ObjectiveThe coronavirus disease 2019 (COVID-19) pandemic illustrated the relationship between cardiac arrhythmias and pro-inflammatory states. Pro-inflammatory cytokines, including interleukin-6 (IL-6), have significant effects on cardiac conduction. Atrial or ventricular arrhythmias occurring while infected results in a doubling of mortality. Tocilizumab, a monoclonal antibody that blocks the IL-6 receptor, is associated with improved mortality and is believed to be related to immune modulation of the COVID-19-related hyperinflammatory state.MethodsA single-center retrospective review of all patients with severe COVID-19, defined as admission to an intensive care unit or requirement of respiratory or circulatory support, from March 2020 through March 2022, was conducted. Patients who received or did not receive tocilizumab were grouped into the treatment and control groups, respectively.ResultsFour hundred seventy-three patients were reviewed and 400 met the criteria for inclusion in our study. There were 305 patients (age, 63 ± 13 years, 58% male) in the control group and 95 (age, 57 ± 15 years, 51% male) in the treatment group. In-hospital mortality was greatly reduced with tocilizumab compared with controls (44.2% vs 85.9%, p < 0.001) and new-onset atrial fibrillation (AF) showed a statistically significant reduction (17.8% vs 29.5%, p = 0.019). New-onset wall motion abnormalities, potentially related to myocarditis or acute coronary syndrome, also trended toward significance with tocilizumab (7.7% vs 15.7%, p = 0.10). Deep vein thrombosis, pulmonary embolism, stroke, and sustained ventricular arrhythmias did not meet statistical significance.ConclusionAs expected, tocilizumab did show significant improvement in mortality. Tocilizumab also showed a significant reduction of new-onset AF. Other cardiac structural endpoints did not reach statistical significance.Abstract PresentationsA preliminary version of this research was presented during a regional conference at the Mid-Atlantic Capital Cardiology Symposium (MACCS) on 19 November 2023.

Background and Objectives: Bulgaria had the highest mortality rate of COVID-19 in Europe and the second highest in the world based on statistical data. This study aimed to determine the mortality predictors in 306 adult patients with COVID-19 infection, treated at the COVID-19 Ward of St. George University Hospital in Plovdiv, Bulgaria in the period of August 2021-April 2022. Materials and Methods: All admitted and treated patients had a positive PCR test for SARS-CoV-2. They were assigned in three groups based on the severity rating scale published in NIH COVID-19 Treatment Guidelines by Stat Pearls Publishing, 2022. Demographic, clinical, and laboratory parameters and pre-existing comorbidities were investigated. Parametric and non-parametric methods were used for statistics. Logistic regression was applied for parameters significantly associated with mortality. Results: Data showed that demographic indicators were not significantly associated with poorer outcome. Among comorbidities, cardiovascular, chronic pulmonary and endocrine disorders were found to be related to poor survival rates (p = 0.003, p = 0.003 and p = 0.017 resp.) Clinical symptoms, such as sore throat, dry or productive cough and breathlessness, were determinants of poor outcome (p = 0.027, p = 0.029, p = 0.004 and p = 0.002 resp.). Laboratory parameters linked to mortality were elevated d-dimers (p = 0.015), ferritin (p = 0.009) and creatinine (p = 0.038). p02 < 50 and saturation < 90 also indicated a higher risk of death (p = 0.006 and p = 0021). Conclusions: Logistic regression showed that each stage of disease severity increased the risk of death 3.6 times, chronic pulmonary disorders increased it by 4.1, endocrine by 2.4 and dyspnea by 3.1 times.

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 coronavirus disease 2019 (COVID-19) pandemic has significantly worsened the health and quality of life of vulnerable populations, particularly elderly patients with heart failure. This study aimed to assess the effect of COVID-19 infection on the quality of life in elderly patients with heart failure during the pandemic.

This retrospective case-control study included elderly heart failure patients admitted to the Second People's Hospital of Lanzhou between December 2022 and December 2023, all of whom were diagnosed during the ongoing COVID-19 pandemic. All patients underwent COVID-19 nucleic acid testing upon admission. Among the 96 heart failure patients who tested positive for COVID-19 and the 68 who tested negative, multiple validated instruments were used to assess both physical and mental health quality of life. These instruments included the Minnesota Living with Heart Failure Questionnaire (MLHFQ), 36-Item Short Form Health Survey physical component summary score (SF-36 PCS), 6-Minute Walking Test (6MWT), Geriatric Depression Scale-15 (GDS-15), Self-Rating Anxiety Scale (SAS) Total, Pittsburgh Sleep Quality Index (PSQI), Mini Nutritional Assessment-Short Form (MNA-SF), and the Fatigue, Resistance, Ambulation, Illness, and Loss of weight (FRAIL) Scale.

Heart failure patients who tested positive for COVID-19 exhibited significantly lower blood pressure, SF-36 scores, and 6MWT distances compared to those who tested negative (P<0.05). Additionally, the COVID-19-positive group had higher MLHFQ scores, older average age, a greater proportion of patients in NYHA class III-IV, more frequent electrolyte imbalances, elevated D-dimer, C-reactive protein (CRP), and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels, and longer hospital stays (P<0.05). These patients also exhibited higher levels of anxiety (SAS total), poorer sleep quality (PSQI), and greater frailty (FRAIL Scale) compared to their COVID-19-negative counterparts (P<0.05). In addition, heart failure patients with COVID-19 infection reported more severe symptoms of dyspnea and fatigue (P<0.05). Both age and COVID-19 infection were identified as significant factors negatively affecting the quality of life in this patient population.

COVID-19 infection significantly exacerbates the decline in quality of life in elderly patients with heart failure. This highlights the urgent need for strengthened, comprehensive treatment and targeted mental health support for this vulnerable group.

