Targeted education for clinicians and clinical coding staff improves the accuracy of clinical coding: A quality improvement project.

The allocation of healthcare resources is reliant upon accurate information generated through clinical coding. Several factors contribute to coding inaccuracies, one of which is interpreting medical documentation. A lack of awareness among medical staff of the clinical coding process and the importance of detailed documentation exacerbates this problem. To investigate this further, 1 month of inpatient clinical coding data from a single hospital ward was reviewed by clinicians experienced in the coding and auditing process. If the reviewing clinician identified inaccuracies in the initial clinical coding, Healthcare Resource Group (HRG) codes were changed. Education sessions were then provided both to junior clinicians working on the hospital ward and to clinical coding staff and a further month of clinical coding data was again reviewed to assess for any difference after the sessions. HRG changes were made in 58.5% of 94 cases initially. Following the educational sessions, 20.5% of HRGs changed in 73 cases (p<0.0001), indicating more accurate initial clinical coding. There were also statistically significant reductions in the extent to which the primary and secondary diagnoses were changed. This study demonstrates that targeted education sessions for both junior clinicians and clinical coding staff can improve the accuracy of inpatient clinical coding.

Marine transmissible cancer navigates urbanized waters, threatening spillover.

Inter-individual transmission of cancer cells represents a unique form of microparasites increasingly reported in marine bivalves. In this study, we sought to understand the ecology of the propagation of Mytilus trossulus Bivalve Transmissible Neoplasia 2 (MtrBTN2), a transmissible cancer affecting four Mytilus mussel species worldwide. We investigated the prevalence of MtrBTN2 in the mosaic hybrid zone of M. edulis and M. galloprovincialis along the French Atlantic coast, sampling contrasting natural and anthropogenic habitats. We observed a similar prevalence in both species, probably due to the spatial proximity of the two species in this region. Our results showed that ports had higher prevalence of MtrBTN2, with a possible hotspot observed at a shuttle landing dock. No cancer was found in natural beds except for two sites close to the hotspot, suggesting spillover. Ports may provide favourable conditions for the transmission of MtrBTN2, such as high mussel density, stressful conditions, sheltered and confined shores or buffered temperatures. Ships may also spread the disease through biofouling. Our results suggest ports may serve as epidemiological hubs, with maritime routes providing artificial gateways for MtrBTN2 propagation. This highlights the importance of preventing biofouling on docks and ship hulls to limit the spread of marine pathogens hosted by fouling species.

Endothelin Receptor Blockade Improves Cerebral Blood Flow-Mediated Dilation in a Mouse Model of Alzheimer's Disease.

INTRODUCTION: Cerebral blood flow (CBF) is reduced in patients with Alzheimer's disease (AD). Flow-mediated dilation (FMD), which plays a key role in the regulation of blood flow, is attenuated by endothelin-1. We hypothesized that endothelin receptor blockade may improve CBF in AD. METHODS: We investigated cerebrovascular reactivity in a mouse model of AD (APP-PS1; 5-6-month-old male subjects). We assessed the in vivo response to normoxic hypercapnia and in vitro FMD in isolated cerebral and mesenteric resistance arteries before and after endothelin receptor blockade (bosentan). RESULTS: Normoxic hypercapnia increased basilar trunk blood flow velocity (+12.3 ± 2.4%; p = 0.006, n = 6) in wild-type (WT) mice but reduced blood flow in APP-PS1 mice (-11.4 ± 1.2%; p < 0.0001, n = 8). Bosentan (50 mg/kg, acute intraperitoneal injection) restored cerebrovascular reactivity in APP-PS1 mice (+10.2 ± 2.2%; p < 0.0001, n = 8) but had no effect in WT. FMD was reduced in the posterior cerebral artery of APP-PS1 compared to WT and was normalized by bosentan (1 µmol/L, 30 min, or 50 mg/kg/day for 28 days). FMD was similar in the mesenteric artery of APPS-PS1 and WT. CONCLUSION: APP-PS1 mice exhibited cerebrovascular endothelial dysfunction. Acute and chronic blockade of endothelin receptors restored endothelial vasomotor function, suggesting a promising therapeutic approach to restoring cerebral vasoreactivity in AD.

The Effectiveness of Common Interventions in the Management of Sickle Cell Disease in Primary Care Settings: A Review.

