Objective Although cardiovascular syndrome X was described many years ago, its causes are still unclear. Many studies have addressed the autonomic function, whereas others have investigated the coronary reserve. The purpose of this study was to investigate the correlations between parasympathetic dysfunction and coronary flow reserve deficiency. Basic methods Eleven consecutive women suffering from cardiovascular syndrome X were enrolled in the study. All the patients underwent the analysis of heart rate and blood pressure variability, the cold face test and noninvasive evaluation of the coronary flow reserve by transthoracic echocardiography. Comparison was made with healthy volunteers. Results Seven patients (64%) showed vagal impairment in the analysis of heart rate and blood pressure variability and a pathological response to the cold face test, whereas four patients (36%) did not show significant differences from the control group. In these three groups, patients with and without vagal impairment and controls, there was a difference in the mean diastolic coronary velocity reserve (1.94±0.48; 3.73±0.95, 2.88±0.55, P=0.0005) and in maximal diastolic velocity reserve (2.00±0.48, 3.26±0.64, 2.65±0.57, P=0.0047). Post-hoc analysis demonstrated that the mean and maximal diastolic velocity reserves of the patients with vagal impairment seemed to be reduced compared with those of the other groups (P<0.05), which were similar. Conclusions This study confirmed that syndrome X patients represent a heterogeneous group. More than half of the patients exhibited vagal dysfunction. In these patients, coronary flow reserve was abnormal compared with controls and other syndrome X patients without vagal impairment.

Background: Central venous access devices (CVADs) are crucial for various medical conditions, but pose risks, including catheter-related bloodstream infections (CRBSI). CRBSI increases comorbidity, mortality, and healthcare costs. Surveillance and evidence-based guidelines have successfully reduced CRBSI rates, although the COVID-19 pandemic has led to increased infection rates. Main body: This review explores strategies for reducing the incidence of CRBSI and examines factors contributing to variations in reported rates across developed countries. Highlighting the significant morbidity, mortality, and healthcare resource burden associated with CRBSI, the analysis delves into evidence-backed preventive measures. It discusses the impact of the COVID-19 pandemic on infection rates and proposes resilient strategies in response to these challenges. The review emphasises the importance of understanding CRBSI pathogenesis, patient, procedure, and device-related risk factors, and the implementation of evidence-guided algorithms and surveillance measures. Recommendations include the use of all-inclusive procedure packs, ultrasound-guided placement, daily dressing changes with antimicrobial treatment, and the use of antimicrobial locks. Conclusions: The review underscores the need for clear, concise algorithms adaptable to various healthcare settings and the scalability of infection prevention systems to ensure resilience.

Despite the proven superiority of the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) over the Cockcroft–Gault (CG) formula, current guidelines recommend the latter to assess renal function in patients treated with non-vitamin K antagonist oral anticoagulants (NOACs). To assess the relationship between the CG and the recommended CKD-EPI formulas, in a cohort of atrial fibrillation (AF) patients treated with NOACs, and the misclassifications introduced by the CG formula for renal function levels, we estimated renal function with three equations: CG, CKD-EPI with body surface adjustment (1.73 mL/m², CKD-EPI) and without such adjustment (CKD-EPI_noBSA), in all consecutive AF patients discharged from NOACs from the Cardiology Division of a main city hospital between February 1st and May 31st 2018. We compared the different estimates of glomerular filtration rate and potential renal function class misclassifications. We reclassified 37/115 patients (32.1%) when switching from the CG to the CKD-EPI; and 24/115 (20.8%) switching from the CG to the CKD-EPI_noBSA formulas. Class reallocation was distributed across all levels of renal function, but mostly affected the “hyper-normal” function. In estimating consequences of such reallocation, a change in NOAC dosages would have occurred in 10/115 patients (8.7%) when switching from the CG to the CKD-EPI formula and in 10/115 patients when switching from the CG to the CKD-EPI_noBSA formula. Although the CG method has been traditionally used to calculate renal function in all NOAC studies, a renal dysfunction class reallocation occurs in a substantial fraction of hospital-admitted AF patients with the use of better estimates of renal function.

Peripartum cardiomyopathy (PCM) is a relatively rare disease with potentially devasting consequences requiring prompt identification and correct treatment. Overall prognosis is good in majority of the cases, although some patients may progress to irreversible heart failure. Early diagnosis is important and effective treatment reduces mortality rates and increases the chance of complete recovery of ventricular systolic function. The aetiology and pathogenesis seems to be multifactorial and poorly understood, with the available literature rather conflicting. In recent years, there has been increased interest in the role played by genetic predisposition in the development of PCM. It probably develops as a result of a complex interaction of pregnancy-associated factors and genetic factors and recently there have been many observations pointing out the central role played by a genetic predisposition. The direct and indirect observations on genetic susceptibility may offer new insights into the pathogenesis of PCM. However, larger studies are needed before advising routine genetic testing in these patients.