The COVID-19 pandemic has had a significant global impact, with more than 280,000,000 people infected and 5,400,000 deaths. The use of personal protective equipment and the anti-SARS-CoV-2 vaccination campaigns have reduced infection and death rates worldwide. However, a recent increase in infection rates has been observed associated with the appearance of SARS-CoV-2 variants, including the more recently described lineage B.1.617.2 (Delta variant) and lineage B.1.1.529/BA.1 (Omicron variant). These new variants put the effectiveness of international vaccination at risk, with the appearance of new outbreaks of COVID-19 throughout the world. This emergence of new variants has been due to multiple predisposing factors, including molecular characteristics of the virus, geographic and environmental conditions, and the impact of social determinants of health that favor the genetic diversification of SARS-CoV-2. We present a literature review on the most recent information available on the emergence of new variants of SARS-CoV-2 in the world. We analyzed the biological, geographical, and sociocultural factors that favor the development of these variants. Finally, we evaluate the surveillance strategies for the early detection of new variants and prevent their distribution outside these regions.

The SARS-CoV-2 pandemic has mobilized many efforts worldwide to curb its impact on morbidity and mortality. Vaccination of the general population has resulted in the administration of more than 6,700,000,000 doses by the end of October 2021, which is the most effective method to prevent hospitalization and death. Among the adverse effects described, myocarditis and pericarditis are low-frequency events (less than 10 per 100,000 people), mainly observed with messenger RNA vaccines. The mechanisms responsible for these effects have not been specified, considering an exacerbated and uncontrolled immune response and an autoimmune response against specific cardiomyocyte proteins. This greater immunogenicity and reactogenicity is clinically manifested in a differential manner in pediatric patients, adults, and the elderly, determining specific characteristics of its presentation for each age group. It generally develops as a condition of mild to moderate severity, whose symptoms and imaging findings are self-limited, resolving favorably in days to weeks and, exceptionally, reporting deaths associated with this complication. The short- and medium-term prognosis is favorable, highlighting the lack of data on long-term evolution, which should be determined in longer follow-ups.

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The CoronaVac vaccine is the most used anti-SARS-CoV-2 vaccine worldwide. Previous data indicate that this vaccine produces a lower immune response than RNA vaccines such as BNT162b2. End-stage renal disease (ESRD) patients have an increased rate of COVID-19 and a reduced immune response to vaccinations. Currently, there is little data on this population’s immune response induced by CoronaVac. Methods: This study involved a prospective cohort of ESRD patients in chronic hemodialysis who received a two-dose immunization scheme of either CoronaVac (Sinovac Biotech) or BNT162b2 vaccines (Pfizer-BioNTech). We measured the plasma levels of anti-SARS-CoV-2 IgG antibodies. We determined antibody titers before immunization, 2 and 4 months after two doses, plus 4 months after a booster dose. Results: We evaluated 208 patients in three hemodialysis centers. The mean age was 62.6 ± 15.6 years, of whom 91 were female (41.75%). Eighty-one patients (38.94%) received the BNT162b2 vaccine and 127 (61.06%) received the CoronaVac vaccine. Patients who received the BNT162b2 vaccine had a higher humoral response compared to those who received the CoronaVac vaccine (4 months after the second dose: BNT162b2: 88.89%, CoronaVac: 51.97%, p < 0.001; 4 months after the booster: BNT162b2: 98.77%, CoronaVac: 86.61%, p < 0.001). Conclusions: Our results suggest that the CoronaVac vaccine induced a lower humoral response than the BNT162b2 vaccine in ESRD patients on hemodialysis.

End-stage renal disease (ESRD) patients are a population with high rates of COVID-19 and mortality. These patients present a low response to anti-SARS-CoV-2 immunization, which is associated with immune dysfunction. ESRD patients also present high plasma titers of Fibroblast Growth Factor 23 (FGF23), a protein hormone that reduces immune response in vivo and in vitro. Increased FGF23 levels associate with higher infection-related hospitalizations and adverse infectious outcomes. Thus, we evaluated whether ESRD patients with high FGF23 titers have an increased rate of SARS-CoV-2 infection. Methods: We performed a prospective cohort of ESRD patients in hemodialysis who had measurements of plasma intact FGF23 in 2019. We determined COVID-19 infections, hospitalizations, and mortality between January 2020 and December 2021. Results: We evaluated 243 patients. Age: 60.4 ± 10.8 years. Female: 120 (49.3%), diabetes: 110 (45.2%). During follow-up, 45 patients developed COVID-19 (18.5%), 35 patients were hospitalized, and 12 patients died (mortality rate: 26.6%). We found that patients with higher FGF23 levels (defined as equal or above median) had a higher rate of SARS-CoV-2 infection versus those with lower levels (18.8% versus 9.9%; Hazard ratio: 1.92 [1.03–3.56], p = 0.039). Multivariate analysis showed that increased plasma FGF23 was independently associated with SARS-CoV-2 infection and severe COVID-19. Discussion: Our results suggest that high plasma FGF23 levels are a risk factor for developing COVID-19 in ESRD patients. These data support the potential immunosuppressive effects of high circulating FGF23 as a factor implicated in the association with worse clinical outcomes. Further data are needed to confirm this hypothesis.

Heart failure with preserved ejection fraction (HFpEF) is a growing public health problem in nearly 50% of patients with heart failure. Therefore, research on new strategies for its diagnosis and management has become imperative in recent years. Few drugs have successfully improved clinical outcomes in this population. Therefore, numerous attempts are being made to find new pharmacological interventions that target the main mechanisms responsible for this disease. In recent years, pathological mechanisms such as cardiac fibrosis and inflammation, alterations in calcium handling, NO pathway disturbance, and neurohumoral or mechanic impairment have been evaluated as new pharmacological targets showing promising results in preliminary studies. This review aims to analyze the new strategies and mechanical devices, along with their initial results in pre-clinical and different phases of ongoing clinical trials for HFpEF patients. Understanding new mechanisms to generate interventions will allow us to create methods to prevent the adverse outcomes of this silent pandemic.

COVID-19 infection presenting as a myocardial infarction. Report of one caseIsolated cardiac involvement of COVID-19 is an infrequent presentation, and myocardial infarction is even less common. We report a 30-year-old man presenting with retrosternal pain of insidious onset whose intensity increases suddenly. On admission, the patient had tachycardia and an EKG showed a 1 mm ST-elevation and diffuse PQ segment depression. Troponin was 26.9 ng/ml (normal value [NV] < 0.03), inflammatory parameters were elevated, and SARS-CoV 2 PCR was positive. He was hospitalized with the diagnosis of myopericarditis secondary to SARS-CoV 2. He progressed favorably without pain during the hospital stay and with decreasing troponin values. A Cardiac Magnetic Resonance Imaging (MRI) was compatible with an infero-lateral transmural infarction. A coronary angiography showed a distal occlusion of the circumflex artery. Consequently, anticoagulation and double platelet anti-aggregation were started. The patient evolved favorably, with a decreasing troponin curve (last at discharge 0.49 ng/ml

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