Inpatient falls pose a significant challenge in hospitals, impacting patient safety and resources. This retrospective study aimed to analyze the impact of the COVID-19 pandemic on fall incidents in a major metropolitan tertiary referral and teaching hospital in New South Wales (NSW), Australia.

Utilizing clinical informatics, data from Clinical Health Information Exchange (CHIE) database, electronic medical records (eMR), and the NSW Health Incident Information Management System (IIMS)/Incident Management System Plus (IMS+) were collected. Inpatient falls reported at the study hospital between July and December 2019, 2020, and 2021 for patients aged 18 years and above were included. Extracted data encompassed patient demographics, medical history, fall characteristics, contributing factors, and fall incident harm scores. Descriptive and inferential statistics were undertaken using SPSS V 25, and inductive content analysis was used to analyze the narratives relating to the contributing factors for falls.

A total of 1399 inpatient falls were reported during the study period. Falls per 1000 occupied bed days (OBD) varied: 3.83 in 2019, 3.41 in 2020, and 4.35 in 2021. A significant increase in fall incidents was observed in 2021 compared to 2020. Most falls occurred on a weekday, particularly between 1400 and 2159 hours. Medicine departments reported the highest number of falls, followed by aged care units. Incident harm scores at level 3, indicating moderate injury, were prevalent across all 3 years. Contributing factors to falls according to the IIMS/IMS+ criteria were diverse, with "Patient complexity/acuity," "Patient engagement and compliance," "Hazard/unsafe," and "Clinical risk screening/assessment" emerging prominently. In addition, 7 distinct themes contributing to inpatient falls were identified through inductive analysis.

The study highlighted increased inpatient falls (4.35 falls per 1000 OBDs) during the July to December 2021 study period. Understanding fall patterns is vital for improving safety protocols. Emphasising incident reporting, staff training, environmental adjustments, and mobility-related risk management is crucial to reducing inpatient falls and fall-related injury during restricted visitor access during pandemics.

The novel coronavirus disease 2019 (COVID-19) is associated with life-threatening complications. Electrocardiogram (ECG) changes associated with COVID-19 have also been reported in the majority of critically ill patients.

In this study, we aimed to investigate the prevalence of fragmented QRS (fQRS) and its prognostic value in hospitalized patients with COVID-19. In addition, we performed a systematic review and meta-analysis of the literature to evaluate the effect of fQRS on the outcomes of COVID-19 patients.

A total of 310 patients with a mean age of 65.7 ± 14.5 years were followed up for 3 months, of whom 139 (44.8%) had fQRS on their ECGs. The rates of in-hospital mortality (8.8% vs. 8.6%), rehospitalization during follow- up (13.7% vs. 12.3%), and 90-day mortality (6.5% vs. 5.3%) were comparable between the patients with and without fQRS, respectively. In the meta-analysis, 9 studies in addition to our study reported outcomes, with a total of 2928 patients with a mean age of 53.8 years, and 1431 (48.9%) were males. The rate of fQRS was 0.31 (95% confidence interval [CI], 0.23-0.38; I2 = 95.21%). In addition, the pooled proportion of in-hospital mortality reported by 5 studies was 0.31 (95% CI, 0.12-0.51; I2 = 98.36). The rate of in-hospital mortality was higher among patients with fQRS compared to those without fQRS (odds ratio, 2.33; 95% CI, 1.52-3.58; p = 0.0001; I2 = 74%).

The rate of fQRS on ECG was relatively high in COVID-19 patients, and according to the meta-analysis, it was associated with worse outcomes in hospitalized COVID-19 patients.

Arrhythmias are a significant cause of cardiovascular mortality in the U.S. This study examines trends in arrhythmia-related mortality from 1999 to 2023, focusing on gender, racial, regional disparities, and specific arrhythmic conditions.

To analyze trends and disparities in arrhythmia-related mortality among U.S. adults aged ≥ 35 years from 1999 to 2023, with a focus on the impact of sex, race, geographic location, and urbanization.

We analyzed mortality data from the CDC WONDER database, focusing on deaths where arrhythmias were a contributing cause. Age-adjusted mortality rates (AAMRs) were calculated and stratified by sex, race/ethnicity, state, and region. The annual percentage change (APC) and average annual percentage change (AAPC) were estimated using Joinpoint regression.

A total of 5,050,271 arrhythmia-related deaths were recorded, with the overall AAMR increasing from 111.4 in 1999 to 137.3 in 2023. Mortality rates declined significantly from 1999 to 2009 (APC: -1.04%; p = 0.003) but rose sharply from 2009 to 2018 (APC: 1.69%; p = 0.003), peaking in 2021 during the COVID-19 pandemic (APC: 8.63%; p < 0.001). A subsequent decline was observed from 2021 to 2023 (APC: -3.91%; p = 0.044). Males consistently exhibited higher AAMRs than females (137.2 vs. 95.3), as did non-Hispanic White individuals compared to other racial groups. Geographic disparities revealed higher mortality rates in Nonmetropolitan areas and the Midwest, with the highest AAMR observed in Oregon and the lowest in Hawaii.

Despite an overall decline in arrhythmia-related mortality, recent increases, especially in West Virginia and among certain racial groups, highlight the need for targeted public health interventions.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic posed a significant global public health challenge, affecting millions of individuals. While some COVID-19 patients remain asymptomatic, others experience severe complications, including multiorgan failure and death. Emerging evidence indicates that COVID-19 is associated with substantial cardiovascular complications, notably an increased risk of arrhythmias, with atrial fibrillation (AF) being particularly prevalent among hospitalized patients. This review analyzes case reports of new-onset AF in COVID-19 patients, synthesizing data on patient demographics, comorbidities, clinical presentations, and outcomes. The cases reviewed indicate that affected patients were predominantly male, covered a broad age range, and frequently had underlying conditions such as hypertension, type 2 diabetes mellitus, and hyperlipidemia. The main outcomes observed included a high incidence of severe complications such as ischemic stroke, acute respiratory failure, myocarditis, and heart failure. Mortality rates were notably elevated among patients with COVID-19-related AF, particularly in those requiring intensive care or mechanical ventilation. The findings emphasize the significant cardiovascular burden of COVID-19, with a focus on its association with increased AF risk. By integrating case-based evidence, this review highlights the complex interplay between COVID-19 and AF, underscoring the need for early recognition and targeted treatment strategies to mitigate cardiovascular complications and improve patient outcomes in this vulnerable population.

