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Clostridioides difficile infection (CDI), though identified nearly five decades ago, still remains a major challenge, being associated with significant mortality rates. The strains classified as hypervirulent, notably 027/NAP1/BI, have garnered substantial attention from researchers and clinicians due to their direct correlation with the severity of the disease. Our study aims to elucidate the significance of toxigenic Clostridioides difficile (CD) strains in the clinical and therapeutic aspects of managing patients diagnosed with CDI. We conducted a single-center prospective study, including patients with CDI from north-eastern Romania. We subsequently conducted molecular biology testing to ascertain the prevalence of the presumptive 027/NAP1/BI strain within aforementioned geographic region. The patients were systematically compared and assessed both clinically and biologically, employing standardized and comparative methodologies. The study enrolled fifty patients with CDI admitted between January 2020 and June 2020. Among the investigated patients, 43 (86%) exhibited infection with toxigenic CD strains positive for toxin B genes (tcdB), binary toxin genes (cdtA and cdtB), and deletion 117 in regulatory genes (tcdC), while the remaining 7 (14%) tested negative for binary toxin genes (cdtA and cdtB) and deletion 117 in tcdC. The presence of the presumptive 027/NAP1/BI strains was linked to a higher recurrence rate (35.56%, p = 0.025), cardiovascular comorbidities (65.1% vs. 14.2%, p = 0.016), and vancomycin treatment (55.8% vs. 14.3%, p = 0.049). The findings of our investigation revealed an elevated incidence of colitis attributed to presumptive 027/NAP1/BI. Despite the prevalence of the presumptive 027 strain and its associated heightened inflammation among the patients studied, no significant differences were observed regarding the clinical course or mortality outcomes.

Background and Objective: In the landscape of heart failure, non-cardiac comorbidities represent a formidable challenge, imparting adverse prognostic implications. Holter ECG monitoring assumes a supplementary role in delineating myocardial susceptibility and autonomic nervous system dynamics. This study aims to explore the potential correlation between Holter ECG parameters and comorbidities in individuals with ischemic cardiomyopathy experiencing heart failure (HF), with a particular focus on the primary utility of these parameters as prognostic indicators. Materials and Methods: In this prospective inquiry, a cohort of 60 individuals diagnosed with heart failure underwent stratification into subgroups based on the presence of comorbidities, including diabetes, chronic kidney disease, obesity, or hyperuricemia. Upon admission, a thorough evaluation of all participants encompassed echocardiography, laboratory panel analysis, and 24 h Holter monitoring. Results: Significant associations were uncovered between diabetes and unconventional physiological indicators, specifically the Triangular index (p = 0.035) and deceleration capacity (p = 0.002). Pertaining to creatinine clearance, notable correlations surfaced with RMSSD (p = 0.026), PNN50 (p = 0.013), and high-frequency power (p = 0.026). An examination of uric acid levels and distinctive Holter ECG patterns unveiled statistical significance, particularly regarding the deceleration capacity (p = 0.045). Nevertheless, in the evaluation of the Body Mass Index, no statistically significant findings emerged concerning Holter ECG parameters. Conclusions: The identified statistical correlations between non-cardiac comorbidities and patterns elucidated in Holter ECG recordings underscore the heightened diagnostic utility of this investigative modality in the comprehensive evaluation of individuals grappling with HF. Furthermore, we underscore the critical importance of the thorough analysis of Holter ECG recordings, particularly with regard to subtle and emerging parameters that may be overlooked or insufficiently acknowledged.

Acute heart failure (AHF) is a life-threatening condition with high morbidity and mortality. Even though this pathology has been extensively researched, there are still challenges in establishing an accurate and early diagnosis, determining the long- and short-term prognosis and choosing a targeted therapeutic strategy. The use of reliable biomarkers to support clinical judgment has been shown to improve the management of AHF patients. Despite a large pool of interesting candidate biomarkers, endothelin-1 (ET-1) appears to be involved in multiple aspects of AHF pathogenesis that include neurohormonal activation, cardiac remodeling, endothelial dysfunction, inflammation, atherosclerosis and alteration of the renal function. Since its discovery, numerous studies have shown that the level of ET-1 is associated with the severity of symptoms and cardiac dysfunction in this pathology. The purpose of this paper is to review the existing information on ET-1 and answer the question of whether this neurohormone could be a promising biomarker in AHF.