Sickle cell disease (SCD), a chronic condition that affects men and women equally, continues to present a public health burden in the United States due to its associated morbidity and complications. Despite advances in medical knowledge and the design of novel therapies for managing the disease, its burden remains compounded because of increasing rates of immigration arising from global displacements and economic unrest in many countries. We thus conducted a comprehensive literature review of publications from 2000 to 2022 to gather guidelines on managing SCD, with a search through four databases, PubMed, Embase, Google Scholar, and Cochrane; 42 articles met the final inclusion criteria after the full-text article screening process. In the United States healthcare system, primary care physicians (PCPs) are generally providers who cater to the lifelong management of chronic medical conditions, SCD not being an exception. While more SCD patients now present to primary care clinics, many PCPs still lack the confidence and adequate experience necessary to manage the condition effectively. The gap created by the shortage of PCPs extensively equipped to provide comprehensive SCD care leads to poor health outcomes for patients. It is imperative now more than ever to continue to raise awareness about this condition at the provider level, to ensure that patients receive well-rounded care to improve their quality of life and clinical outcomes. Providing up-to-date knowledge about existing and novel therapies and/or modalities of SCD treatment would undoubtedly equip the PCPs with self-assurance to manage the condition adeptly. Thus, we explore various public health interventions such as hydroxyurea therapy, pneumococcal vaccination, penicillin therapy, iron chelation therapy, and clinical decision support tools that have been implemented in primary healthcare settings and shown to be effective in improving SCD care. We also discuss recent advancements that can lead to improved outcomes for SCD patients in the future.

Abiraterone-Induced Hypokalemia: A Case Report.

Abiraterone, an androgen biosynthesis inhibitor drug approved by the Food and Drug Administration (FDA) in 2011 for the treatment of metastatic prostate cancer, has seen an increase in prescriptions over the years, owing largely to the aging population and the association of prostate cancer with increasing age. As the rate of abiraterone prescription increases, it is important for physicians to be aware of its adverse effects profile to improve patient outcomes. This case report explains the mechanism, clinical presentation, and management of abiraterone-induced hypokalemia in a 67-year-old male with prostate cancer and highlights the importance of close monitoring and management of electrolyte levels for patients on abiraterone.

Thoracic Aortic Rupture Post Cardiopulmonary Resuscitation in a Patient With Previous Thoracic Aneurysm Repair.

Aortic dissection is characterized by a tear or rupture in the intimal layer of the aorta causing blood to flow between the layers of the arterial wall, thus separating them. While cardiopulmonary resuscitation (CPR) is a life-saving intervention, it can unintentionally contribute to the development or worsening of aortic dissection. The forceful chest compressions involved in CPR can put significant pressure on the fragile aortic wall, potentially leading to a tear or rupture. This highlights the delicate balance between life-saving measures and the potential risks they carry. Though studies have been done on the effects of CPR on the thoracic wall, few reports have studied the effects on the structures that lie in the thoracic cavity. The authors present a 63-year-old with a history of thoracic aneurysm repair who experienced a cardiac arrest while choking on food at home. The patient received CPR and a CT scan done thereafter revealed thoracic dissection and rupture. The patient received medical management in the Intensive Care Unit but eventually expired due to irreversible neurological damage. This highlights the importance of recognizing that CPR can pose a risk for aortic dissection and rupture, particularly in individuals with prior aortic repairs. It emphasizes the need for developing protocols to monitor patients who have undergone aneurysmal repair and adjusting CPR techniques to suit their specific needs. Additionally, further studies are needed to understand how often aortic complications occur after CPR and to provide guidance for follow-up care in patients who have had aortic repairs. By implementing these measures, we can improve outcomes and safety during resuscitation.

VEGF (Vascular Endothelial Growth Factor) Inhibition and Hypertension: Does Microvascular Rarefaction Play a Role?

Drugs acting by inhibition of the angiogenic action of VEGF (vascular endothelial growth factor) have become major instruments in the treatment of cancer. The downside of their favorable effects in cancer treatment is their frequent cardiovascular side effects. The most consistent finding thus far on the cardiovascular side effects of VEGF inhibitors is the high incidence of hypertension. In this short review, we discuss the evidence that hypertension occurring during VEGF inhibitor treatment is caused by microvascular rarefaction. After a review of the role of VEGF in microvascular growth and differentiation, we present evidence from studies in experimental models of hypertension as well as clinical studies on the microvascular network changes during and after VEGF inhibitor treatment.

Suspected neurodevelopmental disorders in adult patients of memory clinics: Start at the beginning. GREDEV proposals for clinical practice.

Neurodevelopmental disorders are frequent but underestimated in adult populations, even though the cognitive profile of those affected remains atypical throughout adulthood and the disorders can cause significant impairment in activities of daily living. Retrospective diagnosis in this population is challenging. In this article, the GREDEV (working group for the assessment of neurodevelopmental disorders in adults) proposes a brief screening questionnaire for patients with suspected neurodevelopmental disorders, a checklist to facilitate taking the patient history, a list of self-administered questionnaires, and the different key steps of diagnosing neurodevelopmental disorders in adults.