The aim of this study was to evaluate how COVID-19 affected acute stroke care and outcome in patients with acute ischemic or hemorrhagic stroke. We performed a retrospective analysis on patients who were admitted with acute ischemic (AIS) or hemorrhagic (ICH) stroke from September 2020 to May 2021 with and without COVID-19. We recorded demographic and clinical data, imaging parameters, functional outcome and mortality at one year. Beside descriptive statistics we performed χ2-probe, Mann-Witney U-test, Student t-probe and multivariate testing. We found a 29%-reduction in the number of AIS cases during the pandemic. The number of the large vessel occlusions /LVOs/ (N = 83, 41.7%), from them 37 (17.7%) had mechanical thrombectomy (MT), was higher than before the COVID-19 period (p = 0.02 and p = 0.001, respectively). From all patients needing acute revascularization therapy (N = 137) 118 patients received it, among them 20 (16.9%) had COVID-19. Those positive for COVID-19 were more likely to have a higher median NIHSS score at baseline and at 24 h (p = 0.02 and p = 0.03, respectively). They also had a lower rate of favourable outcome at discharge (15% vs. 41.8%; p = 0.024) and at three months (25% vs. 52%, p = 0.02), longer median hospitalization (p < 0.0001), and a higher mortality rate (52% vs. 25%; p = 0.03). The incidence of symptomatic intracerebral hemorrhage (sICH) did not differ between the groups. Regarding the ICH patients, NIHSS score at 24 h (p = 0.036), mortality at 3 months (p = 0.004) and at one year (p = 0.00) were higher in the COVID-19 group. We concluded that the pandemic resulted fewer admission due to AIS with an increased number of LVOs and MTs. AIS patients with concomitant SARS-CoV-2 infection have more severe strokes and unfavorable long term outcome. The risk of sICH was not increased in COVID-19 positive patients therefore reperfusion therapies appear to be safe and beneficial for some individuals. Patients with ICH and comorbid COVID-19 have a very poor prognosis.

Cardiac arrhythmias are commonly noted in patients during infections with and recovery from COVID-19. Arrhythmic manifestations span the spectrum of innocuous and benign to life-threatening and deadly. Various pathophysiological mechanisms have been proposed. Debate continues on the impact of incident and exacerbated arrhythmias on the acute and chronic (recovery) phase of the illness. COVID-19 and COVID-19 vaccine-associated myocardial inflammation and autonomic disruption remain concerns. As the pandemic has transformed to an endemic, with discovery of new SARS-CoV-2 variants, updated vaccines, and potent antiviral drugs, vigilance for COVID-19-associated arrhythmic and dysautonomic manifestations remains. The objective of this American Heart Association scientific statement is to review the available evidence on the epidemiology, pathophysiology, clinical presentation, and management of cardiac arrhythmias and autonomic dysfunction in patients infected with and recovering from COVID-19 and to provide evidence-based guidance. The writing committee's consensus on implications for clinical practice, gaps in knowledge, and directions for future research are highlighted.

Bradycardia and dysautonomia observed during SARS-Cov2 infection suggests involvement of the autonomic nervous system (ANS). Limited data exists on ANS dysregulation and its association with outcomes in patients with acute respiratory distress syndrome (ARDS) related to COVID-19 (C-ARDS) or other etiologies (NC-ARDS).

We aimed to explore sympathovagal balance, assessed by heart rate variability (HRV), and its clinical prognostic value in C-ARDS compared with NC-ARDS.

A single-center, prospective case-control study was conducted. Consecutive patients meeting ARDS criteria between 2020 and 2022 were included. HRV was assessed using 1-hour electrographic tracing during a stable, daytime period.

Twenty-four patients with C-ARDS and 19 with NC-ARDS were included. Age, sex and ARDS severity were similar between groups. The median heart rate was markedly lower in the C-ARDS group than in the NC-ARDS group (60 [53-72] versus 101 [91-112] bpm, p<.001). Most of HRV parameters were significantly increased in patients with C-ARDS. HRV correlated with heart rate only in patients with C-ARDS. A positive correlation was found between the low-to high-frequency ratio (LF/HF) and length of intensive care unit stay (r = 0.576, p<.001).

This study confirmed that C-ARDS was associated with marked bradycardia and severe ANS impairment, suggesting a sympathovagal imbalance with vagal overtone. Poor outcomes appeared to be more related to sympathetic rather than parasympathetic hyperactivation.

There exist serious cardiovascular complications subsequent to SARS-Cov2 infection (COVID-19); however, the association between COVID-19 and atrial fibrillation (AF) remains to be elucidated. We aimed to assess the prevalence of AF among COVID-19 patients and its associated risk of death.

The present systematic review was performed in accordance with the PRISMA guidelines. The protocol was registered with CRD42022306523. A comprehensive literature search was performed across PubMed, Embase, and Cochrane databases to identify studies reporting on the prevalence of pre-existing or new-onset fibrillation (AF), and/or the associated clinical outcomes in patients with COVID-19 from January 2020 to December 2023. The random-effect model was used to estimate the prevalence of AF and its related mortality.

A total of 80 studies, including 39,062,868 COVID-19 patients, were identified in the present investigation. The prevalence rates of pre-existing AF or new-onset AF were 10.5% (95% CI [9.3-11.7%]) or 10.3% (95% CI [6.2-14.5%]), respectively. Subgroup analysis revealed a two fold higher incidence of AF in older patients (≥65 years) compared to younger patients (<65 years) (14.4% vs. 6.4%). The highest rate of AF was observed in Europeans (10.7%, 95% CI [10.2-11.2%]), followed by Northern Americans (10.0%, 95% CI [8.2-11.7%]), while Asians demonstrated a lower prevalence (2.7%, 95% CI [2.2-3.3%]). Notably, severe COVID-19 patients displayed a significantly elevated prevalence of AF at 14.l% (95% CI [13.3-14.9%]), which was approximately 2.5-fold higher than that in non-severe patients (5.2%, 95% CI [4.8-5.5%]). Both pre-existing (HR: 1.83, 95% CI [1.49-2.17]) and new-onset AF (HR: 3.47, 95% CI [2.26-5.33]) were associated with an increased mortality risk among COVID-19 patients. Furthermore, the effect on mortality risk was more significant in Asians (HR: 5.33, 95% CI [1.62-9.04]), compared to Europeans (HR: 1.68, 95% CI [1.24-2.13]) and North Americans (HR: 2.01, 95% CI [1.18-2.83]).

This study comprehensively investigated the association between AF and COVID-19 in a real-world setting. Notably, a high prevalence of AF was observed among older individuals, severe COVID-19 patients, and in Europe and Northern America. Moreover, co-existing AF was found to be associated with an increased risk for mortality. Further investigations are warranted to improve the management and outcomes of COVID-19 patients with AF.

The risk of cardiovascular complications due to SARS-CoV-2 are significantly increased within the first 6 months of the infection. Patients with COVID-19 have an increased risk of death, and there is evidence that many may experience a wide range of post-acute cardiovascular complications. Our work aims to provide an update on current clinical aspects of diagnosis and treatment of cardiovascular manifestations during acute and long-term COVID-19.

