Even though nirmatrelvir-ritonavir can improve the short-term morbidity and mortality in COVID-19 patients, the effects of this treatment on long-term major adverse cardiovascular events (MACEs), especially myocardial injury, remains undetermined.

This prospective cohort study identified hospitalized adult patients with COVID-19 between April 19, 2022, and June 9, 2022, amid the omicron wave of the pandemic. Matched nirmatrelvir-ritonavir-treated and non-treated cohorts were formed using the propensity score matching method. The primary outcome of this study was the incidence of MACEs (cardiovascular death, myocardial infarction, stroke, new-onset heart failure or heart failure hospitalization or ventricular arrhythmia) from 30 days to 16 months after the diagnosis of COVID-19.

Two 949-patient cohorts with balanced baseline characteristics were formed by propensity score matching. Patients with nirmatrelvir-ritonavir, compared to those untreated, had a lower level of troponin I peak as well as the incidence of troponin I elevation. During the follow-up period, 59 patients in the nirmatrelvir-ritonavir group and 86 patients in the control group developed MACEs (P = 0.020). Regarding specific constituents of MACEs, the differences are mainly reflected in new-onset heart failure or heart failure hospitalization. COVID-19 clinical severity and troponin I peak were the independent predictors, while nirmatrelvir-ritonavir was the independent protective factor for the occurrence of MACEs in this population.

Nirmatrelvir-ritonavir was effective in reducing myocardial injury as well as long-term adverse cardiovascular outcomes among hospitalized patients with COVID-19 amid the omicron wave of the pandemic.

Middle-aged  and elderly patients with cardiovascular disease (CVD) who have recovered from SARS-CoV-2 infection may experience depressive symptoms due to the physical and psychological impact of the pandemic.

To investigate the prevalence and predictors of depressive symptoms among the middle-aged and elderly with CVD who have recovered from SARS-CoV-2 infection in Wuhan, China, and to develop a prediction model for depressive symptoms.

A cross-sectional study was conducted among 462 former SARS-CoV-2 middle-aged and elderly patients with CVD in Jianghan District, Wuhan, China from June 10 to July 25, 2021. Depressive symptoms were assessed by the Patient Health Questionnaire-9 (PHQ-9). Potential predictors of depressive symptoms were selected by the least absolute shrinkage and selection operator (LASSO) regression. A prediction model was developed by random forest (RF) and logistic regression models and compared by the area under the receiver operating characteristic curve (AUROC). The discrimination, calibration, and practical utility of the prediction model were evaluated by the receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA). Bootstrap sampling was used for internal validation.

The prevalence of depressive symptoms among the participants was 35.93%. The prediction model included age, stethalgia after recovery, insomnia after recovery, post-traumatic stress disorder (PTSD), anxiety, fatigue, and perceived social support as predictors. The AUROC of the logistic regression model was 0.909 (95%CI: 0.879 ~ 0.939), indicating good discrimination. The calibration curve showed good calibration. The DCA showed that the prediction model had a net benefit for a wide range of risk thresholds. The internal validation confirmed the stability of the prediction model.

Depressive symptoms are common among middle-aged and elderly CVD patients who have recovered from SARS-CoV-2 infection in Wuhan, China. A prediction model with satisfactory performance was developed to estimate the risk of depressive symptoms among this population. Interventions targeting long COVID symptoms and social support should be considered to prevent depressive symptoms in CVD patients.

Cardiac aging involves progressive structural, functional, cellular, and molecular changes that impair heart function. This review explores key mechanisms, including oxidative stress, mitochondrial dysfunction, impaired autophagy, and chronic low-grade inflammation. Excess reactive oxygen species (ROS) damage heart muscle cells, contributing to fibrosis and cellular aging. Mitochondrial dysfunction reduces energy production and increases oxidative stress, accelerating cardiac decline. Impaired autophagy limits the removal of damaged proteins and organelles, while inflammation activates signaling molecules that drive tissue remodeling. Gender differences reveal estrogen's protective role in premenopausal women, with men showing greater susceptibility to heart muscle dysfunction and injury. After menopause, women lose this hormonal protection, increasing their risk of cardiovascular conditions. Ethnic disparities, particularly among underserved minority populations, emphasize how social factors such as access to care, environment, and chronic stress contribute to worsening cardiovascular outcomes. The coronavirus disease pandemic has introduced further challenges by increasing the incidence of heart damage through inflammation, blood clots, and long-term heart failure, especially in older adults with existing metabolic conditions like diabetes and high blood pressure. The virus's interaction with receptors on heart and blood vessel cells, along with a weakened immune response in older adults, intensifies cardiac aging. Emerging therapies include delivery of therapeutic extracellular vesicles, immune cell modulation, and treatments targeting mitochondria. In addition, lifestyle strategies such as regular physical activity, nutritional improvements, and stress reduction remain vital to maintaining cardiac health. Understanding how these biological and social factors intersect is critical to developing targeted strategies that promote healthy aging of the heart.

Cardiovascular disease (CVD) is a leading cause of death worldwide, and infections often worsen the clinical condition of these patients. Respiratory infections, either bacterial or viral sources, are important causes of high morbidity and mortality in older adults. Beyond the burden of infection-related complications, they are also associated with non-infection-related complications such as cardiovascular (CV) events. For example, herpes zoster is associated with an increased risk of stroke and myocardial infarction. Vaccination is an effective preventive strategy for patients with CVD by reducing viral and bacterial infections, and minimizing systemic inflammatory responses to support plaque stability and reduce the likelihood of CV events in high-risk patients, thereby reducing the risks of CV and non-CV hospitalizations and mortality. Despite evidence on the effectiveness, safety, and benefits of vaccines and recommendations to vaccinate older patients and those with risk factors, vaccination rates remain sub-optimal in this population. The Taiwan Society of Cardiology and the Infectious Diseases Society of Taiwan recently appointed a task force to formulate a consensus on vaccinations for adults with high CV risk or CVD. Based on the most up-to-date information, the consensus provides current evidence-based important recommendations.

Evidence on the combined impact of air pollution and lifestyle on cardiovascular disease (CVD) risk is limited. We employed the Space-Time Extra-Trees model, an ensemble learning method for spatiotemporal data, to estimate the annual average concentrations of five air pollutants from 2017 to 2019. Cox proportional hazards models were used to assess the associations between air pollutant exposure and CVD incidence. A lifestyle score, based on body mass index, waist circumference, diet, physical activity, alcohol consumption, and smoking, was developed to examine the moderating effect of lifestyle on the air pollution-CVD relationship. Among 5,838,833 baseline participants without CVD, 414,218 developed CVD during follow-up. Long-term exposure to particulate matter (PM1, PM2.5, PM10), ozone (O3), and carbon monoxide (CO) was significantly associated with increased CVD risk. Stratified analyses revealed that exercise had the most significant impact on this association, with exercisers showing a notable reduction in risk compared to non-exercisers. An interaction between air pollution and lifestyle was observed (P-interaction < 0.001). Compared to individuals with a relatively healthy lifestyle and low air pollution exposure, those with an unhealthy lifestyle and high exposure had the highest risk of developing CVD (PM1: HR = 1.660, PM2.5: HR = 1.891, PM10: HR = 1.755, O3: HR = 1.970, CO: HR = 1.426). Further analysis revealed a synergistic additive interaction between lifestyle and air pollution, leading to relative excess risks of 0.151, 0.154, 0.137, 0.171, and 0.095 in groups with relatively unhealthy lifestyles and high exposure to PM1, PM2.5, PM10, O3, and CO, respectively. Thus, in addition to controlling major air pollutant emissions, promoting healthy lifestyle adoption is crucial.