Process optimization, scale-up studies, economic analysis and risk assessment of phenolic rich bioactive extracts production from Carica papaya L. leaves via heat-assisted extraction technology.

This work investigated the influence of process variables of extraction temperature (35-55 °C), solid to liquid ratio (1:20-1:50 g/mL) and time (100-200 min) on the total phenolic content (TPC) and yield (EY) of Carica papaya leaves (CPL) extracts using Box-Behnken experimental design available in Design Expert software. Bi-objective process optimization was also carried out using the desirability function algorithm. The optimum process variables were later used to design an integrated process for the production of CPL extracts with the assistance of SuperPro Designer software. Scale-up studies and economic analysis for CPL extracts production were investigated in the range of 0.638-20.431 × 103 kg CPL extracts/y to determine the most economically feasible production capacity based on the minimum unit production cost (UPC) of CPL extracts. The risk and sensitivity analyses of the most economically feasible production scale were carried out using the Monte Carlo simulation in Oracle Crystal Ball software. Process variables had notable influences on the TPC and EY of CPL extracts. The extraction temperature of 35 °C, solid to liquid ratio of 40.25 g/mL and time of 100 min gave the optimum TPC of 74.65 mg GAE/g d.b and EY of 18.76 % (w/w). HPLC results indicated that CPL extracts were rich in gallic, betulinic, chlorogenic, ellagic, ferulic and caffeic acids. The designed integrated process showed similar behavior with the laboratory scale of 0.18758 g CPL extracts/batch. The preliminary techno-economic analysis indicated that plant capacity has a strong dependence on the material & energy demands and process economics. Plant capacity of 19.857 × 103 kg CPL extracts/y possessed the least UPC and was selected as the most economically feasible scale. The certainty of obtaining base case UPC value of 525.21 US$/kg CPL extracts was 75.20%. Sensitivity analysis showed that extracts recovery, CPL/water, centrifuge purchase cost, extraction time, extractor purchase cost and extraction temperature contributed -5.3 %, +42.8%, +4.0%, +47.1%, +0.1%, and +0.5%, respectively to the variance in UPC of CPL extracts.

Synergistic actions between angiotensin-converting enzyme inhibitors and statins in atherosclerosis.

AIMS: Hypertension and hypercholesterolemia are independent risk factors for atherosclerotic cardiovascular disease (ASCVD) by acting directly on the endothelium and activating the renin-angiotensin aldosterone system (RAAS) and mevalonate pathways. This review examines how the severity and duration of these risk factors may influence the cardiovascular risk through a reciprocal interplay leading to oxidative stress and pro-inflammatory response. DATA SYNTHESIS: The review highlights the clinical evidence supporting the benefits of statins and angiotensin-converting enzyme (ACE) inhibitors for hypertension, lipid disorders and ASCVD management, both individually and combined, at all stages of the cardiovascular continuum. CONCLUSION: Drug strategies incorporating an ACE-inhibitor and a statin, and in particular perindopril and atorvastatin, have consistently demonstrated reductions in the rate of ASCVD events in patients with hypertension and lipid disorders, cementing their position as first-line therapies for the management of atherosclerosis complications.

Renin Angiotensin Blockers and Cardiac Protection: From Basis to Clinical Trials.

Despite a similar beneficial effect on blood pressure lowering observed with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II type 1 receptor (AT1R) blocker (ARBs), several clinical trials and meta-analyses have reported higher cardiovascular mortality and lower protection against myocardial infarction with ARBs when compared with ACEIs. The European guidelines for the management of coronary syndromes and European guidelines on diabetes recommend using ARBs in patients who are intolerant to ACEIs. We reviewed the main pharmacological differences between ACEIs and ARBs, which could provide insights into the differences in the cardiac protection offered by these 2 drug classes. The effect of ACEIs on the tissue and plasma levels of bradykinin and on nitric oxide production and bioavailability is specific to the mechanism of action of ACEIs; it could account for the different effects of ACEIs and ARBs on endothelial function, atherogenesis, and fibrinolysis. Moreover, chronic blockade of AT1 receptors by ARBs induces a significant and permanent increase in plasma angiotensin II and an overstimulation of its still available receptors. In animal models, AT4 receptors have vasoconstrictive, proliferative, and inflammatory effects. Moreover, in models with kidney damage, atherosclerosis, and/or senescence, activation of AT2 receptors could have deleterious fibrotic, vasoconstrictive, and hypertrophic effects and seems prudent and reasonable to reserve the use of ARBs for patients who have presented intolerance to ACE inhibitors.