Given the possible pathophysiological links between myocardial ischemia and SARS-CoV-2 infection, several studies have focused attention on acute coronary syndromes in order to improve patients’ morbidity and mortality. Understanding the pathophysiological aspects of myocardial ischemia in patients infected with SARS-CoV-2 can open a broad perspective on the proper management for each patient. The electrocardiogram (ECG) remains the easiest assessment of cardiac involvement in COVID-19 patients, due to its non-invasive profile, accessibility, low cost, and lack of radiation. The ECG changes provide insight into the patient’s prognosis, indicating either the worsening of an underlying cardiac illnesses or the acute direct injury by the virus. This indicates that the ECG is an important prognostic tool that can affect the outcome of COVID-19 patients, which important to correlate its aspects with the clinical characteristics and patient’s medical history. The ECG changes in myocardial ischemia include a broad spectrum in patients with COVID-19 with different cases reported of ST-segment elevation, ST-segment depression, and T wave inversion, which are associated with severe COVID-19 disease.

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection and it remains the most frequent cause of death amongst critically ill patients worldwide, despite recent medical advancements. The cardiac involvement in sepsis, better known as sepsis-induced cardiomyopathy, represents a form of cardiac dysfunction identified in septic patients, characterized by ventricular dilation, myocardial involvement, decreased ejection fraction and reversibility. Although the implications of cardiac involvement in sepsis can be extremely severe, this affliction has not been intensely debated in literature. Therefore, in order to better understand this affliction, we need to identify new markers. Two biomarkers, endothelin-1 (ET-1) and the soluble form of suppression of tumorigenicity 2 protein (sST2) have previously been linked to both sepsis and acute/chronic heart failure. Endothelin-1 is part of a family of amino acid peptides, that is mainly produced by endothelial cells and exerts a vasoconstrictive effect, but also causes fibrosis of the vascular cells, stimulates production of reactive oxygen species and induces proinflammatory mechanisms. During sepsis, it induces coronary vasoconstriction, decreased cardiac output, increased vascular resistance and permeability and increased fluid flux into the extravascular space on cardiac level, as well as affecting the contractility of myocardial myocytes. High values of serum ET-1 have also been identified in septic shock and in endotoxin-induced febrile responses in rats. The Suppression of tumorigenicity 2 protein (ST2) is a member of the interleukin-1 receptor family and is involved in T helper 2 cells-associated immune response. Recent studies identified a close link between ST2 and both inflammatory and heart diseases. Furthermore, it was recently approved by the Food and Drug Administration as a prognostic biomarker in heart failure and is recommended for the evaluation of additional cardiovascular risk.

Chronic kidney disease represents a complex and multifaceted pathology characterized by the presence of structural or functional renal anomalies associated with a persistent reduction in renal function. As the disease progresses, complications arise due to the chronic inflammatory syndrome, hydro-electrolytic disorders, and toxicity secondary to the uremic environment. Cardiovascular complications are the leading cause of death for these patients. Ischemic cardiac pathology can be both a consequence and complication of chronic kidney disease, highlighting the need to identify specific cardiorenal dysfunction biomarkers targeting pathophysiological mechanisms common to both conditions. This identification is crucial for establishing accurate diagnoses, prognoses, and risk stratifications for patients. This work is intended to elucidate the intricate relationship between chronic kidney disease and ischemic heart disease and to investigate the roles of cardiorenal biomarkers, including cardiac troponin, natriuretic peptides, galectin-3, copeptin, fibroblast growth factor 23 and its co-receptor Klotho, soluble suppression of tumorigenicity 2, and plasma growth differentiation factor 15.

The management of patients with peripheral artery disease (PAD) is integrative and multidisciplinary, in which cardiac rehabilitation (CR) plays a prognostic role in terms of functional status, quality of life, and long-term impact on morbidity and mortality. We conducted a prospective cohort study on 97 patients with PAD admitted to a single tertiary referral center. Based on a prognostic index developed to stratify long-term mortality risk in PAD patients, we divided the cohort into two groups: low and low-intermediate risk group (45 cases) and high-intermediate and high risk group (52 cases). We analyzed demographics, clinical parameters, and paraclinical parameters in the two groups, as well as factors associated with cardiological reassessment prior to the established deadline of 6 months. Obesity (p = 0.048), renal dysfunction (p < 0.001), dyslipidemia (p < 0.001), tobacco use (p = 0.048), and diabetes mellitus (p < 0.001) are comorbidities with long-term prognostic value. Low-density lipoprotein cholesterol (p = 0.002), triglycerides (p = 0.032), fasting glucose (p = 0.011), peak oxygen uptake (p = 0.005), pain-free walking distance (p = 0.011), maximum walking time (p < 0.001), and maximum walking distance (p = 0.002) influence the outcome of PAD patients by being factors associated with clinical improvement at the 6-month follow-up. PAD patients benefit from enrollment in CR programs, improvement of clinical signs, lipid and carbohydrate profile, and weight loss and maintenance of blood pressure profile within normal limits, as well as increased exercise capacity being therapeutic targets.