There had been concerns about the acute complications during or shortly after coronavirus disease 2019 (COVID-19) treatment with nirmatrelvir/ritonavir (NMVr) and molnupiravir (MOL). This study aimed to compare the risks of selected acute safety events in patients treated with or without NMVr or MOL using the COVID-19 oral treatment safety assessment data, constructed through the linkage of nationwide databases: National COVID-19 registry, Real-time Prescription Surveillance, and National Health Insurance data. We identified all adults diagnosed with COVID-19 between January and November 2022, and then constructed two cohorts by matching up to four patients without antiviral treatment records to NMVr or MOL users using propensity score matching. Outcomes of interest were incident-selected cardiac (i.e., atrial fibrillation, other arrhythmia, bradycardia), neurological (i.e., seizure, neuropathy, encephalomyelitis), and miscellaneous (i.e., acute pancreatitis, acute liver injury, dysgeusia) events. A total of 739,935 NMVr users were matched with 2,951,690 comparators and 150,431 MOL users with 759,521 comparators. NMVr users were at lower risk for developing selected cardiac events (hazard ratio 0.74 [95% CI 0.65-0.87] for atrial fibrillation, 0.81 [0.65-0.99] for other arrhythmia, and 0.82 [0.70-0.96] for bradycardia) and dysgeusia (0.58 [0.45-0.74]). For MOL users, the risk was lower for atrial fibrillation (0.72 [0.53-0.96]) and dysgeusia (0.34 [0.18-0.65]). Overall, there were no increased risks of acute complications during and shortly after treatment with oral COVID-19 antivirals. Rather, the findings underscore their effectiveness in attenuating the risk of potential acute sequelae of COVID-19.

Cardiovascular disease (CVD) is the leading cause of morbidity globally, with chronic inflammation as a key modifiable risk factor. Toll-like receptors (TLRs), pivotal components of the innate immune system, including TLR-3, -7, -8, and -9 within endosomes, trigger intracellular cascades, leading to inflammatory cytokine production by various cell types, contributing to systemic inflammation and atherosclerosis. Recent research highlights the role of endosomal TLRs in recognizing self-derived nucleic acids during sterile inflammation, implicated in autoimmune conditions like myocarditis.

This review explores the impact of endosomal TLRs on viral infections, autoimmunity, and inflammatory responses, shedding light on their intricate involvement in cardiovascular health and disease by examining literature on TLR-mediated mechanisms and their roles in CVD pathophysiology.

Removal of endosomal TLRs mitigates myocardial damage and immune reactions, applicable in myocardial injury. Targeting TLRs with agonists enhances innate immunity against fatal viruses, lowering viral loads and mortality. Prophylactic TLR agonist administration upregulates TLRs, protecting against fatal viruses and improving survival. TLRs play a complex role in CVDs like atherosclerosis and myocarditis, with therapeutic potential in modulating TLR reactions for cardiovascular health.

Minerals are essential nutrients that play critical roles in human health by regulating various physiological functions. Examples include bone development, enzyme function, nerve signaling, and the immune response. Both the deficiencies and toxicities of minerals can have significant health implications. Deficiencies in macrominerals such as calcium, magnesium, and phosphate can lead to osteoporosis (associated with falls and fractures), cardiovascular events, and neuromuscular dysfunction. Trace mineral deficiencies, such as iron and zinc. Selenium deficiency impairs oxygen transport, immune function, and antioxidant defenses, contributing to anemia, delaying wound healing, and increasing susceptibility to infectious diseases. Conversely, excessive intake of minerals can have severe health consequences. Hypercalcemia can cause kidney stones and cardiac arrhythmias as well as soft-tissue calcification, whereas excessive iron deposition can lead to oxidative stress and organ/tissue damage. Maintaining adequate mineral levels through a balanced diet, guided supplementation, and monitoring at-risk populations is essential for good health and preventing disorders related to deficiencies and toxicities. Public health interventions and education about dietary sources of minerals are critical for minimizing health risks and ensuring optimal well-being across populations. While a comprehensive analysis of all macro and micronutrients is beyond the scope of this article, we have chosen to focus on calcium, magnesium, and phosphate. We summarize the consequences of deficiency and the adverse events associated with the overconsumption of other minerals.

There are limited national data on the trends and outcomes of patients hospitalized with acute myocardial infarction (AMI) during the coronavirus disease 2019 (COVID-19) pandemic. We aimed to evaluate the impact of early COVID-19 pandemic on the trends and outcomes of AMI using the National Inpatient Sample (NIS) database.

The NIS database was queried from January 2019 to December 2020 to identify adult (age ≥18 years) AMI hospitalizations and were categorized into ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) based on International Classification of Diseases, Tenth Revision, Clinical Modification codes. In addition, the in-hospital mortality, revascularization, and resource utilization of AMI hospitalizations early in the COVID-19 pandemic (2020) were compared to those in the pre-pandemic period (2019) using multivariate logistic and linear regression analysis.

Amongst 1,709,480 AMI hospitalizations, 209,450 STEMI and 677,355 NSTEMI occurred in 2019 while 196,230 STEMI and 626,445 NSTEMI hospitalizations occurred in 2020. Compared with those in 2019, the AMI hospitalizations in 2020 had higher odds of in-hospital mortality (adjusted odds ratio [aOR], 1.27; 95% confidence interval [CI], [1.23-1.32]; p<0.01) and lower odds of percutaneous coronary intervention (aOR, 0.95 [0.92-0.99]; p=0.02), and coronary artery bypass graft (aOR, 0.90 [0.85-0.97]; p<0.01).

We found a significant decline in AMI hospitalizations and use of revascularization, with higher in-hospital mortality, during the early COVID-19 pandemic period (2020) compared with the pre-pandemic period (2019). Further research into the factors associated with increased mortality could help with preparedness in future pandemics.