SARS-CoV-2 has been shown to be associated with increased incidence of cardiovascular complications such as myocardial injury, heart failure, and dysrhythmias, as well as coagulation abnormalities not only during the acute phase but also beyond the first 30 days of the infection, associated with high mortality and poor outcomes. Cardiovascular complications during long-COVID-19 were found regardless of comorbidities such as age, hypertension, and diabetes; nevertheless, these populations remain at high risk for the worst outcomes during post-acute COVID-19. Emphasis should be given to the management of these patients. Treatment with low-dose oral propranolol, a beta blocker, for heart rate management may be considered, since it was found to significantly attenuate tachycardia and improve symptoms in postural tachycardia syndrome, while for patients on ACE inhibitors or angiotensin-receptor blockers (ARBs), under no circumstances should these medications be withdrawn. In addition, in patients at high risk after hospitalization due to COVID-19, thromboprophylaxis with rivaroxaban 10 mg/day for 35 days improved clinical outcomes compared with no extended thromboprophylaxis. In this work we provide a comprehensive review on acute and post-acute COVID-19 cardiovascular complications, symptomatology, and pathophysiology mechanisms. We also discuss therapeutic strategies for these patients during acute and long-term care and highlight populations at risk. Our findings suggest that older patients with risk factors such as hypertension, diabetes, and medical history of vascular disease have worse outcomes during acute SARS-CoV-2 infection and are more likely to develop cardiovascular complications during long-COVID-19.

Deferoxamine is a potent iron chelator that could remove iron from the virus, and severe acute respiratory syndrome coronavirus 2 requires iron to replication. Also, deferoxamine has antioxidant and cytokine-modulating effects. Therefore, we evaluated the efficacy and safety of deferoxamine in patients with moderate coronavirus disease 2019 (COVID-19).

In this randomized controlled trial, patients with moderate COVID-19 were randomly assigned in a 1:1 ratio to the deferoxamine group (received a solution of 500 mg deferoxamine divided into 4 doses a day through a nebulizer for 7 days) and the control group. The main outcomes were viral clearance, oxygen saturation (SPO2), body temperature, and respiratory rate (RR). Intensive care unit admission, hospital length of stay, and hospital mortality were also assessed.

A total of 62 patients, with 30 in the deferoxamine group and 32 in the control group, were randomly assigned. There was no statistically significant improvement in viral clearance after the intervention ended in the deferoxamine group (36.7%) compared to the control group (34.4%). The results showed there was no significant difference between the analyzed groups in terms of SPO2, body temperature, RR, and the number of patients with a worse prognosis (SPO2 < 96%, temperature ≥ 37.5 °C, or RR ≥ 16/min) at the end of the study. There were no significant differences seen between the groups in terms of intensive care unit admission, hospital length of stay, hospital mortality, and the occurrence of adverse medication events during the follow-up period.

Deferoxamine had no significant impact on improving moderately ill patients with COVID-19. However, it was well-tolerated in the patients, and this intervention demonstrated a safe profile of adverse events.

COVID-19 is associated with various cardiovascular complications, including arrhythmias. This study investigated the incidence of new-onset atrial fibrillation (AFB) and atrial flutter (AFL) in COVID-19 patients and identified potential risk factors. We conducted a retrospective cohort study at a tertiary-care safety-net community hospital including 647 patients diagnosed with COVID-19 from March 2020 to March 2021. Patients with a prior history of AFB or AFL were excluded. Data on demographics, clinical characteristics, and outcomes were collected and analyzed using chi-square tests, t-tests, and binary logistic regression. We found that 69 patients (10.66%) developed AFB or AFL, with 41 patients (6.34%) experiencing new-onset arrhythmias. The incidence rates for new-onset AFB and AFL were 5.4% and 0.9%, respectively. Older age (≥65 years) was significantly associated with new-onset AFB/AFL (OR: 5.43; 95% CI: 2.31-12.77; p < 0.001), as was the development of sepsis (OR: 2.73; 95% CI: 1.31-5.70; p = 0.008). No significant association was found with patient sex. Our findings indicate that new-onset atrial arrhythmias are a significant complication in COVID-19 patients, particularly among the elderly and those with sepsis. This highlights the need for targeted monitoring and management strategies to mitigate the burden of atrial arrhythmias in high-risk populations during COVID-19 infection.

This study aimed to investigate alterations in serum markers [creatine kinase-MB (CKMB), cardiac troponin T (cTnT), myoglobin (Myo), B-type natriuretic peptide (BNP), D-dimer (DD), procalcitonin (PCT) and interleukin-6 (IL6)] in early Omicron variant infection and analyzed their correlation with clinical parameters.

Retrospective analysis of 1,138 mild/asymptomatic cases at Tianjin First Central Hospital, including age, gender, serum markers and nucleic acid test results. Statistical analysis used SPSS software, version 24.0.

Elevated cTnT, BNP (125-400), and DD (0.55-1.10) levels were prevalent at 12.92%, 15.64%, and 14.50%, respectively. Females had significantly higher proportions with slightly elevated BNP (19.34%) and DD (19.69%) levels. Patients over 35 had a higher proportion of slight elevation in BNP (20.00%). Abnormal levels of serum markers were significantly associated with older age, increased PCT and IL6 levels, as well as delayed nucleic acid clearance. Additionally, levels of immunoglobulin G (IgG) were notably reduced in these cases. Patients with prolonged nucleic acid clearance (>14 days) had higher BNP and DD levels upon admission. Logistic regression identified PCT (OR = 237.95) as the most significant risk factor for abnormal serum markers for cardiovascular system injury.

Early Omicron infection might do subclinical damage to the cardiovascular system. Elevated cTnT, BNP and DD levels were correlated with age, gender, inflammatory factors, and IgG. Notably, high PCT level emerged as the most robust predictor of abnormal serum biomarkers.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and coronavirus disease 2019 (COVID-19) have been around for more than 3 years now. However, due to constant viral evolution, novel variants are emerging, leaving old treatment protocols redundant. As treatment options dwindle, infection rates continue to rise and seasonal infection surges become progressively common across the world, rapid solutions are required. With genomic and proteomic methods generating enormous amounts of data to expand our understanding of SARS-CoV-2 biology, there is an urgent requirement for the development of novel therapeutic methods that can allow translational research to flourish. In this review, we highlight the current state of COVID-19 in the world and the effects of post-infection sequelae. We present the contribution of translational research in COVID-19, with various current and novel therapeutic approaches, including antivirals, monoclonal antibodies and vaccines, as well as alternate treatment methods such as immunomodulators, currently being studied and reiterate the importance of translational research in the development of various strategies to contain COVID-19.

COVID-19 is an infectious disease caused by SARS-CoV-2. It is unclear whether influenza vaccination reduces the severity of disease symptoms. Previous studies have suggested a beneficial effect of influenza vaccination on the severity of COVID-19. The aim of this study was to evaluate the possible protective effect of the influenza vaccine on the occurrence of SARS-CoV-2 infection symptoms and prognosis in patients hospitalized with COVID-19.

