Early Major Adverse Cardiovascular Event in a Patient With Chronic Kidney Disease: A Case Report.

Acute coronary syndrome (ACS) is common in people with chronic kidney disease (CKD) and is linked to poor short- and long-term outcomes. The diagnosis of myocardial infarction is challenging in patients with CKD as they have baseline elevated troponin levels. To date, there are no widely accepted guidelines to suggest what is a clinically significant change in troponin levels in these patients. We report a case of a patient with CKD who presented with chest pain to the emergency department (ED). His baseline troponin was high; however, the delta change was 11%. He was discharged from the ED for outpatient follow-up, but within 36 hours, he had significant ST elevation myocardial infarction (STEMI) with unstable hemodynamics and acute heart failure requiring urgent intubation and coronary revascularization. This case highlights the gap in clinical knowledge and practice in a relatively not uncommon presentation in emergency departments.

Polycystic ovarian syndrome among women diagnosed with infertility in the Gulf Cooperation Council countries: A protocol for systematic review and meta-analysis of prevalence studies.

BACKGROUND: Polycystic ovarian syndrome, a common endocrine disorder, is an important cause of infertility among women of reproductive age. Within the Gulf Cooperation Council countries, polycystic ovarian syndrome is found to affect women increasingly. No study has been carried out to critically summarize the evidence on the prevalence of polycystic ovarian syndrome among women suffering from infertility in these countries. OBJECTIVE: This protocol aims to conduct a systematic review and meta-analysis of the studies reporting the prevalence of polycystic ovarian syndrome among women seeking infertility treatment in the six Gulf Cooperation Council countries (Bahrain, Kuwait, Oman, Saudi Arabia, Qatar, and United Arab Emirates). DESIGN/METHODS AND ANALYSIS: The systematic review and meta-analysis will follow the following method. DATA SOURCE: Five databases, including PubMed, Embase, CINAHL, Web of Science, and SCOPUS, will be searched for observational studies using a combination of relevant keywords and Medical Subject Headings from inception of databases. DATA EXTRACTION: Two reviewers will screen titles and abstracts, followed by a full-text search based on the eligibility criteria. The main outcome is to measure the proportion of women who have polycystic ovarian syndrome among infertility-diagnosed patients. In addition, the risk of bias in the included studies will be assessed using the national institute of health quality assessment tool for observational studies. DATA SYNTHESIS: The random-effects method of the analysis with the inverse variance will be used to calculate the pooled prevalence of polycystic ovarian syndrome-attributed infertility. Variation in prevalence estimates will be calculated using subgroup analysis based on study and patients' characteristics and publication bias will be assessed via funnel plot inspection and Eggar's test. DISCUSSION: A critical assessment of evidence on the prevalence of polycystic ovarian syndrome in women attending fertility clinics is helpful in risk quantification, enabling better planning for managing infertility in women with polycystic ovarian syndrome. REGISTRATION: This protocol has been registered with PROSPERO, protocol registration number (CRD42022355087).

The Salutary Effects of Catalpol on Diesel Exhaust Particles-Induced Thrombogenic Changes and Cardiac Oxidative Stress, Inflammation and Apoptosis.

Inhaled particulate air pollution exerts pulmonary inflammation and cardiovascular toxicity through secondary systemic effects due to oxidative stress and inflammation. Catalpol, an iridiod glucoside, extracted from the roots of Rehmannia glutinosa Libosch, has been reported to possess anti-inflammatory and antioxidant properties. Yet, the potential ameliorative effects of catalpol on particulate air pollution-induced cardiovascular toxicity, has not been studied so far. Hence, we evaluated the possible mitigating mechanism of catalpol (5 mg/kg) which was administered to mice by intraperitoneal injection one hour before the intratracheal (i.t.) administration of a relevant type of pollutant particle, viz. diesel exhaust particles (DEPs, 30 µg/mouse). Twenty-four hours after the lung deposition of DEPs, several cardiovascular endpoints were evaluated. DEPs caused a significant shortening of the thrombotic occlusion time in pial microvessels in vivo, induced platelet aggregation in vitro, and reduced the prothrombin time and the activated partial thromboplastin time. All these actions were effectively mitigated by catalpol pretreatment. Likewise, catalpol inhibited the increase of the plasma concentration of C-reactive proteins, fibrinogen, plasminogen activator inhibitor-1 and P- and E-selectins, induced by DEPs. Moreover, in heart tissue, catalpol inhibited the increase of markers of oxidative (lipid peroxidation and superoxide dismutase) and nitrosative (nitric oxide) stress, and inflammation (tumor necrosis factor α, interleukin (IL)-6 and IL-1ß) triggered by lung exposure to DEPs. Exposure to DEPs also caused heart DNA damage and increased the levels of cytochrome C and cleaved caspase, and these effects were significantly diminished by the catalpol pretreatment. Moreover, catalpol significantly reduced the DEPs-induced increase of the nuclear factor κB (NFκB) in the heart. In conclusion, catalpol significantly ameliorated DEPs-induced procoagulant events and heart oxidative and nitrosative stress, inflammation, DNA damage and apoptosis, at least partly, through the inhibition of NFκB activation.

Hypocretin/orexin modulates body weight and the metabolism of glucose and insulin.

The hypocretin/orexin (Hcrt/orexin) unit affects the functions of the nervous, cardiovascular, gastrointestinal, and reproductive systems. Hcrt/orexin ligands and receptors have been localized to different parts of the central and peripheral nervous systems, cerebrospinal fluid and blood, exocrine (pancreas, salivary, lacrimal) as well as endocrine (pancreatic islets, pituitary, adrenal) glands. Several factors including stress, glucagon-like peptide-1 agonists, glutamate, nicotine, glucose, and hypoglycaemia stimulate the expression of Hcrt/orexin system, but it is inhibited by ageing, bone morphogenetic protein, hypoxia/hypercapnia, melanocortin receptor accessory protein 2, and glucagon. Literature reports show that Hcrt/orexin can significantly increase insulin secretion from normal and diabetic rat pancreata. Hcrt/orexin decreases blood glucose concentration and reduces insulin resistance partly via increased tissue expression of glucose transporter type 4. It reduces obesity by increasing browning of fat cells and energy expenditure. Taken together, Hcrt/orexin modulates obesity and the metabolism of glucose and insulin. The Hcrt/orexin system may thus be a target in the development of new therapies for the treatment of diabetes mellitus.