Recent studies have suggested an increased incidence of myocarditis and pericarditis following mRNA vaccination or COVID-19. However, the potential interaction effect between vaccine type and COVID-19 on heart disease risk remains uncertain. Our study aimed to examine the impact of COVID-19 status and vaccine type following the first dose on acute heart disease in the Korean population, using data from the National Health Insurance Service COVID-19 database (October 2018-March 2022). We sought to provide insights for public health policies and clinical decisions pertaining to COVID-19 vaccination strategies. We analysed heart disease risk, including acute cardiac injury, acute myocarditis, acute pericarditis, cardiac arrest, and cardiac arrhythmia, in relation to vaccine type and COVID-19 within 21 days after the first vaccination date, employing Cox proportional hazards models with time-varying covariates. This study included 3,350,855 participants. The results revealed higher heart disease risk in individuals receiving mRNA vaccines than other types (adjusted HR, 1.48; 95% CI, 1.35-1.62). Individuals infected by SARS-CoV-2 also exhibited significantly higher heart disease risk than those uninfected (adjusted HR, 3.56; 95% CI, 1.15-11.04). We found no significant interaction effect between vaccine type and COVID-19 status on the risk of acute heart disease. Notably, however, younger individuals who received mRNA vaccines had a higher heart disease risk compared to older individuals. These results may suggest the need to consider alternative vaccine options for the younger population. Further research is needed to understand underlying mechanisms and guide vaccination strategies effectively.

It has been demonstrated that an increase in the diameter of the right ventricle or pulmonary artery in COVID-19 patients could be associated with the severity of lung involvement and may lead to unfavorable outcomes, particularly in the presence of pulmonary vascular diseases. This study investigated the relationship between these right heart strain features, the extent of lung involvement, and their prognostic values in patients without vascular comorbidities.

This study selected 154 consecutive patients with positive chest computed tomography (CT) findings and no evidence of concurrent pulmonary disease. Clinical characteristics and adverse outcomes in in-hospital settings were collected retrospectively. Diameters of cardiac ventricles and arteries, along with lung opacification scores, were obtained using CT pulmonary angiography (CTPA) findings, and the association of these variables was evaluated.

An increase in pulmonary artery (PA) to ascending aorta (AO) diameter ratio and lung parenchymal damage were significantly and positively correlated (P=0.017), but increased right ventricle (RV) to left ventricle (LV) diameter ratio showed no association with the extent of chest opacification (P=0.098). Evaluating the prognostic ability of both ratios using logistic regression and receiver operating characteristic (ROC) analysis proved no significant class separation in regards to predicting adverse outcomes (PA/AO: OR:1.081, P Value:0.638, RV/LV: OR:1.098, P Value:0.344).

In COVID-19 patients without vascular comorbidities, a higher PA/AO diameter ratio was significantly associated with increased lung involvement severity on CT imaging but not with adverse in-hospital outcomes. Conversely, an increased RV/LV ratio on CTPA did not correlate significantly with adverse outcomes or the severity of parenchymal lung damage.

In the post-COVID-19 era, there is growing concern regarding its impact on cardiovascular health and the following effects on the overall quality of life of affected individuals. This research seeks to investigate cardiac magnetic resonance (CMR) findings following COVID-19 and their impact on the quality of life of affected individuals.

An observational, cross-sectional study was conducted in consecutive patients with persistent cardiovascular symptoms after COVID-19 who were referred to CMR due to suspected myocardial injury. In addition, patients completed a questionnaire about symptoms and the quality of life during the post-COVID-19 period.

In this study, 85 patients were included. The study population consisted of patients with a mean age of 42.5 ± 13.4 years, predominantly women, who made up 69.4% of the study population, while men made up 30.6%. CMR findings showed non-ischemic myocardial injury in 78.8% of patients and myocardial edema in 14.1% of patients. Late pericardial enhancement was present in 40% of patients and pericardial effusion in 51.8% of patients. Pericardial effusion (p = 0.001) was more prevalent in patients who reported more pronounced symptoms in the post-COVID-19 period compared to the acute infection phase. Predictors of lower quality of life in the post-COVID-19 period were the presence of irregular heartbeat (p = 0.039), cardiovascular problems that last longer than 12 weeks (p = 0.018), and the presence of pericardial effusion (p = 0.037).

Acute myocarditis was observed in a minority of patients after COVID-19, while non-ischemic LGE pattern and pericardial effusion were observed in the majority. Quality of life was worse during the post-COVID-19 period in patients with CMR abnormalities, primarily in patients with pericardial effusion. Also, irregular heartbeat, cardiovascular symptoms that last longer than 12 weeks, as well as pericardial effusion were independent predictors of lower quality of life during the post-COVID-19 period.

Cardiovascular disease (CVD) and cardiometabolic risk (CMR) are highly prevalent globally. The interplay between CVD/CMR and COVID-19 morbidity and mortality has been intensely studied over the last three years and has yielded some important discoveries and warnings for public health. Despite many advances in cardiovascular medicine, CVD continues to be the global leading cause of death. Much of this disease burden results from high CMR imposed by behaviors centered around poor nutrition related to lifestyle choices and systemic constraints. Increased CVD/CMR contributed to the COVID-19 pandemic's unprecedented wave of disability and death, and the current state of cardiovascular health been equated to a "Population Code Blue." There is an urgent and unmet need to reorient our priorities towards health promotion and disease prevention. This manuscript will review how nutrition and lifestyle affect outcomes in COVID-19 and how some interventions and healthy lifestyle choices can markedly reduce disease burden, morbidity, and mortality.

Ivabradine is a pharmacologic agent that inhibits the funny current responsible for determining heart rate in the sinoatrial node. Ivabradine's clinical potential has been investigated in the context of heart failure since it is associated with reduced myocardial oxygen demand, enhanced diastolic filling, stroke volume, and coronary perfusion time; however, it is yet to demonstrate definitive mortality benefit. Alternative effects of ivabradine include modulation of the renin-angiotensin-aldosterone system, sympathetic activation, and endothelial function. Here, we review key clinical trials informing the clinical use of ivabradine and explore opportunities for leveraging its potential pleiotropic effects in other diseases, including treatment of hyperadrenergic states and mitigating complications of COVID-19 infection.

