Shehanaz Shajahan

Coronavirus disease 2019 (COVID-19) has been reported to cause cardiovascular complications including myocarditis, pericardial effusion, pericarditis, and arrhythmias. With the introduction of the vaccine, there have been reports of myocarditis possibly associated with the mRNA COVID-19 vaccine. We report a case of cardiac involvement following the second dose of Pfizer-BioNTech COVID-19 vaccine in a young male. A healthy 24-year-old male presented to the emergency department with complaints of non-radiating mid-sternal chest pain and pressure. He noticed his symptoms started six hours after he received the second dose of Pfizer COVID vaccine. Laboratory tests revealed elevated cardiac troponin I-CtNI levels. Computed tomography angiography of the chest did not show evidence of pulmonary embolism. Given his presentation of acute chest pain associated with elevated troponin levels, a coronary angiogram was performed which revealed normal coronary arteries. He was subsequently treated for acute peri-myocarditis with colchicine, non-steroidal anti-inflammatory drugs (NSAIDs), and beta-blockers for tachycardia and the prevention of arrhythmia. Although rare, clinicians should be aware of the risk for myocarditis and pericarditis, which should be considered in individuals presenting with chest pain within a week after vaccination, especially in the younger population. Although the long-term risk in these patients is uncertain, early diagnosis and treatment are key to minimizing complications.

Abstract: Introduction: Metabolic diseases dramatically affect life of men and women from infancy up to old age and are a major challenge for clinicians. Sex and gender affect screening and diagnosis of metabolic diseases as well as treatment strategies and outcome. Aims & Objectives: To differentiate the knowledge of diabetes among both the gender and to study some practices like smoking, alcohol & exercise among males and females to avoid diabetes Materials and Methods: Community based cross-sectional study. A questionnaire consisting of questions that were based on the knowledge, awareness and practices regarding the risk factors of Diabetes was prepared. Only students willing to participate in the study were included. The questionnaire was to be filled anonymously. We collected data from 600 adolescents of age group 16-18years out of which 364 were females and 236 were males. Results: According to our study the results showed that 82.63% males and 92% females think that had knowledge about diabetes, 61.8% males, 52.2% females had knowledge about the increase in rates of diabetics. 61.8% males and 52.2% females had knowledge about complications. 70.7%males and 73% females had knowledge about prevention of diabetes. 27.1% males and 24.4% females think there is complete cure for diabetes. Only 16.97%males and 11.8% females thought that they were at increased risk of diabetes.

Introduction: GLP1 receptor agonists (GLP1RA) improves outcomes by reducing event rates of myocardial infarction (MI). Whether GLP1RA also reduce MI size by ameliorating myocardial ischemia-reperfusion (I/R) injury remains incompletely understood. The main cardioprotective pathways to induce myocardial salvage are RISK (activation of Akt) and SAFE (activation of STAT3). We hypothesized that semaglutide increases myocardial salvage, reduces myocardial infarction (MI) size, improves left ventricular (LV) systolic function, and decreases apoptosis and oxidative stress in a porcine model of I/R mediated via activation of both RISK and SAFE pathways Methods: Myocardial I/R injury was induced in Yorkshire pigs by balloon occlusion of the proximal LAD for 60 min, followed by reperfusion. Animals randomly received semaglutide 0.5mg the day before I/R (to mimick patients on chronic GLP1RA), or saline for controls (n=6/group). Animals were evaluated at 1-day post-MI with cardiac MRI, 3D-echo, histology (apoptosis and oxidative stress) and molecular biology (activation of RISK and SAFE). To mechanistically study the effect of each molecular pathway, two additional groups were treated with GLP1RA+wortmannin (inhibitor of RISK) and GLP1RA+AG490 (inhibitor of SAFE) Results: Despite similar of myocardium at risk in both groups (42.8±2.2% vs 42.2±2.7%, p=NS), semaglutide significantly reduced LGE-determined MI size (33.1±2.3% vs 41.1±2.8% of LV, p<0.01), resulting in larger salvaged myocardium (23.2±6.4% vs 4.1±3.9% of AAR, p<0.01), and improved LV systolic function (MRI-determined LVEF 42.6±3.2% vs 34.4±5.4%, p<0.01). Semaglutide reduced apoptosis (19.3±5.1% vs 40.4±9.1% of TUNEL+ cells, p<0.01) and oxidative stress (12.7±4.7% vs 38.2±9.5% of 8-hydroxydoexyguanosine+ cells, p<0.01). Semaglutide increased the phosphorylation of both Akt and STAT3 (ie semaglutide activated RISK and SAFE). Importantly, these cardioprotective effects of semaglutide were mediated via RISK and SAFE activation because both the inhibition of RISK (with wortmannin) and SAFE (with AG490) pathways abrogated these GLP1RA-induced benefits on I/R injury (Figure) Conclusions: The GLP1RA semaglutide increases myocardial salvage, reduces MI size, improves LV systolic function, and decreases apoptosis and oxidative stress in a porcine model of I-R mediated via activation of both RISK and SAFE pathways. This mechanism might explain part of the cardiovascular benefits of semagutide in large clinical trials