Introduction: Antimicrobial resistance (AMR) is currently a growing concern among healthcare providers, underscoring the importance of describing the regional susceptibility profile for common microorganisms that are associated with urinary tract infections (UTIs). This knowledge serves as the foundation for proper empirical therapeutic recommendations tailored to local susceptibility patterns. Results: We found a high prevalence of ESBL-producing strains (36.9%), with Escherichia coli and Klebsiella spp. being the most prevalent isolated bacteria. Among the catheterized patients, Klebsiella spp. emerged as the primary etiology, with a significant correlation between catheterization and Proteus spp. (p = 0.02) and Providencia stuartii (p < 0.0001). We observed significant correlations between urinary catheterization and older age (68.9 ± 13.7 years vs. 64.2 ± 18.1 years in non-catheterized patients, p = 0.026) and with the presence of an isolate with extensive drug resistance (p < 0.0001) or even pandrug resistance (p < 0.0001). Susceptibility rates significantly decreased for almost all the tested antibiotics during the study period. Notably, susceptibility was markedly lower among catheterized patients, with the most pronounced differences observed for carbapenems (59.6% versus 83.4%, p < 0.0001) and aminoglycosides (37.1% versus 46.9%, p = 0.0001). Materials and Methods: We conducted a retrospective study analyzing the susceptibility profiles of 724 extended-spectrum beta-lactamases (ESBL)-producing Enterobacterales isolated from urine cultures. Our focus was on highlighting susceptibility profiles among isolates associated with urinary catheterization and assessing the shifts in the susceptibility rates over time. Conclusions: The constant rise in AMR rates among Enterobacterales presents significant challenges in treating severe infections, particularly among urinary catheterized patients. This trend leaves clinicians with limited or no effective treatment options. Consequently, the development and implementation of personalized treatment protocols are imperative to ensure efficient empirical therapies.

Epicardial adipose tissue (EAT) is a unique fat depot located around the heart, intimately associated with the myocardium and coronary arteries. The secretion of bioactive molecules and their interaction with neighbouring cardiac tissues makes it an active organ with important implications in cardiovascular health and disease. In recent years, omics technologies have provided valuable insights into the molecular characteristics and functional relevance of EAT in patients with coronary atherosclerosis, myocardial infarction, atrial fibrillation and associated metabolic disorders. This review aims to summarize the current understanding of EAT biology through the lens of genomics, transcriptomics, proteomics and lipidomics approaches. We discuss key findings from omics studies on EAT, including gene expression profiles, metabolic activity, signalling pathways and regulatory network, in order to explore in depth the disease mechanisms, possible therapeutic strategies, and cardiovascular risk assessment. Further advances in this field and integrating data from multiple omics platforms hold promise for unlocking personalized cardiometabolic profiles with EAT as a possible biomarker and therapeutic target in cardiovascular disease.

This research focused on establishing a hierarchy concerning the influence of various biological markers and body composition parameters on preventing, diagnosing and managing Metabolic Syndrome (MetS). Our cross-sectional cohort study included 104 subjects without any atherosclerotic antecedent pathology, organized in two groups (with and without MetS). All participants underwent clinical and anthropometric measurements, DEXA investigation and blood tests for all MetS criteria, together with adiponectin, leptin, insulin, uric acid and CRP. Based on mathematical logic, we calculated a normalized sensitivity score to compare the predictive power of biomarkers and parameters associated with MetS, upon the prevalence of MetS. Patients with MetS report higher levels of uric acid (p = 0.02), CRP (p = 0.012) and lower levels of adiponectin (p = 0.025) than patients without MetS. The top three biological markers with the highest predictive power of the prevalence of the disease are HDL, insulin, and adiponectin:leptin ratio, and the top three body composition parameters are trunk fat-free percentage, waist-height ratio and trunk fat percentage. Their high sensitivity scores differentiate them from all the other markers analysed in the study. Our findings report relevant scores for estimating the importance of cardiometabolic risks in the prevalence of MetS. The high rank of protective markers, HDL and trunk fat-free percentage, suggest that positive effects have a stronger association with the prevalence of MetS, than negative ones do. Therefore, this risk stratification study provides important support for prevention and management programs regarding MetS.