As the COVID-19 pandemic shifted into the post-pandemic period in early 2023, following the COVID-19 normalization with relaxation of stringent control measures and high vaccination coverage in Hong Kong, its long-term impact on mortality remains challenging with necessary needs of data-driven insights. This study examined the pattern of post-pandemic excess mortality in Hong Kong.

We analyzed weekly inpatient death data from public hospitals from January 1, 2013, to June 1, 2024, using a mixed model with over-dispersed Poisson regression. Expected mortality was estimated as the difference between observed mortality and baseline derived from pre-pandemic data. Age-stratified analyses of overall and cause-specific mortality were conducted across the pre-Omicron pandemic, Omicron, and post-pandemic periods.

In the post-pandemic period, the excess mortality declined but remained six-fold higher (37.66 [95% CI: 32.72-42.60] per 100,000) than pre-Omicron level, maintaining significance after adjusting for age (32.79 [95% CI: 28.13-37.46] per 100,000). The older population experienced sustained excess mortality, with crude estimates of 100.51 and 586.74 per 100,000 among those aged 65-79 years and ≥80 years, respectively, primarily due to respiratory diseases. Younger population showed near-zero overall excess mortality, whereas increased excess mortality among them occurred in heart disease, cerebrovascular disease, and injuries.

Our findings highlight the lasting mortality impact of pandemic among vulnerable populations, specifically the older population, possibly due to the post-COVID conditions and circulating COVID-19, suggesting the need for targeted interventions for this group.

Health and Medical Research Fund.

While long coronavirus disease 2019 (COVID-19) is linked to prolonged vascular dysfunction in adults, research in children remains poor. In this study, we assessed vascular health in children infected with severe acute respiratory syndrome coronavirus 2 about 6.8 months postinfection, comparing them with healthy controls.

Two hundred twenty-three children were assessed and divided into group 1, which included children with a positive disease history and group 2, which consisted of healthy controls. Anthropometric measurements, lipid profile, biomarkers (interleukin-6, C-reactive protein, tumor necrosis factor-alpha and soluble intracellular adhesion molecule) and long COVID symptoms were assessed, along with pulse wave velocity (PWV) measurements and carotid intima-media thickness (cIMT) to evaluate aortic stiffness.

Children in group 1 were older (mean age: 10.8 ± 3.2 years vs. 8.5 ± 2.8 years, P < 0.001) and had higher body mass index (20.3 ± 5.6 kg/m2 vs. 18.4 ± 3.5 kg/m2, P < 0.001). PWV was increased in group 1 (5.02 ± 0.7 m/s vs. 4.7 ± 0.6, P < 0.001). However, vascular differences between the groups disappeared after adjusting for age, body mass index, and blood pressure. Soluble intracellular adhesion molecule-1 levels were elevated in children with a history of moderate/severe COVID-19 infection compared with controls (555.8 ± 113.2 ng/mL vs. 428 ± 42.6 ng/mL, P < 0.001). Cholesterol levels, inflammatory markers and cIMT were comparable between groups. Long COVID symptoms were reported mainly by participants of group 1 [34 (23.6%) vs. 3 (3.8%), P < 0.001].

This study demonstrates insights into the long-term effects of COVID-19 infection in children. Evidence of endothelial activation without structural arterial changes was found. Persistent inflammation postinfection was absent, yet approximately one-quarter of the participants experienced long COVID symptoms, indicating potential differences in the pathophysiology of postacute COVID-19 infection in childhood.

As age increases, the immune function of elderly individuals gradually decreases, increasing their susceptibility to infectious diseases. Therefore, further research on common viral infections in the elderly population, especially severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and influenza viruses, is crucial for scientific progress. This review delves into the genetic structure, infection mechanisms, and impact of coinfections with these two viruses and provides a detailed analysis of the reasons for the increased susceptibility of elderly individuals to dual viral infections. We evaluated the clinical manifestations in elderly individuals following coinfections, including complications in the respiratory, gastrointestinal, nervous, and cardiovascular systems. Ultimately, we have summarized the current strategies for the prevention, diagnosis, and treatment of SARS-CoV-2 and influenza coinfections in older adults. Through these studies, we aim to reduce the risk of dual infections in elderly individuals and provide a scientific basis for the prevention, diagnosis, and treatment of age-related viral diseases, thereby improving their health status.

Background/Objectives: COVID-19 is associated with various arrhythmias that continue into a post-COVID period and become a concern for patients and healthcare a long time after the infection. This study aimed to assess the incidence of arrhythmias and their relationship to presented symptoms in patients with no history of rhythm disturbances who underwent severe COVID-19 within the past 6 months. Methods: A total of 54 severe COVID-19 survivors with no history of known arrhythmia were enrolled in the study 3-6 months after discharge. All subjects underwent echocardiography, 24 h Holter monitoring, and received a handheld ECG event recorder for 14 days of ambulatory single-lead ECG recording, which was evaluated for supraventricular and ventricular arrhythmias and patient-reported events. After 12 months of follow-up (FU), Holter monitoring and ECG recordings were repeated. Results: The incidence of palpitations was high at baseline and halved after 12 months (65% vs. 36%, p = 0.018), as was the symptom-induced utilization of the event monitor (36% vs. 12%, p0.012). Palpitations were more common in patients with CAD, diabetes, and hypertension, but were not related to any rhythm disturbances except sinus tachycardia (OR of 5.8 for each 10 bpm increase in HR; CI: 1.3-26.5, p = 0.02). Holter monitoring revealed a higher burden of PVCs 3-6 months after COVID vs. FU (PVCs > 200/d in 36% vs. 17%, p < 0.05), and PVCs were more commonly recorded events in symptomatic patients. Symptomatic subjects more frequently reported sinus tachycardia (48% vs. 13%, p < 0.05) and PVC (21% vs. 0%, p < 0.05). Neither arrhythmias nor palpitations were related to the severity of the infection. Conclusions: Palpitations are common after severe COVID-19, but the symptoms are related to sinus tachycardia rather than actual arrhythmia and are more pronounced in patients with cardiovascular conditions. Ventricular ectopy was the predominant finding early after severe COVID-19 and might have been responsible for symptoms in a fraction of symptomatic subjects. Both symptoms and sinus tachycardia resolved over time.

