Air pollution is the most significant environmental risk factor for all-cause mortality, and it has caused substantial disability-adjusted life-years and economic loss. Air pollution intensified the mortality during past pandemics, Spanish flu in 1918 and SARS-CoV-1 in 2003. It increases host susceptibility and virulence of respiratory infections and reduces viral clearance. Thus, a question arises whether there will be any impact of air pollution on the current pandemic coronavirus disease 2019 (COVID-19)? Thus far, history and science are directing towards an immense potential impact of air pollution on the COVID-19 pandemic. Some of the devastated countries with the current pandemic are those with a poor air quality index. Further epidemiological and ecological studies are necessary to confirm this association. Also, countries must mobilize funding for mitigation of air pollution to benefit environmental health and ameliorate its potential effects on pandemics of the future.

Introduction This prospective pharmacodynamic (PD) study aimed to assess the effect of the sodium–glucose cotransporter 2 inhibitor (SGLT2i) empagliflozin on platelet reactivity. Methods Patients with stable coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM) ( n = 20) who were actively treated with dual antiplatelet therapy (DAPT) of aspirin 81 mg daily and clopidogrel 75 mg daily were recruited. Platelet function was measured with the VerifyNow™ P2Y 12 assay (Instrumentation Laboratory, Massachusetts, USA) and assessed before the initiation of and after 10 days of treatment with empagliflozin 25 mg once daily maintenance dose regimen. Results were compared with a paired t test. Results The mean P2Y 12 reaction units (PRU) on empagliflozin was significantly less than without empagliflozin at baseline (187.35, 95% confidence interval (CI) 155.38–219.32 vs. 217.25, CI 180.60–253.90; p < 0.030). The mean difference in PRU was 29.90 (95% CI 3.17–56.63). No patients experienced any serious adverse events (SAEs). Conclusions Significantly attenuated platelet reactivity was observed on empagliflozin as compared to without empagliflozin. This dedicated pharmacodynamic study could be clinically pertinent for Trinidadian patients with stable CAD and T2DM on DAPT. Further studies are required to confirm these exploratory findings. (Funded by the University of the West Indies, St. Augustine; EFFECT). Clinical Trial Registration ClinicalTrials.gov number NCT04342819.

Marked ethnic variations in complications and mortality have been noted following infection with COVID-19, with Black, Asian, and minority ethnic groups (BAME) being particularly hard hit. We hypothesise that glucocorticoid resistance stemming from several intrinsic reasons such as chronic social stress and lower circulating levels of Vitamin D may contribute to the exaggerated inflammatory response, more severe disease and poorer outcomes observed in BAME.

Often described as a clinico-radiological entity, posterior reversible encephalopathy syndrome (PRES) is being increasingly diagnosed nowadays. However, mystery still surrounds its exact etiology. Though there are no standardized diagnostic criteria for this syndrome, there is a consistent feature associated with it: brain vasogenic edema in combination with neurotoxicity. The nonspecific nature of this condition leaves room for the diagnosis to be overlooked, leading to delays in providing appropriate treatment and unfavorable patient outcomes. PRES is associated with a variety of medical conditions including hypertension, eclampsia, autoimmune conditions, renal failure, sepsis, and an immunocompromised state, such as that secondary to the use of immunosuppressive therapy, human immunodeficiency virus (HIV), and organ transplants. Treatment by a multidisciplinary team and prompt identification and reversal of the underlying cause can lead to beneficial outcomes, as in the case we present in this report.

Introduction: This prospective pharmacodynamic (PD) study assessed the effect of the sodium-glucose co-transporter-2 inhibitor (SGLT2i), dapagliflozin, on platelet reactivity. Methods: Patients with stable coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM) (n = 27) who were on maintenance dual antiplatelet therapy (DAPT) of aspirin 81 mg daily, and clopidogrel 75 mg daily were recruited. Platelet function was evaluated with the VerifyNow TM P2Y 12 assay (Werfen, Bedford, MA, USA) and assessed prior to initiation of and after 10 days of treatment with dapagliflozin 10 mg once-daily dose regimen. Results were compared with a paired t test. Results: Treatment with dapagliflozin significantly decreased P2Y12 reaction units (PRU) by 20%, (95% confidence interval (CI) 8.5-32.6%, p value 0.002). The mean difference in PRU was . No patients experienced any serious adverse events (SAEs). Conclusions: Significantly diminished platelet reactivity was observed on dapagliflozin as compared to without dapagliflozin. This dedicated pharmacodynamic study could be potentially informative and applicable for Trinidadian stable CAD patients with T2DM on DAPT. Further studies are required to confirm these exploratory findings. Clinical Trial Registration: EDGE ClinicalTrials.gov number NCT04400760.

Mitral annular calcification (MAC) commonly manifests as an incidental, asymptomatic finding that is associated with several cardiovascular risk factors, atherosclerosis, cardiovascular death, and all-cause mortality. Very rarely, patients with severe MAC can have extensive dystrophic calcification extending into the left atrial wall, termed porcelain left atrium. In this case report, we describe a patient who experienced multiple calcific acute embolic strokes in the setting of severe mitral annular calcification and porcelain left atrium. Our patient presented with multiple, small bilateral acute infarcts scattered throughout the cerebrum and cerebellum confirmed on magnetic resonance imaging (MRI). He was placed on continuous telemetry and underwent multimodal imaging with transthoracic and transesophageal echocardiography, carotid neck ultrasound (US), head and neck computed tomography angiogram (CTA), and cardiac MRI. There were no arrhythmic events detected on telemetry, and all imaging excluded left ventricular thrombi, aortic atheroma, carotid artery stenosis, intracardiac shunting, or large vessel stenosis. Noted on imaging, however, was severe mitral annular calcification with numerous, highly mobile calcific extensions and densely calcified plaque along the posterior left atrial wall, presumed to be the source of this patient's embolic stroke. Cardiac catheterization was significant for severe three-vessel disease requiring coronary artery bypass grafting, and our patient was subsequently discharged to outpatient follow-up on event monitoring and aspirin monotherapy. This case serves to highlight a previously unreported complication of calcific embolic stroke in severe MAC and porcelain left atrium, and highlight the need for further randomized controlled trials to determine the optimum management of these cases.

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