The goal of this study was to determine the potential for right ventricular (RV) and left ventricular (LV) strain to predict cardiopulmonary complications of COVID-19. We identified 276 patients with COVID-19 who underwent transthoracic echocardiography within 30 days of COVID-19 diagnosis at our institution. Patients were excluded if they had a history of any primary outcomes before COVID-19 diagnosis or insufficient imaging. LV global longitudinal strain (GLS) and RV GLS were obtained using 2-dimensional speckle-tracking echocardiography. Primary outcomes were death, pulmonary embolism, congestive heart failure (CHF), cardiomyopathy, pulmonary fibrosis, pulmonary hypertension, acute respiratory distress syndrome (ARDS), and myocardial infarction (MI) occurring after COVID-19 diagnosis. In the final analysis of 163 patients, mean RV GLS and LV GLS were reduced, and 43.6% developed at least one primary outcome. There were significant differences in LV GLS distribution in terms of CHF, cardiomyopathy, and MI in bivariate analysis. However, LV GLS was not significantly associated with CHF after adjusting for LV ejection fraction and RV fractional area change, nor with MI after adjusting for troponin T. RV GLS was significantly associated with ARDS after adjusting for other variables. In the risk stratification of patients with COVID-19, strain imaging can provide incremental prognostic information, as worsened RV GLS is associated with the development of ARDS.

The present study investigated the phytochemicals and in silico anti-nCoV properties of Piper barberi, an endangered and endemic species of Southern Western Ghats. Using conventional soxhlet extraction method, the leaf and stem were extracted separately with methanol (PBLM and PBSM). The bioactive compounds from the extracts were identified using HR-LCMS/MS-qTOF analysis. These compounds were subjected to various in silico analyses to identify potential drug candidates against nCoV. The HR LCMS/MS analysis of PBLM and PBSM revealed the presence of phenols, flavonoids, alkaloids, and terpenoids in it and this is the first report of the phytoconstituents present in the species P. barberi. All the identified bioactive compounds were subjected to predict ADMET. Out of 49 identified compounds, only 31 passed drug-likeness properties and toxicity tests. Molecular interaction studies were conducted using the AutoDockTools 4.2.6., which showed that only 13 compounds exhibited acceptable binding affinity with the nCoV target Mpro. Structural stability and binding free energy analyses of the five compounds with the higher binding affinity indicated that the bioactive compounds Hetisine and Ajaconine are stable with both hydrogen bonds and hydrophobic interactions. Hetisine shows stable binding among these two compounds with two hydrogen bond interactions with the crucial catalytic dyad residue (His41). Thus, this study concludes that these compounds might potentially be used as an alternative drug candidate for managing nCoV. However, further experimental validation, including in vitro and in vivo assays, is required to substantiate the results.Communicated by Ramaswamy H. Sarma.

The Coronavirus Disease 2019, commonly referred to as COVID-19, is responsible for one of the deadliest pandemics in human history. The direct, indirect and lasting repercussions of the COVID-19 pandemic on individuals and public health, as well as health systems can still be observed, even today. In the midst of the initial chaos, the role of tobacco as a prognostic factor for unfavourable COVID-19 outcomes was largely neglected. As of 2023, numerous studies have confirmed that use of tobacco, a leading risk factor for cardiovascular and other diseases, is strongly associated with increased risks of severe COVID-19 complications (e.g., hospitalisation, ICU admission, need for mechanical ventilation, long COVID, etc.) and deaths from COVID-19. In addition, evidence suggests that COVID-19 directly affects multiple organs beyond the respiratory system, disproportionately impacting individuals with comorbidities. Notably, people living with cardiovascular disease are more prone to experiencing worse outcomes, as COVID-19 often inherently manifests as thrombotic cardiovascular complications. As such, the triad of tobacco, COVID-19 and cardiovascular disease constitutes a dangerous cocktail. The lockdowns and social distancing measures imposed by governments have also had adverse effects on our lifestyles (e.g., shifts in diets, physical activity, tobacco consumption patterns, etc.) and mental well-being, all of which affect cardiovascular health. In particular, vulnerable populations are especially susceptible to tobacco use, cardiovascular disease and the psychological fallout from the pandemic. Therefore, national pandemic responses need to consider health equity as well as the social determinants of health. The pandemic has also had catastrophic impacts on many health systems, bringing some to the brink of collapse. As a result, many health services, such as services for cardiovascular disease or tobacco cessation, were severely disrupted due to fears of transmission and redirection of resources for COVID-19 care. Unfortunately, the return to pre-pandemic levels of cardiovascular disease care activity has stagnated. Nevertheless, digital solutions, such as telemedicine and apps, have flourished, and may help reduce the gaps. Advancing tobacco control was especially challenging due to interference from the tobacco industry. The industry exploited lingering uncertainties to propagate misleading information on tobacco and COVID-19 in order to promote its products. Regrettably, the links between tobacco use and risk of SARS-CoV-2 infection remain inconclusive. However, a robust body of evidence has, since then, demonstrated that tobacco use is associated with more severe COVID-19 illness and complications. Additionally, the tobacco industry also repeatedly attempted to forge partnerships with governments under the guise of corporate social responsibility. The implementation of the WHO Framework Convention on Tobacco Control could address many of the aforementioned challenges and alleviate the burden of tobacco, COVID-19, and cardiovascular disease. In particular, the implementation of Article 5.3 could protect public health policies from the vested interests of the industry. The world can learn from the COVID-19 pandemic to better prepare for future health emergencies of international concern. In light of the impact of tobacco on the COVID-19 pandemic, it is imperative that tobacco control remains a central component in pandemic preparedness and response plans.

Abnormal P-wave axis (aPwa) have been correlated with an increased risk of supraventricular arrhythmias. The aim of this study was to analyze whether infection with COVID-19 may cause a predisposition for supraventricular arrhythmia in the long term, following recovery.