This was a retrospective cohort study of patients who tested positive for SARS-CoV-2, identified by quantitative real-time polymerase chain reaction. Chi-square tests, Kaplan-Meier analysis, and multivariate analysis were performed to assess the association between influenza vaccination and the presence of symptoms in hospitalized patients with COVID-19 and their outcome.

In this study, 1712 patients received positive laboratory tests for SARS-CoV-2; influenza vaccination was a protective factor against the presence of characteristic COVID-19 symptoms such as polypnea, anosmia, dysgeusia, and fever (p < 0.001). Influenza-vaccinated patients had fewer days of hospitalization (p = 0.029).

The findings of this study support that influenza vaccination is associated with a decrease in the number of symptoms in patients hospitalized due to COVID-19, with fewer days of hospitalization, but not with the outcome of disease.

COVID-19 is a new infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS CoV-2). Since the outbreak in December 2019, it has caused an unprecedented world pandemic, leading to a global human health crisis. Although SARS CoV-2 mainly affects the lungs, causing interstitial pneumonia and severe acute respiratory distress syndrome, a number of patients often have extensive clinical manifestations, such as gastrointestinal symptoms, cardiovascular damage and renal dysfunction.

This review article discusses the pathogenic mechanisms of cardiovascular damage in COVID-19 patients and provides some useful suggestions for future clinical diagnosis, treatment and prevention.

An English-language literature search was conducted in PubMed and Web of Science databases up to 12th April, 2024 for the terms "COVID-19", "SARS CoV-2", "cardiovascular damage", "myocardial injury", "myocarditis", "hypertension", "arrhythmia", "heart failure" and "coronary heart disease", especially update articles in 2023 and 2024. Salient medical literatures regarding the cardiovascular damage of COVID-19 were selected, extracted and synthesized.

The most common cardiovascular damage was myocarditis and pericarditis, hypertension, arrhythmia, myocardial injury and heart failure, coronary heart disease, stress cardiomyopathy, ischemic stroke, blood coagulation abnormalities, and dyslipidemia. Two important pathogenic mechanisms of the cardiovascular damage may be direct viral cytotoxicity as well as indirect hyperimmune responses of the body to SARS CoV-2 infection.

Cardiovascular damage in COVID-19 patients is common and portends a worse prognosis. Although the underlying pathophysiological mechanisms of cardiovascular damage related to COVID-19 are not completely clear, two important pathogenic mechanisms of cardiovascular damage may be the direct damage of the SARSCoV-2 infection and the indirect hyperimmune responses.

Ginger, a potent antiviral, anti-inflammatory, and antioxidant remedy, is a potential therapeutic option for COVID-19. However, there was not enough clinical evidence about ginger and COVID-19. We evaluated the efficacy and safety of ginger on clinical and paraclinical features in outpatients with COVID-19.

In this randomized controlled trial, the outpatients with confirmed COVID-19 were randomly assigned in a 1:1 ratio to receive ginger (1000 mg 3 times a day for 7 days) or placebo. The primary outcome was viral clearance after the end of the intervention. Oxygen saturation (SPO2), body temperature, respiratory rate (RR), hospital admission, and the incidence of adverse events were also assessed.

A total of 84 patients (42 in the ginger and 42 in the control groups) were randomized. The viral clearance was not statistically improved in the ginger group (41.6%) compared to the placebo group (42.8%). The findings indicated that SPO2, body temperature, and RR had no significant difference between the groups at the end of the intervention. The imaging finding indicated pulmonary infiltrate significantly reduced on the 7th day of the intervention in the ginger group. The percentage of patients with SPO2 <96% in the ginger group decreased over the study compared to the placebo group. Moreover, the need for hospital admission and the incidence of adverse drug events were not different between the groups over the follow-up period.

Ginger had no significant impact on the clinical and paraclinical parameters of patients. However, this intervention demonstrated a safe profile of adverse events and reduced pulmonary infiltrate.

The trial was registered as IRCT20200506047323N1.

In 2019, the emergence of the coronavirus disease 2019 (COVID-19) virus triggered a global pandemic, reminiscent of the magnitude witnessed during the flu pandemic of 1918. Initially, children often presented with either asymptomatic or mild upper respiratory tract infection symptoms. However, in the post-acute phase, a distinct syndrome affecting multiple organ systems emerged, sharing similarities with Kawasaki's disease. This syndrome was later classified as multisystem inflammatory syndrome in children (MIS-C) by the Pediatric Intensive Care Society in April 2020. Notably, cardiac manifestations and complications associated with COVID-19 constitute a significant source of morbidity and mortality, characterized by left ventricular dysfunction, cardiac conduction abnormalities, and arrhythmias. Although cases of arrhythmias with MIS-C are rare in the literature, we present a unique case involving a 14-year-old without known cardiac risk factors who presented with conduction abnormalities and fatal arrhythmias secondary to MIS-C.

Epidemiological studies have demonstrated that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-positive patients often develop atrial fibrillation, premature ventricular contractions (PVCs), and conduction disorders. The manifestation of ventricular cardiac arrhythmias accentuates the risk of sudden cardiac death.

A retrospective study was conducted on the cohort of 1,614 patients admitted for coronavirus disease 2019 (COVID-19). Patients were categorized into two groups based on the occurrence of PVCs. Group I comprised 172 patients diagnosed with PVCs of Lown-Wolf class II - IV upon hospital admission; group II (control group) consisted of 1,442 patients without this arrhythmia. Each patient underwent comprehensive clinical, laboratory, and instrumental evaluations.

The emergence of PVCs in individuals afflicted with COVID-19 was associated with a 5.879-fold heightened risk of lethal outcome, a 2.904-fold elevated risk of acute myocardial infarction, and a 2.437-fold increased risk of pulmonary embolism. Upon application of diagnostic criteria to evaluate the "cytokine storm", it was discovered that the occurrence of the "cytokine storm" was notably more frequent in the group with PVCs, manifesting in six patients (3.5%), compared to 16 patients (1.1%) in the control group (P < 0.05). The mean extent of lung tissue damage in group I was significantly greater than that of patients in group II (P < 0.05). Notably, the average oxygen saturation level, as measured by pulse oximetry upon hospital admission was 92.63±3.84% in group I and 94.20±3.50% in group II (P < 0.05).

The presence of PVCs in COVID-19 patients was found to elevate the risk of cardiovascular complications. Significant independent predictors for the development of PVCs in patients with SARS-CoV-2 infection include: age over 60 years (risk ratio (RR): 4.6; confidence interval (CI): 3.2 - 6.5), a history of myocardial infarction (RR: 3.5; CI: 2.6 - 4.6), congestive heart failure (CHF) with reduced left ventricular ejection fraction (RR: 5.5; CI: 3.9 - 7.6), respiratory failure (RR: 2.3; CI: 1.7 - 3.1), and the presence of a "cytokine storm" (RR: 4.5; CI: 2.9 - 6.0).