Coronavirus infectious disease of 2019 (COVID-19) can lead to cardiac complications, yet the molecular mechanisms driving these effects remain unclear. Protein glycosylation is crucial for viral replication, immune response, and organ function and has been found to change in the lungs and liver of patients with COVID-19. However, how COVID-19 impacts cardiac protein glycosylation has not been defined. Our study combined single nuclei transcriptomics, mass spectrometry (MS)-based glycomics, and lectin-based tissue imaging to investigate alterations in N-glycosylation in the human heart post-COVID-19. We identified significant expression differences in glycogenes involved in N-glycan biosynthesis and MS analysis revealed a reduction in high mannose and isomers of paucimannose structures post-infection, with changes in paucimannose directly correlating with COVID-19 independent of comorbidities. Our observations suggest that COVID-19 primes cardiac tissues to alter the glycome at all levels, namely, metabolism, nucleotide sugar transport, and glycosyltransferase activity. Given the role of N-glycosylation in cardiac function, this study provides a basis for understanding the molecular events leading to cardiac damage post-COVID-19 and informing future therapeutic strategies to treat cardiac complications resulting from coronavirus infections.

The burden of disease measures the total impact of diseases on a population, considering incidence, prevalence, disability, and premature mortality. This study analyzes the burden of ischemic heart disease (IHD) in Tabasco, Mexico, from 2013 to 2021. Ischemic heart disease has a significant incidence of 21,203,479 cases worldwide, and nationally (inside Mexico) a total of 221,747 cases, with more than 9,137,791 deaths due to this pathology globally.

To analyze the burden of ischemic heart disease in Tabasco, Mexico, during the 2013-2021 period.

An observational, descriptive, longitudinal, and retrospective study was conducted in Tabasco. The study population consisted of 2,402,598 people according to INEGI, with a sample of 927,000 adults (462,000 men and 465,000 women). Data were used from the General Directorate of Health Information, IHME, and the World Bank. Analyses were performed in Microsoft Excel, calculating measures of central tendency, dispersion, and Disability-Adjusted Life Years (DALYs).

The DALYs in the adult population of Tabasco were: 2013-23,932; 2014-28,132; 2015-30,197; 2016-30,683; 2017-31,839; 2018-38,599; 2019-40,046; 2020-42,307; and 2021-55,723, totaling 297,576 DALYs from 2013 to 2021.

Ischemic heart disease increased in incidence and mortality in both men and women during the years analyzed. The increase in DALYs indicates a greater impact of ischemic heart disease in Tabasco compared to countries like Costa Rica.

The burden of ischemic heart disease from 2013 to 2021 represents a significant loss of quality and years of life in the population of Tabasco, Mexico.

Aortic valve aneurysm, an extremely rare complication secondary to infective endocarditis (IE), may cause heart failure due to rupture of the aneurysm. Coronavirus disease 2019 (COVID-19) has been reported to cause cardiovascular complications and alter susceptibility to secondary infections such as IE. Herein, we report a case of IE with a fatal outcome caused by rupture of an aortic valve aneurysm in a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-positive autopsy case. The patient was a 67-year-old male diagnosed with heart failure after presenting with edema and weight gain. He was found dead in bed 2 weeks after initial symptom presentation. Autopsy revealed an aneurysmal sac in the center of the noncoronary cusp of the aortic valve with an opening of approximately 1 cm in the center of the aneurysmal wall. Histologically, aortic valve vegetation, destruction of the aortic valve cusp, rupture of the aneurysmal wall, and an abscess under the aortic intima were observed. Gram staining of the aneurysmal wall showed a gram-positive coccus. The reverse transcription quantitative polymerase chain reaction assay was positive for SARS-CoV-2. Because no defined risk factors for IE other than SARS-CoV-2 infection were observed, the association between IE and COVID-19 was highly likely.

Cardiovascular diseases (CVDs) are the major contributor to global mortality and are gaining incremental attention following the COVID-19 outbreak. Epigenetic events such as DNA methylation, histone modifications, and non-coding RNAs have a significant impact on the incidence and onset of CVDs. Altered redox status is one of the major causative factors that regulate epigenetic pathways linked to CVDs. Various bioactive phytocompounds used in alternative therapies including Traditional Chinese Medicines (TCM) regulate redox balance and epigenetic phenomena linked to CVDs. Phytocompound-based medications are in the limelight for the development of cost-effective drugs with the least side effects, which will have immense therapeutic applications.

This review comprehends certain risk factors associated with CVDs and triggered by oxidative stress-driven epigenetic remodelling. Further, it critically evaluates the pharmacological efficacy of phytocompounds as inhibitors of HAT/HDAC and DNMTs as well as miRNAs regulator that lowers the incidence of CVDs, aiming for new candidates as prospective epidrugs.

PRISMA flow approach has been adopted for systematic literature review. Different Journals, computational databases, search engines such as Google Scholar, PubMed, Science Direct, Scopus, and ResearchGate were used to collect online information for literature survey. Statistical information collected from the World Health Organization (WHO) site (https://www.who.int/news-room/fact-sheets/detail/cardiovascular-diseases-(cvds)) and the American Heart Association of Heart Disease and Stroke reported the international and national status of CVDs.

The meta-analysis of various studies is elucidated in the literature, shedding light on major risk factors such as socioeconomic parameters, which contribute highly to redox imbalance, epigenetic modulations, and CVDs. Going forward, redox imbalance driven epigenetic regulations include changes in DNA methylation status, histone modifications and non-coding RNAs expression pattern which further regulates global as well as promoter modification of various transcription factors leading to the onset of CVDs. Further, the role of various bioactive compounds used in herbal medicine, including TCM for redox regulation and epigenetic modifications are discussed. Pharmacological safety doses and different phases of clinical trials of these phytocompounds are elaborated on, which shed light on the acceptance of these phytocompounds as prospective drugs.

This review suggests a strong linkage between therapeutic and preventive measures against CVDs by targeting redox imbalance-driven epigenetic reprogramming using phytocompounds as prospective epidrugs. Future in-depth research is required to evaluate the possible molecular mechanisms behind the phytocompound-mediated epigenetic reprogramming and oxidative stress management during CVD progression.

The regulation of calcium signaling within cardiomyocytes is pivotal for maintaining cardiac function, with disruptions in sarcoplasmic reticulum (SR) calcium handling linked to various heart diseases. This review explores the emerging role of microRNAs (miRNAs) in modulating SR calcium dynamics, highlighting their influence on cardiomyocyte maturation, function, and disease progression. We present a comprehensive overview of the mechanisms by which specific miRNAs, such as miR-1, miR-24, and miR-22, regulate key components of calcium handling, including ryanodine receptors, SERCA, and NCX. Notably, we identify critical research gaps, particularly the inconsistent findings regarding miRNA expression in heart disease and the need for standardized experimental conditions. Furthermore, we emphasize the potential of miRNAs as therapeutic targets, given their ability to influence calcium handling pathways and cardiac remodeling. The review also discusses the challenges in translating miRNA research into clinical applications, including the need for safe and effective delivery methods. By synthesizing current knowledge and identifying areas for future investigation, this review aims to provide insights into the therapeutic potential of miRNAs in diagnosing and treating heart diseases, ultimately contributing to improved patient outcomes.

