Angiotensin-converting enzyme 2 (ACE2), the host cell-binding site for SAR-CoV-2, poses two-fold drug development problems. First, the role of ACE2 itself is still a matter of investigation, and no specific drugs are available targeting ACE2. Second, as a consequence of SARS-CoV-2 interaction with ACE2, there is an impairment of the renin-angiotensin system (RAS) involved in the functioning of vital organs like the heart, kidney, brain, and lungs. In developing antiviral drugs for COVID-19, ACE2, RNA-dependent RNA polymerase (RdRp), and the specific enzymes involved in the viral and cellular gene expression have been the primary targets. SARS-CoV-2 being a new virus with unusually high mortality, there has been a need to get medicines in an emergency, and the drug repurposing has been a primary strategy. Considering extensive mortality and morbidity throughout the world, we have made a maiden attempt to discover the drugs interacting with RAS and identify the lead compounds from herbal plants using molecular docking. Both host ACE2 and viral RNA-dependent RNA polymerase (RdRp) and ORF8 appear to be the primary targets for the treatment of COVID-19. While the drug repurposing of currently approved drugs seems to be one strategy for the treatment of COVID-19, purposing phytochemicals may be another essential strategy for discovering lead compounds. Using in silico molecular docking, we have identified a few phytochemicals that may provide insights into designing herbal and synthetic therapeutics to treat COVID-19.Patients with obstructive sleep apnea (OSA) are susceptible to developing atherosclerosis. Consequently, such patients are at a high risk of developing cardiovascular diseases, leading to poor prognosis. Many physiological parameters have been previously used to predict the development of atherosclerosis. One such parameter, the cardio-ankle vascular index (CAVI), a measure of arterial stiffness, has garnered much attention as it can also predict the degree of atherosclerosis. The CAVI can be calculated based on noninvasive measurements, and is less susceptible to blood pressure variations at the time of measurement. Therefore, the CAVI can assess changes in arterial stiffness and the risk of developing atherosclerosis independent of blood pressure changes. Continuous positive airway pressure (CPAP) is a standard therapy for OSA and can suppress the issue significantly. Several studies have shown that CPAP treatment for OSA could also reduce the CAVI. In this review, we discuss the relationship between OSA and arterial stiffness, primarily focusing on the CAVI. Furthermore, we propose future perspectives for the CAVI and OSA.Since January 2020, coronavirus disease 2019 (COVID-19) has rapidly become a global concern, and its cardiovascular manifestations have highlighted the need for fast, sensitive and specific tools for early identification and risk stratification. Machine learning is a software solution with the ability to analyze large amounts of data and make predictions without prior programming.  https://www.selleckchem.com/products/aspirin-acetylsalicylic-acid.html  When faced with new problems with unique challenges as evident in the COVID-19 pandemic, machine learning can offer solutions that are not apparent on the surface by sifting quickly through massive quantities of data and making associations that may have been missed. Artificial intelligence is a broad term that encompasses different tools, including various types of machine learning and deep learning. Here, we review several cardiovascular applications of machine learning and artificial intelligence and their potential applications to cardiovascular diagnosis, prognosis, and therapy in COVID-19 infection.There is emerging evidence to suggest that vitamin D deficiency is associated with adverse outcomes in COVID-19 patients. Conversely, vitamin D supplementation protects against an initial alveolar diffuse damage of COVID-19 becoming progressively worse. The mechanisms by which vitamin D deficiency exacerbates COVID-19 pneumonia remain poorly understood. In this review we describe the rationale of the putative role of endothelial dysfunction in this event. Herein, we will briefly review (1) anti-inflammatory and anti-thrombotic effects of vitamin D, (2) vitamin D receptor and vitamin D receptor ligand, (3) protective role of vitamin D against endothelial dysfunction, (4) risk of vitamin D deficiency, (5) vitamin D deficiency in association with endothelial dysfunction, (6) the characteristics of vitamin D relevant to COVID-19, (7) the role of vitamin D on innate and adaptive response, (8) biomarkers of endothelial cell activation contributing to cytokine storm, and (9) the bidirectional relationship between inflammation and homeostasis. Finally, we hypothesize that endothelial dysfunction relevant to vitamin D deficiency results from decreased binding of the vitamin D receptor with its ligand on the vascular endothelium and that it may be immune-mediated via increased interferon 1 α. A possible sequence of events may be described as (1) angiotensin II converting enzyme-related initial endothelial injury followed by vitamin D receptor-related endothelial dysfunction, (2) endothelial lesions deteriorating to endothelialitis, coagulopathy and thrombosis, and (3) vascular damage exacerbating pulmonary pathology and making patients with vitamin D deficiency vulnerable to death.Sarcoidosis is a chronic inflammatory disease of unknown etiology characterized by multi-organ involvement. End-organ disease consists of granulomatous inflammation, which if left untreated or not resolved spontaneously, leads to permanent fibrosis and end-organ dysfunction. Cardiac involvement and fibrosis in sarcoidosis occur in 5-10% of cases and is becoming increasingly diagnosed. This is due to increased clinical awareness among clinicians and new diagnostic modalities, since magnetic resonance imaging and positron-emission tomography are emerging as "gold standard" tools replacing endomyocardial biopsy. Despite this progress, isolated cardiac sarcoidosis is difficult to differentiate from other causes of arrhythmogenic cardiomyopathy. Cardiac fibrosis leads to congestive heart failure, arrhythmias and sudden cardiac death. Immunosuppressives (mostly corticosteroids) are used for the treatment of cardiac sarcoidosis. Implantable devices like a cardioverter-defibrillator may be warranted in order to prevent sudden cardiac death.