In this study, a total of 252 subjects with a confirmed history of COVID-19 (recovered COVID-19) and 251 healthy subjects without a history of COVID-19 were included. The recovered COVID-19 group was divided into three subgroups designated as mild, moderate, and severe according to the severity score of their chest CT. The aPwa data were obtained using 12-lead electrocardiography (ECG) and compared between the healthy subjects and the recovered COVID-19 subgroups.

This study showed that in the recovered severe COVID-19 subgroup the prevalence of aPwa was significantly increased compared to the controls and the other COVID-19 subgroups. No correlation could be detected in Spearman's Rho correlation between the existence of aPwa and the number of positive PCR tests for COVID-19 and the time elapsed after infection with COVID-19. The binary logistic regression analysis showed that recovery from severe COVID-19, the severity score of the chest CT in the recovered from COVID-19 subjects, and the existence of hypertension (HT) were all independent predictors of aPwa (hazard ratio: 3.542, 95% confidence interval: 1.398-8.969, p: 0.01; hazard ratio: 0.896, 95% confidence interval: 0.840-0.955, p < 0.001; hazard ratio: 2.710, 95% confidence interval: 1.079-6.804, p: 0.03, respectively).

Individuals who have recovered from severe COVID-19 have shown an increased prevalence of aPwa. The existence of aPwa was not associated with the number of positive PCR tests for COVID-19 or the time elapsed after infection with COVID-19. Therefore, recovery from severe COVID-19 is an independent predictor of electrocardiographic abnormal P-wave axis.

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.

Coronavirus disease 2019 (COVID-19) triggers multiple components of the immune system and causes inflammation of endothelial walls across vascular beds, resulting in respiratory failure, arterial and venous thrombosis, myocardial injury, and multi-organ failure leading to death. Early in the COVID-19 pandemic, aspirin was suggested for the treatment of symptomatic individuals, given its analgesic, antipyretic, anti-inflammatory, anti-thrombotic, and antiviral effects. This study aimed to evaluate the association of aspirin use with various clinical outcomes in patients hospitalized for COVID-19.

This was a retrospective study involving patients aged ≥ 18 years and hospitalized for COVID-19 from March 2020 to October 2020. Primary outcomes were acute cardiovascular events (ST elevation myocardial infarction (STEMI), type 1 non-ST elevation myocardial infarction (NSTEMI), acute congestive heart failure (CHF), and acute stroke) and death. Secondary outcomes were respiratory failure, need for mechanical ventilation, and acute deep vein thrombosis (DVT)/pulmonary embolism (PE).

Of 376 patients hospitalized for COVID-19, 128 were taking aspirin. Significant proportions of native Americans were hospitalized for COVID-19 in both aspirin (22.7%) and non-aspirin (24.6%) groups. Between aspirin and non-aspirin groups, no significant differences were found with regard to mechanical ventilator support (21.1% vs. 15.3%, P = 0.16), acute cardiovascular events (7.8% vs. 5.2%, P = 0.32), acute DVT/PE (3.9% vs. 5.2%, P = 0.9), readmission rate (13.3% vs. 12.9%, P = 0.91) and mortality (23.4% vs. 20.2%, P = 0.5); however, the median duration of mechanical ventilation was significantly shorter (7 vs. 9 days, P = 0.04) and median length of hospitalization was significantly longer (5.5 vs. 4 days, P = 0.01) in aspirin group compared to non-aspirin group.

No significant differences were found in acute cardiovascular events, acute DVT/PE, mechanical ventilator support, and mortality rate between hospitalized COVID-19 patients who were taking aspirin compared to those not taking aspirin. However, larger studies are required to confirm our findings.

Background: The new coronavirus disease (COVID-19), a pandemic infection caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2), had a deep global influence on morbidity and mortality profiles. Comorbidities, especially cardiovascular diseases, were identified to strongly modify the clinical course of COVID-19. However, the prognostic role of incident or prevalent atrial fibrillation has not been fully explained. The aim of this study was to evaluate the association between atrial fibrillation and outcomes following hospitalization in patients with severe COVID-19. Methods: We analyzed 199 patients (72 female, median age 70 years) with severe COVID-19 hospitalized between November 2020 and February 2021, due to SARS-CoV-2 infection. The study cohort included 68 patients with a history of AF (34 patients with paroxysmal AF, 19 with permanent AF, 15 patients with persistent AF), and 51 patients presented with AF during hospitalization. Results: Overall mortality during 90 days from the admission to hospital was 41% (n = 82). Non-survivors were older, had significantly elevated inflammation markers (CRP, WBC, procalcitonin, IL-6), NT-proBNP and D-dimer on the first day of hospitalization, lower left ventricular ejection fraction and worse kidney function, as compared to those who stayed alive during the follow-up. Among the hospitalized patients with COVID-19, a history of AF and the presence of AF during hospitalization contributed to higher mortality. Patients with permanent and persistent AF were at the highest risk of death. Different presentations of AF (any history of AF, the subtypes of AF-paroxysmal, permanent, persistent-and the presence of AF during hospitalization) were included in multivariate analysis, aiming to identify independent risk factors of death in the study period. We found that AF was related to worse prognosis, and persistent or permanent forms represented an independent predictor of mortality. Conclusions: Different clinical presentations of AF have varying impacts on survival in severe COVID-19. Mortality in hospitalized patients with severe COVID-19 was higher among patients with a history of AF, especially with persistent and permanent types of AF, and with AF present during hospitalization.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) leads to coronavirus disease-2019 (COVID-19) which can cause severe cardiovascular complications including myocardial injury, arrhythmias, acute coronary syndrome and others. Among these complications, arrhythmias are considered serious and life-threatening. Although arrhythmias have been associated with factors such as direct virus invasion leading to myocardial injury, myocarditis, immune response disorder, cytokine storms, myocardial ischemia/hypoxia, electrolyte abnormalities, intravascular volume imbalances, drug interactions, side effects of COVID-19 vaccines and autonomic nervous system dysfunction, the exact mechanisms of arrhythmic complications in patients with COVID-19 are complex and not well understood. In the present review, the literature was extensively searched to investigate the potential mechanisms of arrhythmias in patients with COVID-19. The aim of the current review is to provide clinicians with a comprehensive foundation for the prevention and treatment of arrhythmias associated with long COVID-19.