This study aimed to assess the risk of ocular adverse events, including retinal artery occlusion (RAO), retinal vein occlusion (RVO), noninfectious uveitis (NIU), noninfectious scleritis (NIS), optic neuritis (ON), ischemic optic neuropathy (ION), and ocular motor cranial nerve palsy (OMCNP), after coronavirus disease 2019 (COVID-19) infection.

Population-based self-controlled case series (SCCS).

The study included patients from the entire Korean population of 52 million who experienced incident RAO, RVO, anterior NIU, nonanterior NIU, NIS, ON, ION, or OMCNP between January 1, 2021, and October 29, 2022.

This nationwide SCCS utilized data from the Korea National Health Insurance Service and the Korea Disease Control and Prevention Agency. The risk period after infection was defined as up to 24 weeks after COVID-19 infection. Conditional Poisson regression was used to calculate the relative incidence rate ratios (IRRs) for RAO, RVO, anterior NIU, nonanterior NIU, NIS, ON, ION, and OMCNP during the designated risk periods.

The IRRs for RAO, RVO, anterior NIU, nonanterior NIU, NIS, ON, ION, and OMCNP during the risk periods.

The study included 9336, 103 362, 201 010, 25 428, 23 744, 3026, 69 933, and 16 335 cases of incident RAO, RVO, anterior NIU, nonanterior NIU, NIS, ON, ION, and OMCNP, respectively. The IRRs (95% confidence interval) during the early risk period (1-8 weeks) were 0.94 (0.83-1.07), 1.01 (0.97-1.04), 1.00 (0.98-1.03), 0.96 (0.90-1.03), 1.00 (0.94-1.07), 0.97 (0.81-1.17), 0.97 (0.93-1.01), and 1.02 (0.94-1.11), respectively. In the late risk period (9-24 weeks), the IRRs were 1.02 (0.92-1.12), 1.01 (0.98-1.04), 1.01 (0.99-1.03), 1.02 (0.97-1.08), 1.02 (0.97-1.08), 0.99 (0.85-1.15), 1.02 (0.99-1.06), and 0.97 (0.90-1.03), respectively. Stratified analyses showed that in patients with a history of cerebro-cardiovascular disease, the risk of RAO increased during the late risk period, with an IRR (95% confidence interval) of 1.19 (1.02-1.40).

The risk of incident RVO, anterior NIU, nonanterior NIU, NIS, ON, ION, or OMCNP did not increase after COVID-19 infection. The risk of incident RAO increased only in individuals with preexisting cardio-cerebrovascular disease.

Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

Prions are considered as sub-viral protein particles that have exceptional ability for multiple structural or functional conformational changes, that any might affect the regulation of viral infections. The aim of this study is to utilize two computational platforms to predict the prion-forming potential of the spike protein (S) in Betacoronavirus, including SARS-CoV-2 clades. The abovementioned computational platforms included two algorithms; the Prion Aggregation Prediction Algorithm (PAPA) and the Supervised Machine Learning Algorithm Called Prion RANKing and Classification (pRANK) have been adopted due to their high classifier performance proteome-wide when compared with other algorithms, such as PLAAC-LLR and prionW. The findings of this study imply the propensity of some Betacorona viruses, including the Wild type of SARS-CoV-2 and some variants, specifically as Gamma and Delta, to develop prion-like sequence which can act as a regulator for viral pathogenicity or as a biochemical threat.

Since its emergence in 2019, COVID-19 has continued to pose significant threats to both the physical and mental health of the global population, as well as to healthcare systems worldwide (Raman et al., Eur Heart J 43:1157-1172, 2022). Emerging evidence indicates that COVID-19 may lead to post-acute COVID-19 syndrome (PACS) with cardiovascular implications, potentially driven by factors such as ACE2 interaction with viruses, systemic inflammation, and endothelial dysfunction. However, there remains a limited amount of research on the cardiovascular manifestations of PACS, which may delay the development of optimal treatment strategies for affected patients. Therefore, it is crucial to investigate the prevalence of cardiovascular sequelae in COVID-19 patients and to determine whether COVID-19 infection acts as an independent risk factor for these outcomes.

This meta-analysis adhered to PRISMA guidelines and was registered in PROSPERO (CRD42024524290). A systematic search of PubMed, Embase, and the Cochrane Library was conducted up to March 17, 2024. The primary outcomes included hypertension, palpitations, and chest pain, with pooled effect estimate reported as proportions and odds ratios (ORs) with 95% confidence intervals (CIs). Sensitivity and subgroup analysis were performed to assess the robustness of the results and to identify sources of heterogeneity.

A total of 37 studies, encompassing 2,965,467 patients, were included in the analysis. Pooled results from case-control studies revealed that, compared to the control group, the ORs of chest pain in the COVID-19 group was 4.0 (95% CI: 1.6, 10.0). The ORs for palpitation and hypertension were 3.4 (95% CI: 1.1, 10.2) and 1.7 (95% CI: 1.6, 1.8), respectively. The proportions of PACS patients experiencing chest pain, palpitation, and hypertension as sequelae were 22% (95% CI: 14%, 33%), 18% (95% CI: 13%, 24%), and 19% (95% CI: 12%, 31%), respectively.

Our findings indicate that 15% of COVID-19 patients experience cardiovascular sequelae. Furthermore, COVID-19 infection significantly increases the likelihood of developing these sequelae compared to uninfected individuals. Future research should prioritize investigating the underlying pathological mechanisms and developing targeted preventive and management strategies.

CRD42024524290.

COVID-19 is a highly contagious viral disease caused by SARS-CoV-2, leading to a tragic global pandemic, where it was ranked in 2020 as the third leading cause of death in the USA, causing approximately 375,000 deaths, following heart disease and cancer. The CDC reports that the risk of death increases with age and preexisting comorbidities such as such as hypertension, diabetes, respiratory system disease, and cardiovascular disease. this report will delineate and analyze the paramount comorbidities and their repercussions on individuals infected with SARS-CoV-2.

The Coronavirus Disease 2019 (COVID-19) recently emerged as a life-threatening global pandemic that has ravaged millions of lives. The affected patients are known to frequently register numerous comorbidities induced by COVID-19 such as diabetes, asthma, cardiac arrest, hypertension, and neurodegenerative diseases, to name a few. The expensiveness and probability of false negative results of conventional screening tests often delay timely diagnosis and treatment. In such cases, the deployment of a suitable biosensing platform can readily expedite the rapid diagnosis process for enhanced patient outcomes. We report the development of an electrochemical genosensor based on DNA/OGCN (DNA/oxygenated graphitic carbon nitride) nanohybrids for the quantification of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) DNA─the key biomarker for COVID-19. This is achieved by exploiting the molecular nanowire-formation capability of the [Ru(NH3)6]2+/3+ redox probe onto the DNA phosphate backbone via electrostatic interactions. The microstructural characterization of OGCN was performed using scanning electron microscopy (SEM) coupled with an energy-dispersive X-ray (EDX) module, X-ray diffraction (XRD), and Fourier transform infrared spectroscopy. The electrochemical analyses were performed using cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS), while the analytical performance of the sensor was evaluated using square wave voltammetry (SWV). The developed sensor exhibited a wide linear detection range within 10 fM-10 μM, with a limit of detection (LoD) of ∼7.23 fM with a high degree of selectivity toward SARS-CoV-2 target DNA, thereby indicating its potential to be employed in a point-of-care scenario toward providing affordable healthcare to the global populace.

