Hypertension nowadays still becomes one of the severe problems in Indonesia, with a prevalence of 34% in 2018. The complication of hypertension causes the most deaths and disabilities in Indonesia and cost 75% of The Social Security Organizing Agency (BPJS) budget or IDR 15 trillion in 2019. This problem was probably caused by patients' lack of knowledge and limited personnel at the primary health centre (PHC). Telemedicine is a health care provider without any direct contact, which has various methods. Today, telemedicine in Indonesia is growing rapidly along with technology and legal regulation in its implementation, increasing users by 700% in the first year of 2020. Despite the rise of those numbers, telemedicine in PHC is still limited. Recently, the Ministry of Health and various organizations have issued telemedicine regulations at primary level health facilities in collaboration with The Social Security Organizing Agency. This review aims to discuss the current implementation and the potential future of telemedicine-based hypertension management in collaboration with the Social Security Organizing Agency in PHC.

Vaccination is significant to control, mitigate, and recover from the destructive effects of coronavirus disease 2019 (COVID-19). The incidence of myocarditis following COVID-19 vaccination has been increasing and growing public concern; however, little is known about it. This study aimed to systematically review myocarditis following COVID-19 vaccination. We included studies containing individual patient data of myocarditis following COVID-19 vaccination published between January 1, 2020 and September 7, 2022 and excluded review articles. Joanna Briggs Institute critical appraisals were used for risk of bias assessment. Descriptive and analytic statistics were performed. A total of 121 reports and 43 case series from five databases were included. We identified 396 published cases of myocarditis and observed that the majority of cases was male patients, happened following the second dose of mRNA vaccine administration, and experienced chest pain as a symptom. Previous COVID-19 infection was significantly associated (p < 0.01; OR, 5.74; 95% CI, 2.42–13.64) with the risk of myocarditis following the administration of the first dose, indicating that its primary mechanism is immune-mediated. Moreover, 63 histopathology examinations were dominated by non-infective subtypes. Electrocardiography and cardiac marker combination is a sensitive screening modality. However, cardiac magnetic resonance is a significant noninvasive examination to confirm myocarditis. Endomyocardial biopsy may be considered in confusing and severe cases. Myocarditis following COVID-19 vaccination is relatively benign, with a median length of hospitalization of 5 days, intensive care unit admission of <12%, and mortality of <2%. The majority was treated with nonsteroidal anti-inflammatory drugs, colchicine, and steroids. Surprisingly, deceased cases had characteristics of being female, older age, non-chest pain symptoms, first-dose vaccination, left ventricular ejection fraction of <30%, fulminant myocarditis, and eosinophil infiltrate histopathology.

Chronic obstructive pulmonary disease (COPD) is one of the leading causes of mortality globally. It is associated with a low quality of life and socio-economic burden. Airway destruction in COPD pathogenesis is primarily due to the three mechanisms: protease-antiprotease imbalance, chronic airway inflammation, and oxidative stress, which is triggered by exposure to harmful particles, such as cigarette smoking. Neutrophil elastase (NE), a serine protease stored in azurophilic granules of neutrophils, actively participates in airway remodeling and microbiocidal activity. It hydrolyzes elastin, collagen, and other vital extracellular matrix proteins (EMP) in the respiratory tissue. In addition, neutrophil elastase activates other principal proteinases such as matrix metalloprotease (MMP)-2, MMP-9, Cathepsin B, Meprin α protease, and Calpain that amplify EMP degradation. Macrophage, the primary leukocyte, responsible for lung parenchymal inflammation in COPD, is also activated by NE. However, neutrophil elastase level is positively correlated with the degree of airway inflammation and disease severity. Neutrophil elastase activates reactive oxygengenerating systems such as nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and myeloperoxidase and it also generates mitochondrial-derived-reactive oxygen species formation by inducing the secretion of Interleukin (IL)-1 andTumour necrosis factor (TNF)- α. In addition, neutrophil elastase stimulates respiratory cell apoptosis by direct (e.g., activating the caspase-3 pathway) and indirect mechanisms (e.g., by secretion of Neutrophil Extracellular Traps). Surprisingly, neutrophil elastase may have small anti-inflammatory properties. In conclusion, neutrophil elastase is one of the main culprits responsible for COPD pathogenesis by mediating the activation of Triad COPD pathogenesis.