Controversial Roles of the Renin Angiotensin System and Its Modulators During the COVID-19 Pandemic.

Since December 2019, the coronavirus 2019 (COVID-19) pandemic has rapidly spread and overwhelmed healthcare systems worldwide, urging physicians to understand how to manage this novel infection. Early in the pandemic, more severe forms of COVID-19 have been observed in patients with cardiovascular comorbidities, who are often treated with renin-angiotensin aldosterone system (RAAS)-blockers, such as angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs), but whether these are indeed independent risk factors is unknown. The cellular receptor for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the membrane-bound angiotensin converting enzyme 2 (ACE2), as for SARS-CoV(-1). Experimental data suggest that expression of ACE2 may be increased by RAAS-blockers, raising concerns that these drugs may facilitate viral cell entry. On the other hand, ACE2 is a key counter-regulator of the RAAS, by degrading angiotensin II into angiotensin (1-7), and may thereby mediate beneficial effects in COVID-19. These considerations have raised concerns about the management of these drugs, and early comments shed vivid controversy among physicians. This review will describe the homeostatic balance between ACE-angiotensin II and ACE2-angiotensin (1-7) and summarize the pathophysiological rationale underlying the debated role of the RAAS and its modulators in the context of the pandemic. In addition, we will review available evidence investigating the impact of RAAS blockers on the course and prognosis of COVID-19 and discuss why retrospective observational studies should be interpreted with caution. These considerations highlight the importance of solid evidence-based data in order to guide physicians in the management of RAAS-interfering drugs in the general population as well as in patients with more or less severe forms of SARS-CoV-2 infection.

Renin-angiotensin system blockers and severe acute respiratory syndrome coronavirus 2.

Severe acute respiratory syndrome coronavirus 2, which is responsible for the current coronavirus disease 2019 pandemic, uses angiotensin-converting enzyme 2 as a gateway into host cells. In this review, we summarise the biology of this enzyme, which plays a key role in cardiovascular homeostasis. Blockers of the renin-angiotensin system modify the expression and activity of angiotensin-converting enzyme 2 in different ways. The effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on the expression and enzyme activity of angiotensin-converting enzyme 2 are reviewed, and the consequences of these treatments for the severity of coronavirus disease 2019 infection are discussed.

Wall Shear Stress in the Feeding Native Conduit Arteries of Superficial Arteriovenous Malformations of the Lower Face is a Reliable Marker of Disease Progression.

PURPOSE: To assess the prognostic value of the wall shear stress (WSS) measured in the feeding native arteries upstream from facial superficial arteriovenous malformations (sAVMs). Reliable prognostic criteria are needed to distinguish progressive from stable sAVMs and thus support the indication for an aggressive or a conservative management to avoid severe facial disfigurement. MATERIALS AND METHODS: We prospectively included 25 patients with untreated facial sAVMs, 15 patients with surgically resected sAVMs and 15 controls. All had undergone Doppler ultrasound examination (DUS) with measurements of inner diameters, blood flow velocities, computation of blood flow and WSS of the feeding arteries. Based on the absence or presence of progression in clinical and imaging examinations 6 months after, we discriminated untreated patients as stable or progressive. RESULTS: WSS in the ipsilateral external carotid artery was higher in progressive compared to stable sAVMs (15.8 ±â€Š3.3dynes/cm² vs. 9.6 ±â€Š2.0dynes/cm², mean±SD, p < 0.0001) with a cut-off of 11.5dynes/cm² (sensitivity: 92 %, specificity: 92 %, AUC: 0.955, [95 %CI: 0.789-0.998], p = 0.0001). WSS in the ipsilateral facial artery was also higher in progressive compared to stable sAVMs (50.7 ±â€Š14.5dynes/cm² vs. 25.2 ±â€Š7.1dynes/cm², p < 0.0001) with a cut-off of 34.0dynes/cm² (sensitivity: 100 %, specificity: 92 %, AUC: 0.974, [95 %CI: 0.819-1.000], p = 0.0001). The hemodynamic data of operated patients were not different from those of the control group. CONCLUSION: WSS measured in the feeding arteries of an sAVM may be a simple reliable criterion to distinguish stable from progressive sAVMs. This value should be considered to guide the therapeutic strategy as well as the long-term follow-up of patients with facial sAVMs.

Implementation of various approaches to study the prevalence, incidence and progression of disseminated neoplasia in mussel stocks.