This study aims at automatically quantifying and modelling the uncertainty of facts in biomedical knowledge graphs (BKGs) based on their textual supporting evidence using deep learning techniques.

A sentence transformer is employed to extract deep features of sentences used to classify sentence factuality using a naive Bayes classifier. For each fact and its supporting evidence in a source KG, the deep feature extractor and the classifier are used to quantify the factuality of each sentence which are then transformed to numerical values in [0,1] before being averaged to get the confidence score of the fact.

The fact classification feature extractor enhances the separability of classes in the embedding space. This helped the fact classification model to achieve a better performance than existing factuality classification with hand-crafted features. Uncertainty quantification and modelling were demonstrated on SemMedDB by creating USemMedDB, showing KGB2U's ability to process large BKGs. A subset of USemMedDB facts is modelled to demonstrate the correlation between the structure of the uncertain BKG and the confidence scores. The best-trained model is used to predict confidence scores of existing and unseen facts. The top-ranked unseen facts were grounded using scientific evidence showing KGB2U's ability to discover new knowledge.

Supporting literature of BKG facts can be used to automatically quantify their uncertainty. Additionally, the resulting uncertain biomedical KGs can be used for knowledge discovery. BKG2U interface and source code are available at http://biofunk.datanets.org/ and https://github.com/BahajAdil/KBG2U respectively.

COVID-19, caused by severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), is primarily a respiratory illness but significantly affects the cardiovascular system as well. After entering the body through the respiratory tract, the virus directly and indirectly disrupts the vascular system. Vascular endothelial cells (ECs), which express ACE2 and TMPRSS2, are targets for viral invasion. However, the predominant cause of widespread vascular damage is the "cytokine storm" induced by the immune response. This leads to EC activation, inflammation, neutrophil activation, and neutrophil-platelet aggregation, causing endothelial injury. Additionally, increased expression of plasminogen activator inhibitor-1 disrupts the balance between prothrombotic and fibrinolytic processes, while activation of the renin-angiotensin-aldosterone system adds oxidative stress to the vascular endothelium. In the heart, SARS-CoV-2 invades ECs, leading to apoptosis and pyroptosis, exacerbated by inflammation and elevated catecholamines. These factors contribute to arrhythmias, strokes, and myocardial infarction in severe cases of COVID-19. This narrative review aims to explore the mechanisms by which SARS-CoV-2 affects the cardiovascular system and to highlight the resulting complications. It also identifies research gaps and discusses potential therapeutic strategies to mitigate the cardiovascular impacts of COVID-19.

Post-COVID Sequelae are considered as the signs and symptoms that develop during or after an infection consistent with COVID-19 which continue for more than 12 weeks and are not explained by alternative diagnosis. The prevalence of post-COVID cardiac sequelae ranges from 2% to 71% across the globe and it is reported to be around 22% in India. With this background, the study was conducted to assess the prevalence of probable post-COVID cardiac sequelae (PCCS) and delay in health-seeking for post-COVID cardiac sequelae among healthcare workers.

A facility-based cross-sectional study was conducted among health workers and students in a medical educational institute in Karnataka from May 2022 to July 2022. Health workers and students who had a past history of COVID-19 during the COVID pandemic were included in the study. Socio-demographic details, clinical profile, symptoms of post-COVID cardiac sequelae, and health-seeking behavior were collected. Data were collected in Epicollect5 and analyzed using STATA statistical software. The prevalence of probable PCCS was expressed with 95% confidence interval. Univariate binomial logistic regression was done to assess the determinants of probable post-COVID sequelae.

A total of 336 health workers were included in the study with a mean (SD) age of 25.6 (8.6) years. A majority (68.2%) of them were females and only 25 (7.4%) belonged to the age group of 45-60 years. The prevalence of probable post-COVID cardiac sequelae among health workers and medical students was 11.9% (95% CI: 8.76-15.7). Among the 40 participants who had probable post-COVID cardiac sequelae, 55% (95% CI: 40%-70%) were not evaluated further which was their treatment-seeking behavior. Females, hypertensive individuals, and those who had moderate-severe disease during acute COVID-19 disease were at higher risk of developing probable post-COVID cardiac sequelae.

Around one out of ten individuals had experienced probable post-COVID cardiac sequelae, but only half of them got evaluated for it. An appropriate screening program for post-COVID cardiac sequelae needs to be implemented along with awareness-raising activities about long COVID to prevent the morbidity and mortality associated with it.

The COVID-19 pandemic adversely affected the severity and prognosis of patients with acute myocardial infarction (MI) caused by atherothrombosis (type 1 MI). The effect, if any, of COVID-19 vaccination and natural SARS-CoV2 serologic immunity in these patients is unclear. Our aim was to analyze the association between the severity and outcome of patients with type 1 MI and their previous SARS-CoV2 vaccination and serostatus.

A single-center retrospective cohort study conducted between March 1, 2020 and March 1, 2023. Clinical and follow-up information was collected from medical records and patients. Total antibodies (IgM, IgA, IgG) to nucleocapsid (N) antigens were measured by ECLIA (electrochemiluminescence-based immunoassay) to test the immune response to natural infection. If positive, IgM and IgG antibodies to spike (S) surface antigens were measured by CLIA to test the immune response to vaccine or natural infection. Multivariable logistic regression analysis was performed, adjusting for age, sex, hypertension, diabetes, and dyslipidemia.

Total sample of 949 patients, 656 with ST-segment elevation MI (STEMI) and 293 with non-ST-segment elevation MI (NSTEMI). Mean age was 64 (SD 13) years, 80 % men. Pre-admission vaccination status was: ≥ 1 dose, 53 % of patients; complete vaccination, 49 %; first booster dose, 25 %. The majority (84 %) of vaccines administered were mRNA-based. Six months after MI, 92 (9.7 %) patients had a major adverse cardiac event (MACE) and 50 died; 11 % of patients had severe heart failure or cardiogenic shock (Killip III-IV) after STEMI. Vaccinated patients with STEMI and positive serology (Pos/Vax group) had a higher risk of Killip III-IV on admission: OR 2.63 (1.27-5.44), p = 0.010. SARS-CoV-2 S-specific IgG titers were highest in this group (median > 2080 AU/mL, [IQR 1560- >2080] vs 91 [32-198] in the unvaccinated group). In the overall sample, a higher incidence of 6-month MACE was not demonstrated (OR 1.89 [0.98-3.61], p = 0.055).