Background/Objectives: The newly emergent COVID-19 pandemic involved primarily the respiratory system and had also major cardiovascular system (CVS) implications, revealed by acute myocardial infarction (AMI), arrhythmias, myocardial injury, and thromboembolism. CVS involvement is done through main mechanisms-direct and indirect heart muscle injury, with high mortality rates, worse short-term outcomes, and severe complications. AMI is the echo of myocardial injury (revealed by increases in CK, CK-MB, and troponin serum markers-which are taken into consideration as possible COVID-19 risk stratification markers). When studying myocardial injury, physicians can make use of imaging studies, such as cardiac MRI, transthoracic (or transesophageal) echocardiography, coronary angiography, cardiac computed tomography, and nuclear imaging (which have been used in cases where angiography was not possible), or even endomyocardial biopsy (which is not always available or feasible). Two-case-series presentations: We present the cases of two COVID-19 positive male patients who were admitted into the Clinical Department of Cardiology in "Sfântul Apostol Andrei" Emergency Clinical Hospital of Galați (Romania), who presented with acute cardiac distress symptoms and have been diagnosed with ST elevation AMI. The patients were 82 and 57 years old, respectively, with moderate and severe forms of COVID-19, and were diagnosed with anteroseptal left ventricular AMI and extensive anterior transmural left ventricular AMI (with ventricular fibrillation at presentation), respectively. The first patient was a non-smoker and non-drinker with no associated comorbidities, and was later discharged, while the second one died due to AMI complications. Conclusions: From this two-case series, we extract the following: old age alone is not a significant risk factor for adverse outcomes in COVID-19-related CVS events, and that the cumulative effects of several patient-associated risk factors (be it either for severe forms of COVID-19 and/or acute cardiac injury) will most probably lead to poor patient prognosis (death). At the same time, serum cardiac enzymes, dynamic ECG changes, along with newly developed echocardiographic modifications are indicators for poor prognosis in acute cardiac injury in COVID-19 patients with acute myocardial injury, regardless of the presence of right ventricular dysfunction (due to pulmonary hypertension).

This study aimed to explore the association between cardiac fibroblast activation and cardiac magnetic resonance (CMR) imaging parameters in patients with myocarditis following infection with coronavirus 2019 (COVID-19).

In this prospective study, four patients with COVID-19-related myocarditis underwent 99mTc-labeled-hydrazinonicotinamide-fibroblast activation protein inhibitor-04 (99mTc-HFAPi) single photon emission computed tomography/computed tomography (SPECT/CT) and CMR imaging. Segmental 99mTc-HFAPi activity was quantified as the percentage of average segmental myocardial count × global left ventricular target-to-background ratio. T1/T2 values, extracellular volume (ECV), and late gadolinium enhancement (LGE) were analyzed by CMR. The consistency between myocardial 99mTc-HFAPi activity and CMR parameters was explored.

In patients with myocarditis, the proportion of segments with abnormal 99mTc-HFAPi activity was significantly higher than in those with abnormal LGE (81.25% vs. 60.93%, p = 0.011), abnormal T2 (81.25% vs. 50.00%, p < 0.001), and abnormal ECV (81.25% vs. 59.38%, p = 0.007); however, they were similar in those with abnormal native T1 (81.25% vs. 73.43%, p = 0.291). Meanwhile, 99mTc-HFAPi imaging exhibited good consistency with native T1 (kappa = 0.69).

Increased cardiac 99mTc-HFAPi activity is present in COVID-19-related myocarditis, which is correlated with the native T1 values in CMR.

Background: Many people infected with COVID-19 develop myocardial injury. Epicardial adipose tissue (EAT) is among the various risk factors contributing to coronary artery disease. However, its correlation with myocardial injury in patients diagnosed with COVID-19 remains uncertain. Methods: We examined myocardial biomarkers in population affected by COVID-19 during the period from December 2022 to January 2023. The patients without myocardial injury were referred to as group A (n = 152) and those with myocardial injury were referred to as group B (n = 212). Results: 1) The A group and the B group exhibitedstatistically significant differences in terms of age, TC, CRP, Cr, BUN, LDL-C, IL-6, BNP, LVEF and EAT (p < 0.05). 2) EAT volumehad a close relationship with IL-6, LDL-C, cTnI, and CRP (p < 0.05); the corresponding correlation coefficient values were 0.24, 0.21, 0.24, and 0.16. In contrast to those with lower EAT volume, more subjects with a higher volume of EAT had myocardial injury (p < 0.05). Regression analysis showed that EAT, LDL-C, Age and Cr were established as independent risk variables for myocardial injury in subjects affected by COVID-19. 3) In COVID-19 patients, the likelihood of myocardial injury rised notably as EAT levels increase (p < 0.001). Addition of EAT to the basic risk model for myocardial injury resulted in improved reclassification. (Net reclassification index: 58.17%, 95% CI: 38.35%, 77.99%, p < 0.001). Conclusion: Patients suffering from COVID-19 with higher volume EAT was prone to follow myocardial injury and EAT was an independent predictor of heart damage in these individuals.