Marine mussel production is of substantial economic interest in numerous coastal areas worldwide, making crucial the study of pathologies that affect them. Disseminated neoplasia (DN) has recently been suggested to be linked to blue mussel, Mytilus edulis, mortality outbreaks observed in France since 2014, although the evidence remains indirect. In order to improve DN detection and monitoring, we compared the sensitivity of four diagnostic tools, namely haemocytology, histology, flow cytometry, and genetics. Haemocytological examination gave the best results in sensitivity and had the advantage of being non-invasive, allowing disease progression to be followed in affected mussels. Using this approach, we showed that DN progression is usually slow, and we provide evidence of remission events. We observed a high diversity of forms and mitotic features of neoplastic cells located in the vesicular connective tissue but rarely in the haemolymph. Circulating cells occur as four main types but are homogenous in morphology and DNA content within a single individual. Polyploidy proved very high, from 8 N to 18 N. Genetic analysis of haemolymph DNA showed that a Mytilus trossulus genetic signal was associated with almost all the DN cases here diagnosed by haemocytological examination, regardless of the DN type. This result corroborates DN is a transmissible cancer that first originated in a M. trossulus host and subsequently crossed into M. edulis. No pre-neoplastic conditions were detectable. The prevalence of the disease was quite low, which, together with the low morbidity observed in the lab, suggest DN is unlikely to be the direct cause of mortality outbreaks in France.

The many faces of myocardial ischaemia and angina.

Obstructive disease of the epicardial coronary arteries is the main cause of angina. However, a number of patients with anginal symptoms have normal coronaries or non-obstructive coronary artery disease (CAD) despite electrocardiographic evidence of ischaemia during stress testing. In addition to limited microvascular vasodilator capacity, the coronary microcirculation of these patients is particularly sensitive to vasoconstrictor stimuli, in a condition known as microvascular angina. This review briefly summarizes the determinants and control of coronary blood flow (CBF) and myocardial perfusion. It subsequently analyses the mechanisms responsible for transient myocardial ischaemia: obstructive CAD, coronary spasm and coronary microvascular dysfunction in the absence of epicardial coronary lesions, and variable combinations of structural anomalies, impaired endothelium-dependent and/or -independent vasodilation, and enhanced perception of pain. Lastly, we exemplify mechanism of angina during tachycardia. Distal to a coronary stenosis, coronary dilator reserve is already recruited and can be nearly exhausted at rest distal to a severe stenosis. Increased heart rate reduces the duration of diastole and thus CBF when metabolic vasodilation is no longer able to increase CBF. The increase in myocardial oxygen consumption and resulting metabolic vasodilation in adjacent myocardium without stenotic coronary arteries further acts to divert blood flow away from the post-stenotic coronary vascular bed through collaterals.

Non-Alcoholic Fatty Liver Disease, and the Underlying Altered Fatty Acid Metabolism, Reveals Brain Hypoperfusion and Contributes to the Cognitive Decline in APP/PS1 Mice.

Non-alcoholic fatty liver disease (NAFLD), the leading cause of chronic liver disease, is associated with cognitive decline in middle-aged adults, but the mechanisms underlying this association are not clear. We hypothesized that NAFLD would unveil the appearance of brain hypoperfusion in association with altered plasma and brain lipid metabolism. To test our hypothesis, amyloid precursor protein/presenilin-1 (APP/PS1) transgenic mice were fed a standard diet or a high-fat, cholesterol and cholate diet, inducing NAFLD without obesity and hyperglycemia. The diet-induced NAFLD disturbed monounsaturated and polyunsaturated fatty acid (MUFAs, PUFAs) metabolism in the plasma, liver, and brain, and particularly reduced n-3 PUFAs levels. These alterations in lipid homeostasis were associated in the brain with an increased expression of Tnfα, Cox2, p21, and Nox2, reminiscent of brain inflammation, senescence, and oxidative stress. In addition, compared to wild-type (WT) mice, while brain perfusion was similar in APP/PS1 mice fed with a chow diet, NAFLD in APP/PS1 mice reveals cerebral hypoperfusion and furthered cognitive decline. NAFLD reduced plasma ß40- and ß42-amyloid levels and altered hepatic but not brain expression of genes involved in ß-amyloid peptide production and clearance. Altogether, our results suggest that in a mouse model of Alzheimer disease (AD) diet-induced NAFLD contributes to the development and progression of brain abnormalities through unbalanced brain MUFAs and PUFAs metabolism and cerebral hypoperfusion, irrespective of brain amyloid pathology that may ultimately contribute to the pathogenesis of AD.