Melatonin: A potential protective multifaceted force for sepsis-induced cardiomyopathy.

Sepsis is a life-threatening condition manifested by organ dysfunction caused by a dysregulated host response to infection. Lung, brain, liver, kidney, and heart are among the affected organs. Sepsis-induced cardiomyopathy is a common cause of death among septic patients. Sepsis-induced cardiomyopathy is characterized by an acute and reversible significant decline in biventricular both systolic and diastolic function. This is accompanied by left ventricular dilatation. The pathogenesis underlying sepsis-induced cardiomyopathy is multifactorial. Hence, targeting an individual pathway may not be effective in halting the extensive dysregulated immune response. Despite major advances in sepsis management strategies, no effective pharmacological strategies have been shown to treat or even reverse sepsis-induced cardiomyopathy. Melatonin, namely, N-acetyl-5-methoxytryptamine, is synthesized in the pineal gland of mammals and can also be produced in many cells and tissues. Melatonin has cardioprotective, neuroprotective, and anti-tumor activity. Several literature reviews have explored the role of melatonin in preventing sepsis-induced organ failure. Melatonin was found to act on different pathways that are involved in the pathogenesis of sepsis-induced cardiomyopathy. Through its antimicrobial, anti-inflammatory, and antioxidant activity, it offers a potential role in sepsis-induced cardiomyopathy. Its antioxidant activity is through free radical scavenging against reactive oxygen and nitrogen species and modulating the expression and activity of antioxidant enzymes. Melatonin anti-inflammatory activities control the overactive immune system and mitigate cytokine storm. Also, it mitigates mitochondrial dysfunction, a major mechanism involved in sepsis-induced cardiomyopathy, and thus controls apoptosis. Therefore, this review discusses melatonin as a promising drug for the management of sepsis-induced cardiomyopathy.

The crosstalk between Nrf2 and NF-κB pathways in coronary artery disease: Can it be regulated by SIRT6?

Coronary artery disease (CAD) is the leading cause of death worldwide. Oxidative stress and inflammation are major mechanisms responsible for the progression of CAD. Nuclear transcription factor erythroid-2 related factor 2 (Nrf2) is a transcription factor that modulates the cellular redox status. Nrf2 upregulation increases the expression of antioxidant genes, decreases the expression of Nuclear factor-kappa B (NF-kB), and increases free radical metabolism. Activated NF-kB increases the production of inflammatory cytokines causing endothelial dysfunction. The two pathways of Nrf2 and NF-kB can regulate the expression of each other. Foremost, the Nrf2 pathway can decrease the level of active NF-κB by increasing the level of antioxidants and cytoprotective enzymes. Furthermore, the Nrf2 pathway prevents IκB-α degradation, an inhibitor of NF-kB, and thus inhibits NF-κB mediated transcription. Also, NF-kB transcription inhibits Nrf2 activation by reducing the antioxidant response element (ARE) transcription. Sirtuin 6 (SIRT6) is a member of the Sirtuins family that was found to protect against cardiovascular diseases. SIRT6 can suppress the production of Reactive oxygen species (ROS) through deacetylation of NRF2 which results in NRF2 activation. Furthermore, SIRT6 can inhibit the inflammatory process through the downregulation of NF-kB transcription. Therefore, targeting sirtuins could be a therapeutic strategy to treat CAD. This review describes the potential role of SIRT6 in regulating the crosstalk between NRF2 and NF-kB signaling pathways in CAD.

Occupational health risk among healthcare workers during COVID-19 pandemic: actions to limit the risk.

The World Health Organization declared coronavirus infection 2019 (COVID-19) as a pandemic in March 2020. The infection with coronavirus started in Wuhan city, China, in December 2019. As of October 2020, the disease was reported in 235 countries. The coronavirus infection 2019 (COVID-19) is a disease with high morbidity and mortality. As of February 2021, the number of confirmed cases of COVID-19 globally is 102,942,987 and 2,232,233 deaths according to WHO report. This infection is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which is a ribonucleic acid (RNA) ß-coronavirus. The infection is mainly transmitted through respiratory droplets.Healthcare workers (HCWs) play an essential role at the front lines, providing care for patients infected with this highly transmittable disease. They are exposed to very high occupational health risk as they frequently contact the infective persons. In order to limit the number of infected cases and deaths among healthcare workers, it is crucial to have better awareness, optimistic attitude, efficient PPE, and adequate health practices about COVID-19.

Management of pharmacotherapy-related problems in acute coronary syndrome: Role of clinical pharmacist in cardiac rehabilitation unit.

Acute coronary syndrome (ACS) is one of the leading causes of mortality worldwide and negatively impacts healthcare costs, productivity and quality of life. Polymorbidity and polypharmacy predispose ACS patients to medication discrepancies between cardiologist-prescribed medication and drug use by the patient, drug-related problems (DRPs) and inadequate drug adherence. This study aimed to evaluate the impact of clinical pharmacist-provided services on the outcome of ACS patients. This was a prospective, randomized, controlled study on ACS patients participating in a cardiac rehabilitation programme. Forty ACS patients were randomly assigned to either control group, who received standard medical care, or intervention group, who received standard medical care plus clinical pharmacist-provided services. Services included DRP management, clinical assessment and enforcing the patient education and adherence. For both groups, the following were assessed at baseline and after 3 months: DRPs, adherence (assessed by 8-item Morisky Adherence Questionnaire), patient's knowledge (assessed by Coronary Artery Disease Questionnaire), 36-Short Form Health Survey (SF-36), heart rate, systolic and diastolic blood pressure, low-density lipoprotein (LDL), total cholesterol (TC) and fasting blood glucose (FBG). After 3 months, there was a significant difference between the intervention and control groups in the per cent change of DRPs (median: -100 vs 5.882, P = 0.0001), patient's adherence score (median: 39.13 vs -14.58, P = 0.0001), knowledge score (median: 30.28 vs -5.196, P = 0.0001), SF-36 scores, heart rate (mean: -10.04 vs 6.791, P = 0.0001), diastolic blood pressure (mean: -17.87 vs 10.45, P = 0.0001), systolic blood pressure (mean: -16.22 vs 4.751, P = 0.0001), LDL (median: -25.73 vs -0.2538, P = 0.0071), TC (median: -14.62 vs 4.123, P = 0.0005) and FBG (median: -11.42 vs 5.422, P = 0.0098). Clinical pharmacists can play an important role as part of a cardiac rehabilitation team through patient education and interventions to minimize DRPs.