All elective procedures were stopped in March 2020 because of the coronavirus disease 2019 (COVID-19) pandemic. We report the 90-day mortality and complications of patients who underwent primary arthroplasty before the stopping of elective procedures at a single academic medical center. A retrospective cohort study was conducted including patients who underwent elective primary arthroplasty between December 2019 and mid-March 2020. Their 90-day postoperative mortality and medical complications were statistically compared with those of a historical cohort from the same operative period in 2019. The 2020 and 2019 cohorts included 372 and 410 patients, respectively. Except for the prevalence of diabetes, there was no significant difference between the two cohorts regarding baseline characteristics or preoperative health. The 2020 cohort had statistically significant higher rates of pneumonia (2.7% vs 0.7%; P=.03), readmission (9.1% vs 5.4%; P=.04), pulmonary embolism (1.6% vs 0.2%; P=.04), and 90-day mortality (1.1% vs 0%; P=.04). The 2020 cohort also had a trend for increased rates of deep venous thrombosis (1.1% vs 0.7%; P=.7) and cardiac complications (1.9% vs 0.5%; P=.07) and no change in emergency department visits (14.0% vs 11.7%; P=.3). There were 7 confirmed cases of COVID-19 in the 2020 cohort and 1 death. This study demonstrates that patients who underwent primary arthroplasty procedures at our institution close to the time of the first wave of the COVID-19 pandemic experienced a statistically significant increase in mortality, pneumonia, pulmonary embolism, and readmission compared with a historical cohort. As elective procedures have resumed during the ongoing pandemic, providers and patients should be aware of these increased risks. [Orthopedics. 2024;47(3):135-140.].

The novel coronavirus of 2019 (COVID-19) has inflicted significant harm on the cardiovascular system. Patients presenting with fatal chronic arrhythmias after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are rare, arrhythmia caused by SARS-CoV-2 infection need to be taken seriously.

Three female patients were admitted to the hospital with syncopal symptoms. Previously, they had been identified to have COVID-19 infection and none of the patients had a preexisting history of arrhythmia, and upon hospital admission, no electrolyte imbalances associated with arrhythmias were observed. However, following SARS-CoV-2 infection, patients exhibit varying degrees of syncope symptoms.

A high-degree atrioventricular block was diagnosed after a comprehensive evaluation of the patient's clinical manifestations and electrocardiogram (ECG) performance.

We performed ECG monitoring of the patient and excluded other causes of arrhythmia. The patient was discharged from the hospital after permanent pacemaker implantation and symptomatic treatment.

The outpatient follow-ups did not reveal a recurrence of syncope or complications related to the pacemaker in any of the three patients.

Some patients did not exhibit any obvious respiratory symptoms or signs following SARS-CoV-2 infection. This suggests that the cardiac conduction system may be the preferred target for some SARS-CoV-2 variants. Therefore, in addition to investigating the causes of malignant arrhythmias, special attention should be paid to SARS-CoV-2 infection in patients with developing arrhythmias. Additionally, permanent pacemaker implantation may be the most suitable option for patients who already have malignant arrhythmias.

Infection with Sars-CoV-2 is known to cause cardiac injury and coronary artery changes in moderate to severe acute COVID-19 and post-acute multisystem inflammatory syndrome in children (MIS-C). However, little is known about the potential for cardiac involvement, in particular coronary artery dilation, in asymptomatic or mild cases of COVID-19.

A retrospective review of children ≤ 18 years of age with a history of asymptomatic or mild COVID-19 disease who underwent echocardiography after Sars-CoV-2 infection is conducted. Patients were excluded if they had been hospitalised for COVID-19/MIS-C or had a history of cardiac disease that could affect coronary artery dimension. Coronary artery dilation was defined as the Boston Z-score greater than 2.0.

One hundred and fifty-seven patients met inclusion criteria with a mean age of 9.4 years (+/- 5.4 years). Eighty-four (54%) patients were identified as having COVID-19 through positive antibody testing. All patients underwent electrocardiogram and echocardiogram as part of their cardiology evaluation. One hundred and thirty-five (86%) patients had a normal evaluation or only a minor variant on electrocardiogram, while 22 patients had abnormalities on echocardiogram, 4 of which demonstrated coronary artery dilation based on the Boston Z-score.

Much of the literature for post-infectious screening and follow-up focuses on patients with a history of moderate to severe COVID-19 disease, emphasising the need for surveillance for the potential development of myocarditis. In this study, 4 out of 157 (2.5%) children with a history of asymptomatic or mild COVID-19 disease without MIS-C were found to have some degree of coronary artery dilation. The significance of this finding currently remains unknown.

Viral infections have been linked to a variety of cardiac pathology, which may include acute myocarditis, dilated cardiomyopathy, heart failure, cardiogenic shock, pericarditis, acute coronary syndromes, and arrhythmias. We performed a systematic review of literature focusing on the cardiovascular effects of various viral infections, as well as providing an update on the current understanding of the pathophysiology of Coronavirus disease-2019 (COVID-19). Cardiac manifestations of viral illnesses are usually self-limiting, have variable clinical presentations, and require sufficient clinical suspicion for diagnosis and optimal management.

The coronavirus disease 2019 (COVID-19) was first introduced in December 2019, which is known as severe acute respiratory syndrome caused by coronavirus-2 (SARS-CoV-2) that is a serious and life-threatening disease. Although pneumonia is the most common manifestation of COVID-19 and was initially introduced as a respiratory infection, in fact, the infection of COVID-19 is a subset of complications and damage to various organs. There are several reports of cardiac involvement with COVID-19. A wide range of cardiac complications may occur following COVID-19 infection, including systolic heart failure, myocarditis, pericarditis, atrial and ventricular arrhythmias, and thromboembolic events. There are various hypotheses about the pathophysiology of cardiovascular involvement by this virus. At the top of these hypotheses is the release of cytokines to the heart. Although there are other assumptions, considering that one of the causes of death in patients with COVID-19 is arrhythmia. It is necessary to know correctly about its pathophysiology and etiology. Therefore, in this study, we have reviewed the articles of recent years in the field of pathophysiology and etiology of arrhythmia in patients with COVID-19 infection. The purpose of this study was to provide a basis for a correct and more comprehensive understanding of the pathogenesis of arrhythmia in patients with COVID-19 infection.

We compared the effect of perioperative COVID-19, before and after vaccination, on 30-day mortality after cardiac surgery.

Data was extracted from several national registries. The study period was March 1st, 2020-March 31st, 2022.