The combination of vaccination and natural SARS-CoV2 infection was associated with the development of severe heart failure and cardiogenic shock in patients with STEMI, possibly related to an increased serological response.

Risk of cardiovascular events is increased after COVID-19. However, information on cardiovascular risk trends after COVID-19 infection is lacking and estimates by sex are inconsistent. Our aim was to examine cardiovascular outcomes and mortality in a large cohort (164,346 participants) of SARS-CoV-2 positive individuals compared to non-positive individuals, stratified by sex. Data were obtained from the Spanish Health System's electronic medical records. Selected individuals were ≥ 45 years old with/without a positive SARS-CoV-2 test in the period March-May 2020. Follow-up was obtained until January 31, 2021, for cardiovascular events (angina/myocardial infarction, arrhythmias, bypass/revascularization, heart failure, peripheral artery disease, stroke/transient ischemic attack, and thrombosis), and until March 31, 2021, for mortality. Individuals were matched by propensity score. Incidence of cardiovascular events and mortality was compared with accelerated failure time models. The effect of matching and of COVID-19 severity was assessed with sensitivity analyses. In the first 3 months of follow-up, SARS-CoV-2 positive individuals had a higher risk of mortality and of all cardiovascular events. From 4-12 months, there was increased risk of mortality in SARS-CoV-2 positive individuals overall, of heart failure in SARS-CoV-2 positive females (HR= 1.26 [1.11-1.42]), and of arrhythmias and thrombosis in SARS-CoV-2 positive males (HR= 1.29 [1.14-1.47] and HR= 1.35 [1.03-1.77], respectively). When COVID-19 patients admitted to the ICU were excluded, incidence of thrombosis was similar in males regardless of positive/non-positive SARS-CoV-2 status. In the full year of follow-up, increased incidence of heart failure and of arrhythmias and thrombosis was observed in SARS-CoV-2 positive females and males, respectively.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiologic agent of coronavirus disease 2019 (COVID-19). Severe and fatal COVID-19 cases often display cytokine storm i.e. significant elevation of pro-inflammatory cytokines and acute respiratory distress syndrome (ARDS) with systemic hypoxia. Understanding the mechanisms of these pathogenic manifestations would be essential for the prevention and especially treatment of COVID-19 patients. Here, using a dual luciferase reporter assay for hypoxia-response element (HRE), we initially identified SARS-CoV-2 nonstructural protein 5 (NSP5), NSP16, and open reading frame 3a (ORF3a) to upregulate hypoxia-inducible factor-1α (HIF-1α) signaling. Further experiments showed NSP16 to have the most prominent effect on HIF-1α, thus contributing to the induction of COVID-19 associated pro-inflammatory response. We demonstrate that NSP16 interrupts von Hippel-Lindau (VHL) protein interaction with HIF-1α, thereby inhibiting ubiquitin-dependent degradation of HIF-1α and allowing it to bind HRE region in the IL-6 promoter region. Taken together, the findings imply that SARS-CoV-2 NSP16 induces HIF-1α expression, which in turn exacerbates the production of IL-6.

Although the end of COVID-19 as a public health emergency was declared on May 2023, still new cases of the infection are reported and the risk remains of new variants emerging that may cause new surges in cases and deaths. While clinical symptoms have been rapidly defined worldwide, the basic body responses and pathogenetic mechanisms acting in patients with SARS-CoV-2 infection over time until recovery or death require further investigation. The understanding of the molecular mechanisms underlying the development and course of the disease is essential in designing effective preventive and therapeutic approaches, and ultimately reducing mortality and disease spreading.

The current investigation aimed to identify the key genes engaged in SARS-CoV-2 infection. To achieve this goal high-throughput RNA sequencing of peripheral blood samples collected from healthy donors and COVID-19 patients was performed. The resulting sequence data were processed using a wide range of bioinformatics tools to obtain detailed modifications within five transcriptomic phenomena: expression of genes and long non-coding RNAs, alternative splicing, allel-specific expression and circRNA production. The in silico procedure was completed with a functional analysis of the identified alterations.

The transcriptomic analysis revealed that SARS-CoV-2 has a significant impact on multiple genes encoding ribosomal proteins (RPs). Results show that these genes differ not only in terms of expression but also manifest biases in alternative splicing and ASE ratios. The integrated functional analysis exposed that RPs mostly affected pathways and processes related to infection-COVID-19 and NOD-like receptor signaling pathway, SARS-CoV-2-host interactions and response to the virus. Furthermore, our results linked the multiple intronic ASE variants and exonic circular RNA differentiations with SARS-CoV-2 infection, suggesting that these molecular events play a crucial role in mRNA maturation and transcription during COVID-19 disease.

By elucidating the genetic mechanisms induced by the virus, the current research provides significant information that can be employed to create new targeted therapeutic strategies for future research and treatment related to COVID-19. Moreover, the findings highlight potentially promising therapeutic biomarkers for early risk assessment of critically ill patients.

Although the novel coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), primarily manifests as severe respiratory distress, its impact on the cardiovascular system is also notable. Studies reveal that COVID-19 patients often suffer from certain vascular diseases, partly attributed to increased proliferation or altered phenotype of vascular smooth muscle cells (VSMCs). Although the association between COVID-19 and VSMCs is recognized, the precise mechanism underlying SARS-CoV-2's influence on VSMC phenotype remains largely under-reviewed. In this context, while there is a consistent body of literature dissecting the effect of COVID-19 on the cardiovascular system, few reports delve into the potential role of VSMC switching in the pathophysiology associated with COVID-19 and the molecular mechanisms involved therein. This review dissects and critiques the link between COVID-19 and VSMCs, with particular attention to pathways involving cholesterol, calcium, and phosphate. These pathways underpin the interaction between the virus and VSMCs. Such interaction promotes VSMC proliferation, and eventually potentiates vascular calcification as well as worsens prognosis in patients with COVID-19.

To evaluate common endocrine responses of the patients hospitalized with COVID 19 Infection at Hayatabad Medical Complex Peshawar.

This was a prospective cross sectional study which included 66 patients having age 18 years and above with positive COVID 19 PCR, who were reported in COVID OPD for hospitalization in Isolation Units and Intensive Care Unit of Hayatabad Medical Complex Peshawar between June 15, 2020 to December 15, 2020. Patients with preexisting kidney or liver disease, those who had used steroids before enrollment and pregnant and lactating females were excluded. Patients were clinically assessed, and investigations were performed which included C- reactive protein (CRP), complete blood count (CBC), Covid PCR, thyroid function tests (TFTs), and cortisol levels.

The mean age of the study participants was 54.38±15.81 years. At baseline, 75%, 17%, and 3% patients had mild, moderate, and severe COVID-19, respectively. Thyroid Stimulating Hormones (TSH) levels were suppressed in 25% of patients, more significant in those with more severe infection. Raised cortisol levels were found in 94% of patients at admission without any prior use of steroids. As per clinical outcome is concerned, mortality occurred in 20% of patients while 80% recovered healthy.

