of severe infections caused by Gram-negative bacteria, particularly in critically ill and immunocompromised patients. However, the global rise of carbapenem-resistant Enterobacterales (CRE), Pseudomonas aeruginosa, and Acinetobacter baumannii has significantly eroded their effectiveness, and the phenomenon is now recognized as a major public health threat. Resistance is driven by the complex and evolving interplay of enzymatic and non-enzymatic mechanisms, occurring within highly successful clonal lineages and mobile genetic platforms. This review summarizes advances since 2020 in the molecular basis of carbapenem resistance, integrating enzymatic mechanisms across Ambler classes A, B, C, and D with emerging non-enzymatic contributors, including porin remodeling, efflux pump upregulation, target-site alterations, and outer-membrane adaptations. Particular attention is given to adaptive genome dynamics, such as IS26-mediated gene amplification, plasmid multimerization, and heteroresistance, that generate unstable resistance phenotypes and complicate routine susceptibility testing. Newly introduced β-lactam/β-lactamase inhibitor combinations exert distinct selective pressures: ceftazidime–avibactam favors KPC Ω-loop variants and permeability defects, often restoring carbapenem susceptibility, whereas meropenem–vaborbactam and imipenem–relebactam resistance is driven mainly by porin loss and β-lactamase gene amplification. Cefiderocol resistance is multifactorial, frequently involving impaired siderophore uptake and heteroresistance, while sulbactam–durlobactam remains active against OXA-producing A. baumannii but is compromised by metallo-β-lactamases and PBP3 alterations. Carbapenem resistance is increasingly characterized by convergent, multi-layered adaptations that undermine both established and novel therapies. While high-level randomized evidence remains limited for some resistance mechanisms, emerging mechanistic, microbiological, and clinical data support the need for mechanism-aware diagnostics, repeated susceptibility assessment during therapy, and stewardship strategies informed by resistance biology. Integrating molecular context into routine practice will be critical to preserving emerging treatment options and limiting the global impact of carbapenem resistance.

Early research into the implications concerning the evolution of the infection caused by the new coronavirus in people with glucose metabolism dysfunction, in this case diabetics, shows that severe forms of the disease predominate in this risk category. Moreover, it seems that even in patients with normal glycaemic status, COVID-19 may predispose to the development of hyperglycaemia which modulates immune mechanisms and inflammatory responses, with direct effects on morbidity and mortality. Thus, taking into account these scientific data, as well as the increased frequency of diabetes in the general population, we aimed to assess the risk of an unfavourable outcome of diabetic patients, which is in a strong connection with the presence and severity of pulmonary disease such as interstitial pneumonia/bronchopneumonia, as well as the effectiveness of Tocilizumab administration. The results of our study indicate a three-fold higher risk of death in patients with diabetes and COVID-19 (RR = 3.03; IC95%: 2.37–3.86; p = 0.001),compared to nondiabetic patients, and the risk of developing severe forms of acute respiratory failure was 1.5 times higher in the first studied category. In conclusion, we can say that the diabetic diagnosed with SARS-CoV-2 infection is more predisposed to immunological and organic dysfunctions that may ultimately result in death, and treatment with monoclonal anti-IL-6 antibodies was more effective in diabetic patients than non-diabetics (p < 0.05). The effectiveness of Tocilizumab was significant in both studied groups, but diabetic patients responded better to this therapy compared to non-diabetes-mellitus (DM) ones (76.7% vs. 35% p = 0.001).

Sepsis, defined as a dysregulated host response to infection, is one of the leading causes of mortality worldwide. It unleashes in the organism a cascade of molecules, cytokines, and proteins which leads to an inflammatory storm. If this response to infection is uncontrolled, any organ is susceptible to damage. Acute kidney injury (AKI) is one of the most frequent organ dysfunctions in septic patients, and while it can be reversible, its presence leads to a higher burden of morbidity and mortality. While serum creatinine is essential in evaluating kidney function, the pathophysiology of AKI is not completely elucidated, and a plethora of novel biomarkers have been studied in the hope of an early diagnosis and fast treatment. While the liver is not as affected by sepsis, it plays an important role as a guardian by providing acute-phase proteins, activating neutrophils, and controlling iron balance. Acute liver failure (ALF) could impair the organism’s capacity to contain and eliminate pathogens. Some molecules have been associated with either AKI or ALF, although biomarkers specific for organ dysfunction are difficult to validate. The aim of this review is to understand the role of several molecules in the pathophysiology of sepsis and their clinical ability for diagnosing or predicting sepsis-induced hepato-renal dysfunction.

Sepsis represents a life-threatening organ dysfunction caused by a dysregulated host response to infection, and is considered a medical emergency. Therefore, quick diagnosis and treatment are required in order to improve survivability. Currently, patient evaluation in sepsis is based on the Sequential Organ Failure Assessment (SOFA) score to determine the severity of the disease; however, novel biomarkers are also actively researched with the aim to develop quicker diagnostic tools and better therapy. Endothelin-1 is one of the most potent vasoconstrictors found in the human body and is involved in the pathophysiology of both sepsis and other conditions involving organs that make up the SOFA score. In this narrative review, we aimed to gather information of this peptide’s multiple effects and to help determine whether or not it could prove a valuable biomarker in the evaluation of patients with multi-organ dysfunction in sepsis.