ABSTRACT
INTRODUCTION: Pregnant women and their offspring are often at increased direct and indirect risks of adverse outcomes during epidemics and pandemics. A coordinated research response is paramount to ensure that this group is offered at least the same level of disease prevention, diagnosis, and care as the general population. We conducted a landscape analysis and held expert consultations to identify research efforts relevant to pregnant women affected by disease outbreaks, highlight gaps and challenges, and propose solutions to addressing them in a coordinated manner. METHODS: Literature searches were conducted from 1 January 2015 to 22 March 2022 using Web of Science, Google Scholar and PubMed augmented by key informant interviews. Findings were reviewed and Quid analysis was performed to identify clusters and connectors across research networks followed by two expert consultations. These formed the basis for the development of an operational framework for maternal and perinatal research during epidemics. RESULTS: Ninety-four relevant research efforts were identified. Although well suited to generating epidemiological data, the entire infrastructure to support a robust research response remains insufficient, particularly for use of medical products in pregnancy. Limitations in global governance, coordination, funding and data-gathering systems have slowed down research responses. CONCLUSION: Leveraging current research efforts while engaging multinational and regional networks may be the most effective way to scale up maternal and perinatal research preparedness and response. The findings of this landscape analysis and proposed operational framework will pave the way for developing a roadmap to guide coordination efforts, facilitate collaboration and ultimately promote rapid access to countermeasures and clinical care for pregnant women and their offspring in future epidemics.
Subject(s)
Delivery of Health Care , Pandemics , Humans , Pregnancy , Female , Disease OutbreaksABSTRACT
INTRODUCTION: Urotensin II (UII) is a vasoactive peptide secreted by endothelial cells. Increased plasma UII concentration was observed in patients with heart failure, liver cirrhosis, diabetic nephropathy and renal insufficiency. In patients with myocardial infarction both increased and decreased plasma UII concentrations were demonstrated. The aim of this study was to analyze whether plasma UII concentration reflects the severity of acute coronary syndrome (ACS). MATERIAL AND METHODS: One hundred and forty-nine consecutive patients with ACS, without age limit, were enrolled in the study. In all patients plasma concentration of creatinine, creatine kinase isoenzyme MB (CK-MB), troponin C, N-terminal prohormone of brain natriuretic peptide (NT-pro BNP), and UII were assessed, and echocardiography was performed in order to assess the degree of left ventricular hypertrophy, ejection fraction (EF) and mass (LVM). RESULTS: In patients with the highest risk (TIMI 5-7) plasma UII concentration was significantly lower than in those with low risk (TIMI 1-2): 2.61±1.47 ng/ml vs. 3.60±2.20 ng/ml. Significantly lower plasma UII concentration was found in patients with increased concentration of troponin C (2.60±1.52 ng/ml vs. 3.41±2.09 ng/ml). There was a significant negative correlation between plasma UII concentration and TIMI score or concentration of troponin C, but not CK-MB. Borderline correlation between plasma UII and ejection fraction (R = 0.157; p=0.063) or NT-proBNP (R = - 0.156; p=0.058) was found. CONCLUSIONS: Decreased plasma urotensin II concentration in patients with ACS could be associated with more severe injury of myocardium.
ABSTRACT
Chronic kidney disease is a worldwide growing problem in public health. It is a risk factor for complications in patients with acute coronary syndrome (ACS). Diabetes, hypertension (hypertrophy and left ventricular failure), impaired fibrinolysis and coagulation processes, as well as the rapid development of atherosclerosis (partly associated with chronic inflammation) are responsible for higher prevalence of cardiovascular diseases in patients with chronic kidney disease. Inflammatory process of unknown aetiology belongs to the so-called non-traditional risk factors in development of cardiovascular system diseases. It is thought that this process is responsible for adverse remodelling of atherosclerosis plaque and its instability which causes plaque rupture and as a result a coronary syndrome occurrence. Important inflammatory mediators, which take part in pathogenesis of ACS, are acute phase proteins such as: C-reactive protein, adhesion molecules VCAM-1, ICAM-1, selectins, plasma amyloid A, metalloproteinases, interleukins-1 and -6, tumour necrosis factor-a and vascular endothelial growth factor.