In the context of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, significant attention was given to pulmonary manifestations. However, cardiac involvement is increasingly recognized as a critical factor influencing the prognosis, leading to myocardial damage, heart failure, acute coronary syndromes, potentially lethal arrhythmic events, and sudden cardiac death. Despite these findings, there is a lack of studies detailing the necroscopic, macroscopic, and microscopic cardiac changes associated with SARS-CoV-2. This study aimed to investigate the presence of SARS-CoV-2 viral proteins in cardiac tissue using immunohistochemical techniques to assess viral tropism. The analysis of cardiac tissue samples from deceased subjects, in different stages of conservation, confirmed to be positive for SARS-CoV-2 via reverse transcriptase-polymerase chain reaction (RT-PCR), showed immunopositivity for the SARS-CoV-2-NP viral antigen in 33% of cases. Notably, the presence of leukocyte infiltrates sufficient for diagnosing lymphocytic myocarditis was not observed. The central proinflammatory cytokines involved in the pathogenetic mechanism of coronavirus disease 19 (COVID-19) were researched using the immunohistochemical method. A significant increase in cytokine expression was detected, indicating myocardial involvement and dysfunction during SARS-CoV-2 infection. These findings suggest that the immunohistochemical detection of SARS-CoV-2 viral antigens and inflammatory cytokine expression in cardiac tissue could be crucial for a proper forensic assessment of the cause of death, even in sudden cardiac death.

Hospitalized patients with Coronavirus disease 2019 (COVID-19) are highly susceptible to in-hospital mortality and cardiac complications such as atrial arrhythmias (AA). However, the utilization of biomarkers such as potassium, B-type natriuretic peptide, albumin, and others for diagnosis or the prediction of in-hospital mortality and cardiac complications has not been well established. The study aims to investigate whether biomarkers can be utilized to predict mortality and cardiac complications among hospitalized COVID-19 patients. Data were collected from 6,927 hospitalized COVID-19 patients from March 1, 2020, to March 31, 2021 at one quaternary (Henry Ford Health) and five community hospital registries (Trinity Health Systems). A multivariable logistic regression prediction model was derived using a random sample of 70% for derivation and 30% for validation. Serum values, demographic variables, and comorbidities were used as input predictors. The primary outcome was in-hospital mortality, and the secondary outcome was onset of AA. The associations between predictor variables and outcomes are presented as odds ratio (OR) with 95% confidence intervals (CIs). Discrimination was assessed using area under ROC curve (AUC). Calibration was assessed using Brier score. The model predicted in-hospital mortality with an AUC of 90% [95% CI: 88%, 92%]. In addition, potassium showed promise as an independent prognostic biomarker that predicted both in-hospital mortality, with an AUC of 71.51% [95% Cl: 69.51%, 73.50%], and AA with AUC of 63.6% [95% Cl: 58.86%, 68.34%]. Within the test cohort, an increase of 1 mEq/L potassium was associated with an in-hospital mortality risk of 1.40 [95% CI: 1.14, 1.73] and a risk of new onset of AA of 1.55 [95% CI: 1.25, 1.93]. This cross-sectional study suggests that biomarkers can be used as prognostic variables for in-hospital mortality and onset of AA among hospitalized COVID-19 patients.

This study assessed medication patterns for inpatients at a central hospital in Portugal and explored their relationships with clinical outcomes in COVID-19 cases.

A retrospective study analyzed inpatient medication data, coded using the Anatomical Therapeutic Chemical classification system, from electronic patient records. It investigated the association between medications and clinical severity outcomes such as ICU admissions, respiratory/circulatory support needs, and hospital discharge status, including mortality (identified by ICD-10-CM/PCS codes). Multivariate analyses incorporating demographic data and comorbidities were used to adjust for potential confounders and understand the impact of medication patterns on disease progression and outcomes.

The analysis of 2688 hospitalized COVID-19 patients (55.3% male, average age 62.8 years) revealed a significant correlation between medication types and intensity and disease severity. Cases requiring ICU admission or ECMO support often involved blood and blood-forming organ drugs. Increased use of nervous system and genitourinary hormones was observed in nonsurvivors. Corticosteroids, like dexamethasone, were common in critically ill patients, while tocilizumab was used in ECMO cases. Medications for the alimentary tract, metabolism, and cardiovascular system, although widely prescribed, were linked to more severe cases. Invasive mechanical ventilation correlated with higher usage of systemic anti-infectives and musculoskeletal medications. Trends in co-prescribing blood-forming drugs with those for acid-related disorders, analgesics, and antibacterials were associated with intensive interventions and worse outcomes.

The study highlights complex medication regimens in managing severe COVID-19, underscoring specific drug patterns associated with critical health outcomes. Further research is needed to explore these patterns.

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.

Severe and critical forms of SARS-CoV-2 pneumonia are associated with high morbidity and mortality. Numerous research studies have been conducted around the world to investigate various variables (demographic, clinical, laboratory, etc.) in an attempt to understand the relationships between them and the course and outcome of patients with COVID-19 infection and pneumonia.

Clinical experience and several large studies in the field have found that SARS-CoV-2 infection can cause long-term persistent cardiovascular (CV) impairment beyond the acute phase of the disease. This has resulted in a major public health concern worldwide. Regarding COVID-related long-term involvement of various organs and systems, using specific definitions and terminology is crucial to point out time relationships, lingering damage, and outcome, mostly when symptoms and signs of CV disease persist beyond the acute phase. Due to a lack of a common standardized definition, investigators have used interchangeable terms such as "long COVID," "post-COVID," or "post-acute sequelae of COVID-19" to describe CV involvement, thus causing some confusion. For the sake of clarity, the aim of this paper is to discuss the definition and terminology used in defining sequelae after the acute phase of COVID-19, thus pointing out the meaning of definitions like acute cardiac injury, post-acute sequelae of COVID-19, long COVID syndrome, and increased risk of atherosclerotic cardiovascular disease.

Remodeling of sympathetic nerves and ACE2 has been implicated in cardiac pathology, and ACE2 also serves as a receptor for SARS-CoV-2. However, there is limited histological knowledge about the transmural distribution of sympathetic nerves and the cellular localization and distribution of ACE2 in human left ventricles from normal or diseased hearts. Goals of this study were to establish the normal pattern for these parameters and determine changes that occurred in decedents with cardiovascular disease alone compared to those with cardiac pathology and severe COVID-19.