2594 adult patients underwent cardiac surgery before the availability of a universal COVID-19 vaccine. 33 patients were diagnosed with COVID-19 prior to surgery (mean age 58.3±10.0, mean length of time 73.6±60.1 days) and 7 patients were diagnosed with COVID-19 0-14 days after surgery (age 66.4±7.6). These were compared to 4426 patients who underwent cardiac surgery after the availability of a universal vaccine: 469 patients were diagnosed with COVID-19 prior to surgery (age 62.1±10.1, length of time 175.8±158.2) and 32 patients diagnosed with COVID-19 0-14 days after surgery (age 60.8±14.5). In patients diagnosed with COVID-19 prior to surgery, there was no excess 30-day mortality either before or after vaccination (1 (3.0%) vs. 57 (2.2%), respectively, P<0.8, and 8 (1.7%) vs. 87 (2.2%), respectively, P<0.5). Patients diagnosed with COVID-19 after surgery, but before vaccination, had significantly higher 30-day mortality compared to COVID-19 negative patients (2 (28.6%) vs. 56 (2.2%) respectively, P<0.0001). This excess mortality disappeared after universal vaccination (1 (3.1%) vs. 94 (2.1%) respectively, P<0.7).

COVID-19, when diagnosed in the early post-operative period, was a risk factor for mortality before available vaccinations, but not after vaccination was widely available. Pre-surgery screening and post-surgical isolation is essential until vaccines are available. This data may be useful for patient management in future respiratory pandemics.

Introduction: Significant attention has been paid to myocardial damage mediated by the single-stranded RNA virus. Qingfei Paidu decoction (QFPDD) has been proved to protect the damage caused by the influenza virus A/PR/8/1934 (PR8), but its specific mechanism is unclear. Methods: Molecular biological methods, together with network pharmacology, were used to analyze the effects and underlying mechanism of QFPDD treatment on PR8-induced myocardial damage to obtain insights into the treatment of COVID-19-mediated myocardial damage. Results: Increased apoptosis and subcellular damage were observed in myocardial cells of mice infected by PR8. QFPDD treatment significantly inhibited the apoptosis and subcellular damage induced by the PR8 virus. The inflammatory factors IFN-β, TNF-α, and IL-18 were statistically increased in the myocardia of the mice infected by PR8, and the increase in inflammatory factors was prevented by QFPDD treatment. Furthermore, the expression levels or phosphorylation of necroptosis-related proteins RIPK1, RIPK3, and MLKL were abnormally elevated in the group of infected mice, while QFPDD restored the levels or phosphorylation of these proteins. Our study demonstrated that HIF-1α is a key target of QFPDD in the treatment of influenza virus-mediated injury. The HIF-α level was significantly increased by PR8 infection. Both the knockdown of HIF-1α and treatment of the myocardial cell with QFPDD significantly reversed the increased inflammatory factors during infection. Overexpression of HIF-1α reversed the inhibition effects of QFPDD on cytokine expression. Meanwhile, seven compounds from QFPDD may target HIF-1α. Conclusion: QFPDD can ameliorate influenza virus-mediated myocardial damage by reducing the degree of cell necroptosis and apoptosis, inhibiting inflammatory response and the expression of HIF-1α. Thus, our results provide new insights into the treatment of respiratory virus-mediated myocardial damage.

Since 2019, Coronavirus disease-2019 (COVID-19) has raised unprecedented global health crisis. The incidence and impact of atrial fibrillation (AF) on patients with COVID-19 remain unclearly defined.

We conducted a retrospective cohort study using ICD-10 codes to identify patients with a primary diagnosis of COVID-19 with or without AF in National Inpatient Sample Database 2020. We compared the outcome of COVID-19 patients with a concurrent diagnosis of AF with those without.

AF will adversely affect the prognosis of hospitalized COVID-19 patients.

A total of 211 619 patients with a primary diagnosis of COVID-19 were identified. Among these patients, 31 923 (15.08%) had a secondary diagnosis of AF. Before propensity score matching, COVID-AF cohort was older (75.8 vs. 62.2-year-old, p < .001) and had more men (57.5% vs. 52.0%, p < .001). It is associated with more comorbidities, mainly including diabetes mellitus (43.7% vs. 39.9%, p < .001), hyperlipidemia (54.6% vs. 39.8%, p < .001), chronic kidney disease (34.5% vs. 17.0%, p < .001), coronary artery disease (35.3% vs. 14.4%, p < .001), anemia (27.8% vs. 18.6%, p < .001), and cancer (4.8% vs. 3.4%, p < .001). After performing propensity score match, a total of 31 862 patients were matched within each group. COVID-AF cohort had higher inpatient mortality (22.2% vs. 15.3%, p < .001) and more complications, mainly including cardiac arrest (3.9% vs. 2.3%, p < .001), cardiogenic shock (0.9% vs. 0.3%, p < .001), hemorrhagic stroke (0.4% vs. 0.3%, p = .025), and ischemic stroke (1.3% vs. 0.7%, p < .001). COVID-AF cohort was more costly, with a longer length of stay, and a higher total charge.

AF is common in patients hospitalized for COVID-19, and is associated with poorer in-hospital mortality, immediate complications and increased healthcare resource utilization.

In the past several years, the coronavirus pandemic has introduced multiple medical disciplines to various new forms of disease previously unknown and has shown us a unique presentation of already existing diseases. We continue to understand the long-term effects of the pandemic on the population's health and continue to find new unique features previously unknown. This paper presents the unique feature of lung uptake abnormalities discovered on nuclear stress testing for cardiac perfusion defects, a consistent finding in multiple individuals with recent COVID-19 or ongoing infection.

The respiratory illness known as COVID-19 is caused by the novel coronavirus, SARS-CoV-2. While the precise pathogenic mechanism of COVID-19 remains unclear, the occurrence of a cytokine storm subsequent to viral infection plays a pivotal role in the initiation and advancement of the disease. The infection of SARS-CoV-2 induces a state of immune system hyperactivity, leading to an excessive production of inflammatory cytokines. Consequently, the identification of the various signaling pathways implicated in the inflammation induced by COVID-19 will enable researchers to investigate new targets for therapeutic intervention.

Patients diagnosed with coronavirus disease (CVD) who experience cardiovascular complications or have pre-existing cardiovascular disease are at an increased risk of death. The primary heart-related consequences associated with COVID-19 encompass venous thromboembolism, shock, heart failure, arrhythmias, myocarditis, acute myocardial infarction, and acute cardiac damage. The coronavirus has the potential to induce cardiovascular complications or exacerbate pre-existing CVD through various mechanisms. These mechanisms include dysregulation of the renin-angiotensin-aldosterone system; direct viral toxicity; damage to endothelial cells; formation of blood clots and subsequent inflammation, a phenomenon known as thromboinflammation; an excessive immune response known as cytokine storm; and an imbalance between the demand and supply of oxygen in the body. In this study, we comprehensively analyze the cardiovascular symptoms, histology, and underlying mechanisms associated with COVID-19. Our aim is to contribute to the identification of future research objectives and aid in the advancement of therapeutic management approaches.