The findings of the results suggest an appropriate response of endocrine system to covid infection. The amount of cortisol and TSH changes were also associated with the severity of sickness.

Viral myocarditis is associated with the development of dilated cardiomyopathy (DCM), left ventricular dysfunction, and heart failure. This review addresses the mechanisms of viral myocarditis and its treatment.

Heart failure (HF) affects 64 million people worldwide and is one of the most prevalent causes of hospitalization in adults. Infection is believed to be one of the potential triggers that may facilitate HF decompensation and the need for hospitalization. Therefore, it seems crucial to safeguard against such a situation. Vaccinations seem to be a very reasonable option. However, this remains an underutilized solution among HF patients. This review investigates the impact of available vaccinations, including influenza, COVID-19, pneumococcal, and RSV, on prognosis in specific HF populations only, as there are pathophysiological reasons to believe that this population of patients may benefit the most from the intervention. It will provide information about the safety profile of these vaccines and summarize the available evidence on their impact on hard clinical outcomes. In summary, this article will discuss the impact of preventive vaccinations against seasonal infections in the HF population.

COVID-19 is associated with acute risk of major adverse cardiac events (MACE), including myocardial infarction, stroke, and mortality (all-cause). However, the duration and underlying determinants of heightened risk of cardiovascular disease and MACE post-COVID-19 are not known.

Data from the UK Biobank was used to identify COVID-19 cases (n=10 005) who were positive for polymerase chain reaction (PCR+)-based tests for SARS-CoV-2 infection (n=8062) or received hospital-based International Classification of Diseases version-10 (ICD-10) codes for COVID-19 (n=1943) between February 1, 2020 and December 31, 2020. Population controls (n=217 730) and propensity score-matched controls (n=38 860) were also drawn from the UK Biobank during the same period. Proportional hazard models were used to evaluate COVID-19 for association with long-term (>1000 days) risk of MACE and as a coronary artery disease risk equivalent. Additional analyses examined whether COVID-19 interacted with genetic determinants to affect the risk of MACE and its components.

The risk of MACE was elevated in COVID-19 cases at all levels of severity (HR, 2.09 [95% CI, 1.94-2.25]; P<0.0005) and to a greater extent in cases hospitalized for COVID-19 (HR, 3.85 [95% CI, 3.51-4.24]; P<0.0005). Hospitalization for COVID-19 represented a coronary artery disease risk equivalent since incident MACE risk among cases without history of cardiovascular disease was even higher than that observed in patients with cardiovascular disease without COVID-19 (HR, 1.21 [95% CI, 1.08-1.37]; P<0.005). A significant genetic interaction was observed between the ABO locus and hospitalization for COVID-19 (Pinteraction=0.01), with risk of thrombotic events being increased in subjects with non-O blood types (HR, 1.65 [95% CI, 1.29-2.09]; P=4.8×10-5) to a greater extent than subjects with blood type O (HR, 0.96 [95% CI, 0.66-1.39]; P=0.82).

Hospitalization for COVID-19 represents a coronary artery disease risk equivalent, with post-acute myocardial infarction and stroke risk particularly heightened in non-O blood types. These results may have important clinical implications and represent, to our knowledge, one of the first examples of a gene-pathogen exposure interaction for thrombotic events.

Factors associated with cardiovascular complications of COVID-19 remain understudied.

Here we investigate the occurrence and risk factors of arrythmias, myocardial infarction and/or stroke, and thromboembolism in the course of COVID-19.

We have performed an observational study with prospectively designed data collection. Data of patients diagnosed with COVID-19 who were admitted from March 6th 2020 to November 30th 2021 in our Hospital were analyzed. Logistic regression was used to identify variables associated with the odds of early hospital death due to COVID-19.

Fourteen-point three percent of 1964 patients had cardiovascular complications, 6.36 % arrhythmias, 5.5 % thromboembolic events and 2.39 % myocardial infarction and/or stroke. Factors independently increasing the odds of arrhythmia were older age (OR=1.49 [95 % CI: 1.17-1.92], p = 0.02), longer time between admission and the first onset of symptoms (1.02 [0.99-1.05], p = 0.049), concomitant atrial fibrillation/flutter (2.84 [1.37-5.70], p = 0.004), nicotinism (2.49 [1.37-4.49], p = 0.002), and eGFR<60 ml/min/1.73m2 (2.44 [1.08-5.59], p = 0.033). Factors independently increasing the odds of myocardial infarction and/or stroke were dementia (4.55 [0.97-19.3], p = 0.044), hemiplegia (12.67 [3.12-46.1], p < 0.001), nicotinism (3.36 [1.30-10.4], p = 0.013) and higher C-reactive protein concentration (1.01 [1.00-1.01], p = 0.040). Factors independently increasing the odds of thromboembolic events were longer hospitalization (1.08 [1.05-1.10], p < 0.001) and higher d-dimers (1.04 [1.02-1.05], <0.001).

The risk of cardiovascular complications was especially pronounced in patients with older age, pre-existing cardiovascular disease and more sever pneumonia at presentation to care. This underlines the importance of close and careful clinical follow-up in the course of COVID-19 for specific patients' populations, including a pro-active approach in diagnosis.

This study investigated the long-term cardiovascular effects of coronavirus disease (COVID-19) in elite male athletes by comparing the heart rate variability (HRV), arterial stiffness, and other cardiovascular parameters between those with and without prior COVID-19 infection. Methods: This cross-sectional study evaluated 120 elite male athletes (60 post COVID-19, 60 controls) using anthropometric measurements, body composition analysis, pulmonary function tests, HRV analysis, arterial stiffness assessments, hemodynamic monitoring, and microcirculatory function tests. Results: Athletes post COVID-19 showed significantly higher lean mass (p = 0.007), forced vital capacity (p = 0.001), and forced expiratory volume in 1 s (p = 0.007) than controls. HRV parameters did not significantly differ between the groups. Post-COVID-19 athletes exhibited peripheral vascular resistance (p = 0.048) and reflection index (p = 0.038). No significant differences were observed in the blood pressure, cardiac output, oxygen saturation, or microcirculatory oxygen absorption. Conclusions: Elite male athletes showed notable cardiovascular resilience after COVID-19, with only minor differences in vascular function. The maintained cardiac autonomic function and improved lung parameters in post-COVID-19 athletes suggests an adaptive response. These findings support the cardiovascular health of elite athletes following COVID-19 but emphasize the importance of continued monitoring.

Previous research highlighted variability in electrocardiogram (ECG) readings across patient positions, particularly in the context of COVID-19 patients with pulmonary complications requiring prone positioning as part of the treatment.

This study aimed to elucidate the effects of prone positioning on ECG parameters and explore its association with the severity of COVID-19.