<p>Hypertension is still one of the leading causes of morbidity and mortality globally. Complications of hypertension cause innumerable social, economic, and health cost burdens, reaching 131 million dollars per year in the United States. However, blood pressure control through lifestyle modifications and pharmacological intervention, achieving blood pressure targets is often unsatisfying. With its simple, cost-efficient, multifunctional, and enormous coverage characteristics, social media is promising to be utilized in health programs. Social media could provide massive information and accommodate the hypertension community to increase hypertension awareness. Incorporating social media in hypertension management improves patients’ lifestyles and pharmacological adherence more than conventional methods. The exact mechanism of how social media-based health programs increase treatmentadherence is complex and has not been well-defined; raised awareness, bidirectional communication, and a qualified coach (physician) seem to be the essential factors. It should also be well aware that screen time duration and emotional alteration due to social media exposure could also potentially increase blood pressure.</p><p>Hipertensi masih menjadi salah satu penyebab utama morbiditas dan mortalitas global. Komplikasi hipertensi menimbulkan beban sosial, ekonomi, dan biaya kesehatan yang mencapai 131 juta dollar setiap tahun di Amerika Serikat. Kontrol tekanan darah melalui modifikasi gaya hidup dan intevensi farmakologis, hasilnya seringkali masih belum memuaskan. Media sosial dengan karakteristiknya yang simpel, murah, multifungsi, dengan cakupan sangat luas tampak menjanjikan untuk digunakan dalam program-program kesehatan. Media sosial dapat menyediakan berbagai informasi dan mengakomodasi komunitas untuk meningkatkan kesadaran terhadap hipertensi. Penggunaan media sosial dalam manajemen hipertensi tampak mampu memperbaiki pola hidup dan ketaatan farmakologi lebih baik daripada metode konvensional. Mekanisme pastinya bersifat kompleks dan masih belum dapat dijelaskan dengan baik; namun peningkatan kesadaraan, komunikasi dua arah, dan pendamping (dokter) terkualifikasi tampak sebagai<br />faktor-faktor penting. Hal yang seharusnya juga diperhatikan adalah durasi screen time dan perubahan emosional karena saat menggunakan media sosial juga dapat berpotensi meningkatkan tekanan darah.</p>

Current research supports the evidence that the gut microbiome (GM), which consist of gut microbiota and their biologically active metabolites, is associated with atherosclerosis development. Trimethylamine-N-oxide (TMAO), a metabolite produced by the GM through trimethylamine (TMA) oxidation, significantly enhances the formation and vulnerability of atherosclerotic plaques. TMAO promotes inflammation and oxidative stress in endothelial cells, leading to vascular dysfunction and plaque formation. Dimethyl-1-butanol (DMB), iodomethylcholine (IMC) and fluoromethylcholine (FMC) have been recognized for their ability to reduce plasma TMAO by inhibiting trimethylamine lyase, a bacterial enzyme involved in the choline cleavage anaerobic process, thus reducing TMA formation. Conversely, indole-3-carbinol (I3C) and trigonelline inhibit TMA oxidation by inhibiting flavin-containing monooxygenase-3 (FMO3), resulting in reduced plasma TMAO. The combined use of inhibitors of choline trimethylamine lyase and flavin-containing monooxygenase-3 could provide novel therapeutic strategies for cardiovascular disease prevention by stabilizing existing atherosclerotic plaques. This review aims to present the current evidence of the roles of TMA/TMAO in atherosclerosis as well as its potential therapeutic prevention aspects.