Licorice extract (glycyrrhizin), a potent antiviral, anti-inflammatory, and antioxidant remedy, is a potential therapeutic option for COVID-19. We evaluated the efficacy and safety of licorice in patients with moderate COVID-19. In this study, 60 patients with confirmed COVID-19 were randomly assigned in a 1:1 ratio to receive licorice (at a dose of 760 mg three times a day for seven days) or control groups. The primary outcomes were SPO2, body temperature, and respiratory rate (RR) after the end of the intervention. The findings indicated that SPO2, body temperature, and RR had no significant difference between the groups at the end of the intervention. However, CRP and ALT improved in the licorice group toward the baseline. The number of patients with worse prognoses, LOS, mortality, and the incidence of adverse events were not different between the groups at the end of the study. Licorice had no beneficial effect on the clinical symptoms of COVID-19. Moreover, this intervention demonstrated a safe profile of adverse events. The confirmation of the results of this preparatory trial requires more detailed multiple-center trials with a larger sample size.

New-onset atrial fibrillation (NOAF) is the most frequently encountered cardiac arrhythmia observed in patients with COVID-19 infection, particularly in Intensive Care Unit (ICU) patients. The purpose of the present review is to delve into the occurrence of NOAF in COVID-19 and thoroughly review recent, pertinent data. However, the causality behind this connection has yet to be thoroughly explored. The proposed mechanisms that could contribute to the development of AF in these patients include myocardial damage resulting from direct virus-induced cardiac injury, potentially leading to perimyocarditis; a cytokine crisis and heightened inflammatory response; hypoxemia due to acute respiratory distress; disturbances in acid-base and electrolyte levels; as well as the frequent use of adrenergic drugs in critically ill patients. Additionally, secondary bacterial sepsis and septic shock have been suggested as primary causes of NOAF in ICU patients. This notion gains strength from the observation of a similar prevalence of NOAF in septic non-COVID ICU patients with ARDS. It is plausible that both myocardial involvement from SARS-CoV-2 and secondary sepsis play pivotal roles in the onset of arrhythmia in ICU patients. Nonetheless, there exists a significant variation in the prevalence of NOAF among studies focused on severe COVID-19 cases with ARDS. This discrepancy could be attributed to the inclusion of mixed populations with varying degrees of illness severity, encompassing not only patients in general wards but also those admitted to the ICU, whether intubated or not. Furthermore, the occurrence of NOAF is linked to increased morbidity and mortality. However, it remains to be determined whether NOAF independently influences outcomes in critically ill COVID-19 ICU patients or if it merely reflects the disease's severity. Lastly, the management of NOAF in these patients has not been extensively studied. Nevertheless, the current guidelines for NOAF in non-COVID ICU patients appear to be effective, while accounting for the specific drugs used in COVID-19 treatment that may prolong the QT interval (although drugs like lopinavir/ritonavir, hydrochlorothiazide, and azithromycin have been discontinued) or induce bradycardia (e.g., remdesivir).

This scoping review sought to identify the nature and extent of clinical evidence regarding the acute and long-term cardiovascular complications associated with COVID-19. Forty-nine studies published between 2020 and 2023 were selected for review. The studies were divided into two groups. The referential group included 22 studies. The second group of 27 studies was used for a detailed review to assess the strength of the evidence. The aggregate evidence indicates that the most common cardiac complications associated with COVID-19 include but are not limited to acute pericarditis, acute myocardial injury, acute myocarditis, various arrhythmias, microvascular angiopathy, left ventricular dysfunction, heart failure, acute cardiac injury, and acute coronary syndrome. Clinical and epidemiological implications of the findings are investigated, and future research recommendations are proposed.

Coronavirus disease-2019 (COVID-19) has cardiac manifestations. Data about electrocardiogram (ECG) changes after COVID-19 recovery is limited in hemodialysis patients. We aimed to investigate the changes in ventricular repolarization parameters after COVID-19 recovery in hemodialysis patients.

Fifty-five hemodialysis patients who recovered from COVID-19 infection were included. QT interval, Tp-e interval, corrected QT (QTc), QTc dispersion, and Tp-e dispersion values were determined on the patients' ECGs, taken before COVID-19 and at least 1 month after recovery. The patients' data before COVID-19 infection and after recovery were compared.

It was found that longest QTc (QTcmax) and QTc dispersion values after recovery were prolonged compared with pre-infection period (427 ± 28 ms vs. 455 ± 26 ms, p = 0.000 and 39 ± 16 ms vs. 65 ± 20 ms, p = 0.000).

In our hemodialysis patients, ventricular repolarization parameters increased after COVİD-19 recovery. In hemodialysis patients, already predisposed to arrhythmic deaths, arrhythmia risk after COVİD-19 recovery may become more pronounced.

Mimicry of host proteins is a strategy employed by pathogens to hijack host functions. Domain and motif mimicry was explored in the experimental and predicted SARS-CoV-2-human interactome. The host first interactor proteins were also added to capture the continuum of the interactions. The domains and motifs of the proteins were annotated using NCBI CD Search and ScanProsite, respectively. Host and pathogen proteins with a common host interactor and similar domain/motif constitute a mimicry pair indicating global structural similarity (domain mimicry pair; DMP) or local sequence similarity (motif mimicry pair; MMP). 593 DMPs and 7,02,472 MMPs were determined. AAA, DEXDc and Macro domains were frequent among DMPs whereas glycosylation, myristoylation and RGD motifs were abundant among MMP. The proteins involved in mimicry were visualised as a SARS-CoV-2 mimicry interaction network. The host proteins were enriched in multiple CVD pathways indicating the role of mimicry in COVID-19 associated CVDs. Bridging nodes were identified as potential drug targets. Approved antihypertensive and anti-inflammatory drugs are proposed for repurposing against COVID-19 associated CVDs. The SARS-CoV-2 mimicry data has been updated in ImitateDB (http://imitatedb.sblab-nsit.net/SARSCoV2Mimicry). Determination of key mechanisms, proteins, pathways, drug targets and repurposing candidates is critical for developing therapeutics for SARS CoV-2 associated CVDs.

Coronavirus disease 2019 is a "Public Health Emergency of International Concern" from 30 January 2020 to 5 May 2023. While battling Coronavirus disease 2019, the Chinese government has actively promoted the collaborative treatment model of Western medicine and traditional Chinese medicine, and clinical and scientific research has applied appropriate and rigorous methodology. Severe acute respiratory syndrome coronavirus 2 infection may damage the cardiovascular system via an unclarified pathogenic mechanism. The National Health Commission of China recommends 'three formulas and three medicines' for the treatment of coronavirus disease 2019, which have been shown to be most effective in the treatments. Data from randomized controlled trials of 'three formulas and three medicines' suggested that the traditional Chinese medicine is safe and can alleviate the symptoms of cardiac injury. Therefore, we further evaluate the benefits and safety of traditional Chinese medicine treatment for Coronavirus disease 2019 patients with cardiac injury across the care continuum.