A prospective cohort study involved 60 patients diagnosed with COVID-19 and presenting pulmonary complications. ECGs were recorded in both supine and prone positions, and analyzed for various parameters including heart rate, QRS axis, and QTc interval. Clinical severity was assessed using APACHE II scores and SpO2/FiO2 ratios.

Prone positioning led to an increase in heart rate (mean difference: 2.100, 95% CI: 0.471-3.729, p = 0.012), with minor shifts in the QRS axis. Heart rate and QRS axis demonstrated strong positive correlations between positions, with Pearson's correlation coefficients of 0.927 and 0.894, respectively. The study also found a significant association between prolonged QTc intervals in the prone position and elevated APACHE II scores, with a relative risk of 10.75 (95% CI: 1.82-63.64, p = 0.008).

The prone positioning caused minor yet significant changes in heart rate and QRS axis. The correlation of prolonged QTc intervals in the prone position with higher APACHE II scores suggests the prognostic relevance of prone ECG in COVID-19 patients. However, further research is needed to fully understand the clinical implications and mechanisms of these findings.

This study seeks to evaluate how recent COVID-19 infection affects myocardial perfusion and functional parameters derived from gated myocardial perfusion imaging in patients undergoing evaluation for coronary artery disease. The goal is to enhance our understanding of COVID-19's influence on the cardiovascular system.

Conducted at Farshchian Heart Hospital from 2022 to 2023, this case-control study enrolled patients suspected of coronary artery disease, stratified into two groups: those with confirmed COVID-19 infection within the past 6 months (study group) and those without prior COVID-19 infection (control group). Employing a 2-day protocol, stress testing and gated SPECT MPI were performed. Statistical analysis included descriptive statistics, Chi-square test, Student's t test, and Mann-Whitney U test.

Among the 86 patients included, 43 were in each group. Significantly higher summed stress core and summed difference score values were observed in the study group compared to the control group (p < 0.05). In addition, the study group exhibited significantly altered global left ventricular ejection fraction, end-diastolic volume, and end-systolic volume (p < 0.05). Non-perfusion findings, including transient ischemic dilation and transient right ventricular visualization, were more prevalent in the study group.

Recent COVID-19 infection is associated with impaired myocardial perfusion and altered functional parameters as detected by MPI. These findings underscore the intricate interplay between COVID-19 and cardiovascular health, emphasizing the importance of comprehensive evaluation and management strategies to address cardiac complications in affected individuals. Further research is warranted to elucidate the underlying mechanisms and optimize patient care in the context of COVID-19-associated cardiovascular manifestations.

The coronavirus disease 2019 (COVID-19) was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which led to a huge mortality rate and imposed significant costs on the health system, causing severe damage to the cells of different organs such as the heart. However, the exact details and mechanisms behind this damage are not clarified. Therefore, we aimed to identify the cell and molecular mechanism behind the heart damage caused by SARS-Cov-2 infection.

RNA-seq data for COVID-19 patients' hearts was analyzed to obtain differentially expressed genes (DEGs) and differentially expressed ferroptosis-related genes (DEFRGs). Then, DEFRGs were used for analyzing GO and KEGG enrichment, and perdition of metabolites and drugs. we also constructed a PPI network and identified hub genes and functional modules for the DEFRGs. Subsequently, the hub genes were validated using two independent RNA-seq datasets. Finally, the miRNA-gene interaction networks were predicted in addition to a miRNA-TF co-regulatory network, and important miRNAs and transcription factors (TFs) were highlighted.

We found ferroptosis transcriptomic alterations within the hearts of COVID-19 patients. The enrichment analyses suggested the involvement of DEFRGs in the citrate cycle pathway, ferroptosis, carbon metabolism, amino acid biosynthesis, and response to oxidative stress. IL6, CDH1, AR, EGR1, SIRT3, GPT2, VDR, PCK2, VDR, and MUC1 were identified as the ferroptosis-related hub genes. The important miRNAs and TFs were miR-124-3P, miR-26b-5p, miR-183-5p, miR-34a-5p and miR-155-5p; EGR1, AR, IL6, HNF4A, SRC, EZH2, PPARA, and VDR.

These results provide a useful context and a cellular snapshot of how ferroptosis affects cardiomyocytes (CMs) in COVID-19 patients' hearts. Besides, suppressing ferroptosis seems to be a beneficial therapeutic approach to mitigate heart damage in COVID-19.

Little is known about post-hospital health care resource use (HRU) of patients admitted for severe COVID-19, specifically for the care of patients with postacute COVID-19 syndrome (PACS).

A list of HRU domains and items potentially related to PACS was defined, and potential PACS-related HRU (PPRH) was compared between the pre- and post-COVID-19 periods, to identify new outpatient care likely related to PACS.

A retrospective cohort study was conducted with the French National Health System claims data (SNDS). All patients hospitalized for COVID-19 between February 1, 2020, and June 30, 2020 were described and investigated for 6 months, using discharge date as index date. Patients who died during index stay or within 30 days after discharge were excluded. PPRH was assessed over the 5 months from day 31 after index date to end of follow-up, that is, for the post-COVID-19 period. For each patient, a pre-COVID-19 period was defined that covered the same calendar time in 2019, and pre-COVID-19 PPRH was assessed. Post- or pre- ratios (PP ratios) of the percentage of users were computed with their 95% CIs, and PP ratios>1.2 were considered as "major HRU change."

The final study population included 68,822 patients (median age 64.8 years, 47% women, median follow-up duration 179.3 days). Altogether, 23% of the patients admitted due to severe COVID-19 died during the hospital stay or within the 6 months following discharge. A total of 8 HRU domains were selected to study PPRH: medical visits, technical procedures, dispensed medications, biological analyses, oxygen therapy, rehabilitation, rehospitalizations, and nurse visits. PPRs showed novel outpatient care in all domains and in most items, without specificity, with the highest ratios observed for the care of thoracic conditions.

Patients hospitalized for severe COVID-19 during the initial pandemic wave had high morbi-mortality. The analysis of HRU domains and items most likely to be related to PACS showed that new care was commonly initiated after discharge but with no specificity, potentially suggesting that any impact of PACS was part of the overall high HRU of this population after hospital discharge. These purely descriptive results need to be completed with methods for controlling for confusion bias through subgroup analyses.

ClinicalTrials.gov NCT05073328; https://clinicaltrials.gov/ct2/show/NCT05073328.

The acute phase of severe acute respiratory syndrome coronavirus 2 [coronavirus disease (COVID)] infection has many well-documented cardiovascular manifestations, however, the long-term sequelae are less understood. In this focused review, we explore the risk factors, character, and rates of cardiovascular events in patients with Long COVID, which is defined as symptoms occurring more than 4 weeks following initial infection. Research has identified increased rates of cerebrovascular disease, dysrhythmias, ischemic and inflammatory heart disease, cardiopulmonary symptoms, and thrombotic events among those with Long COVID, though the risk rates and potential mechanisms behind each cardiovascular event vary. Finally, we discuss the current gaps in the literature as well as how COVID compares to other viral infections when it comes to causing long-term cardiovascular sequelae.