R wave peak time (RWPT) is also known as intrinsicoid deflection time or ventricular activation time. It shows the conduction time from the endocardium in the ventricle to the epicardium. It provides diagnostic and prognostic information for many cardiovascular diseases, such as RWPT prolongation, left ventricular hypertrophy, volume overload, conduction system abnormalities, and myocardial ischemia. Objectives The aim of this study is to investigate the relationship between COVID-19 mortality and RWPT in superficial ECG.

This study retrospectively examined 640 patients diagnosed with COVID-19 and treated in an intensive care unit at a single center between January 2021 and June 2022. All patients included in the study had clinical and radiological characteristics and signs of COVID-19 pneumonia.

640 patients included in the study were divided into 2 groups: surviving and deceased. There were 510 patients in the surviving group and 130 patients in the deceased group. The deceased group was found to be significantly older. The number of patients with COPD was higher in the deceased group. Troponin, lactate dehydrogenase (LDH), C-reactive protein (CRP), D-dimer and T-peak to T-end interval(Tpe) and RWPT were found to be significantly increased in the deceased group. In binary logistic regression analysis; age, COPD, LDH, CRP, troponin, D-dimer, Tpe interval, RWPT were determined as independent risk factors for mortality.

Prolonged RWPT is useful in risk stratification for COVID-19 pneumonia mortality.

Remdesivir has been used for coronavirus disease 2019 (COVID-19) pneumonia with oxygen requirements that do not require mechanical intubation, and several studies showed a reduction in disease duration. However, there is a concern about bradycardia as its side effect. We aimed to investigate the association between Remdesivir and bradycardia by integrating findings from prior studies. We queried PubMed and EMBASE in February 2023 and performed a meta-analysis of studies investigating bradycardia in patients who did or did not receive Remdesivir. The outcome of interest was the rate of bradycardia and in-hospital mortality. We identified eight studies involving 8993 patients, of which seven studies investigated bradycardia. Six studies were observational, one was a case-control, and one was a randomized trial. Incidence of bradycardia was 400/3480 patients (22.3%, 95% confidence interval, CI: [6.5-54.4], I2  = 99%) in the Remdesivir group and 294/5005 (9.8%, 95% CI: [2.8-29], I2  = 98.61) in the non-Remdesivir group. The odds ratio of bradycardia was 2.11 (95% CI: [1.65-2.71], I2  = 22%, p < 0.001) for the Remdesivir group. There was no difference in mortality between the two groups. Patients who received Remdesivir for COVID-19 were more likely to develop bradycardia. The effect of confounding factors should be considered to further clarify the possible association.

To study the effect of coronavirus disease of 2019 (COVID-19) on retinal vasculature by Optical Coherence Tomography Angiography (OCTA).

Macular OCTA images of patients recovered from COVID-19 infections were studied including foveal avascular zone (FAZ), capillary vascular densities (CVD) of the superficial and deep capillary network (SCP, DCP), and central foveal thickness (CFT).

The FAZ area was significantly larger in post COVID-19 cases compared to the healthy controls (p=0.032). Post COVID-19 cases had significant lower CVDs in perifoveal quadrants of the SCP. They also had lower CVD in the whole area, parafoveal, temporal and inferior perifoveal areas in the DCP. The parafoveal DCP area showed a positive correlation with disease duration (r=0.249, p-value=0.018). The whole SCP was significantly larger in cases with lymphopenia (p-value=0.004).

This study found asymptomatic retinal vascular affection in post COVID-19 eyes showing a relation with disease clinical and laboratory features.

Healthcare professionals consider predicting heart disease an essential task and deep learning has proven to be a promising approach for achieving this goal. This research paper introduces a novel method called the asynchronous federated deep learning approach for cardiac prediction (AFLCP), which combines a heart disease dataset and deep neural networks (DNNs) with an asynchronous learning technique. The proposed approach employs a method for asynchronously updating the parameters of DNNs and incorporates a temporally weighted aggregation technique to enhance the accuracy and convergence of the central model. To evaluate the effectiveness of the proposed AFLCP method, two datasets with various DNN architectures are tested, and the results demonstrate that the AFLCP approach outperforms the baseline method in terms of both communication cost and model accuracy.

Since 2019, the global pandemic caused by the SARS-CoV-2 virus, also known as COVID-19, has dramatically affected every aspect of health and society. With wide-ranging socio-economic ramifications and the morbidity/mortality associated with the disease, a lot of research has been done on this disease. With recent surges and new variants of the COVID-19 virus, we must have regularly updated information on this disease to effectively manage this disease and to maximize outcomes for patients. Worldwide data, so far, has suggested that children have milder or asymptomatic acute infectious phase, most often presenting with mild upper respiratory infection (URI) symptoms compared to the adult population. However, in the post-acute phase, it was observed that children presented with a syndrome that strongly resembled Kawasaki's disease (KD), and like in KD, they could potentially develop severe life-threatening complications. The significant difference between KD and this syndrome is the association with COVID-19 infection. This syndrome was observed to affect almost all organ systems including cardiovascular, gastrointestinal, and integumentary and was later named multisystem inflammatory syndrome in children (MIS-C) by the Pediatric Intensive Care Society in April 2020. The cardiovascular manifestations of this clinical entity have been associated with significant morbidity and mortality. This review is an attempt to give consolidated information from the studies done so far about the cardiac changes that occur from SARS-CoV-2 infection/MIS-C.

The coronavirus disease 2019 (COVID-19) pandemic has presented substantial challenges for providing health care due to the numerous complications on the respiratory and cardiovascular systems of people. Cardiac arrhythmia is one of the cardiac complications, and it was observed in COVID-19 patients. Moreover, arrhythmia and cardiac arrest are common in COVID-19 patients in the intensive care unit. The occurrence of cardiac arrhythmia in COVID-19 patients is associated with hypoxia, cytokine storm, myocardial ischemia and inflammatory disease such as congestive heart failure. It is necessary to know the occurrence and mechanisms of tachyarrhythmia and bradyarrhythmia in patients with COVID-19 infection for their proper management. This review provides an overview of the association between COVID-19 and arrhythmias by detailing possible pathophysiological mechanisms.

Since the Corona Virus Disease 2019 (COVID-19) pandemic, there has been increasing evidence that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is associated with acute cerebrovascular events such as cerebral infarction, cerebral hemorrhage, and cerebral venous thrombosis. Although the mechanism of cerebrovascular complications among COVID-19 patients has not been adequately elucidated, the hypercoagulable state, excessive inflammation and ACE-2-associated alterations in the renin-angiotensin-aldosterone system after SARS-CoV-2 infection probably play an essential role. In this overview, we discuss the possible mechanisms underlying the SARS-CoV-2 infection leading to acute cerebrovascular events and review the characteristics of COVID-19-related acute cerebrovascular events cases and treatment options available worldwide.