We performed immunohistochemical analysis on sections of left ventricular wall from twenty autopsied human hearts consisting of a control group, a cardiovascular disease group, and COVID-19 ARDS, and COVID-19 non-ARDS groups.

Using tyrosine hydroxylase as a noradrenergic marker, we found substantial sympathetic nerve loss in cardiovascular disease samples compared to controls. Additionally, we found heterogeneous nerve loss in both COVID-19 groups. Using an ACE2 antibody, we observed robust transmural staining localized to pericytes in the control group. The cardiovascular disease hearts displayed regional loss of ACE2 in pericytes and regional increases in staining of cardiomyocytes for ACE2. Similar changes were observed in both COVID-19 groups.

Heterogeneity of sympathetic innervation, which occurs in cardiac disease and is not increased by severe COVID-19, could contribute to arrhythmogenesis. The dominant localization of ACE2 to pericytes suggests that these cells would be the primary target for potential cardiac infection by SARS-CoV-2. Regional changes in ACE2 staining by myocytes and pericytes could have complex effects on cardiac pathophysiology.

Myocardial injury has been described in coronavirus-2019 (COVID-19). Few studies have reported cardiovascular imaging data with transthoracic echocardiography (TTE) and electrocardiography (ECG) findings in COVID-19 patients, and their correlation with mortality.

We conducted a retrospective cohort study that included COVID-19 patients from March 2020 through February 2021 who had TTE and ECG during hospital admission. Myocardial injury was defined by an elevated high-sensitivity troponin T level > 20 ng/L. Bivariate analysis was used to compare patients with myocardial injury and those without. Multivariate logistic regression analysis was performed to identify the variables associated with mortality.

A total of 438 patients were included. The mean age was 62.1 ± 14.9 years, and 58.9% were male. A total of 149 patients died, with a mortality rate of 34%. A total of 260 patients (59.4%) had myocardial injury. The average left ventricular ejection fraction was 59.8% ± 11.2%, with 30 patients (6.8%) having an ejection fraction of < 40%. Patients with myocardial injury had higher mortality than those without (P < 0.05, χ2 test). A multiple regression analysis model indicated that age, race and/or ethnicity, the development of acute respiratory distress syndrome, shock, the need for vasopressors, mechanical ventilation, and hemodialysis were the variables significantly associated with mortality.

COVID-19 patients with myocardial injury had higher mortality than those without. Age, race and/or ethnicity, acute respiratory distress syndrome, shock, the need for vasopressors, mechanical ventilation, and hemodialysis were the clinical variables associated with mortality. The TEE and ECG variables studied were not significantly associated with mortality.

Studies show that with the COVID-19 pandemic, the world's population went through multiple stress and anxiety factors, generating serious psychological problems, in addition, the virus also caused damage and physical stress to those contaminated. In this way, the intense emotional experiences and stressful effects on the body caused by SARS-CoV-2 are capable of triggering the excessive release of catecholamines in the body. Thus, the framework of Takotsubo Syndrome is characterized by myocardial dysfunction as a response of cardiac receptors to the spillage of such hormones in an unregulated way in the human body. The purinergic system plays a central role in this process, as it actively participates in actions responsible for the syndromic cascade, such as the stress generated by the cytokine storm triggered by the virus and the stimulation of deregulated catecholamine release. Therefore, further pharmacological studies on the role of purines in this pathology should be developed in order to avoid the evolution of the syndrome and to modulate its P1 and P2 receptors aiming at developing means of reversing or treating the Takotsubo Syndrome.

A growing body of research shows that COVID-19 is now recognized as a multi-organ disease with a wide range of manifestations that can have long-lasting repercussions, referred to as post-COVID-19 syndrome. It is unknown why the vast majority of COVID-19 patients develop post-COVID-19 syndrome, or why patients with pre-existing disorders are more likely to experience severe COVID-19. This study used an integrated network biology approach to obtain a comprehensive understanding of the relationship between COVID-19 and other disorders. The approach involved building a PPI network with COVID-19 genes and identifying highly interconnected regions. The molecular information contained within these subnetworks, as well as the pathway annotations, were used to reveal the link between COVID-19 and other disorders. Using Fisher's exact test and disease-specific gene information, significant COVID-19-disease associations were discovered. The study discovered diseases that affect multiple organs and organ systems, thus proving the theory of multiple organ damage caused by COVID-19. Cancers, neurological disorders, hepatic diseases, cardiac disorders, pulmonary diseases, and hypertensive diseases are just a few of the conditions linked to COVID-19. Pathway enrichment analysis of shared proteins revealed the shared molecular mechanism of COVID-19 and these diseases. The findings of the study shed new light on the major COVID-19-associated disease conditions and how their molecular mechanisms interact with COVID-19. The novelty of studying disease associations in the context of COVID-19 provides new insights into the management of rapidly evolving long-COVID and post-COVID syndromes, which have significant global implications.Communicated by Ramaswamy H. Sarma.

The novel 2019 coronavirus disease (COVID-19) was first reported in the last days of December 2019 in Wuhan, China. The presence of certain co-morbidities, including cardiovascular diseases (CVDs), are the basis for worse outcomes in patients with COVID-19. Relevant English-language literature was searched and retrieved from the Google Scholar search engine and PubMed database up to 2023 using COVID-19, SARS-CoV-2, Heart failure, Myocardial infarction, and Arrhythmia and Cardiac complication as keywords. Increased hemodynamic load, ischemia-related dysfunction, ventricular remodeling, excessive neurohumoral stimulation, abnormal myocyte calcium cycling, and excessive or insufficient extracellular matrix proliferation are associated with heart failure (HF) in COVID-19 patients. Inflammatory reaction due to the excessive release of inflammatory cytokines, leads to myocardial infarction (MI) in these patients. The virus can induce heart arrhythmia through cardiac complications, hypoxia, decreased heart hemodynamics, and remarkable inflammatory markers. Moreover, studies have linked cardiac complications in COVID-19 with poor outcomes, extended hospitalization time, and increased mortality rate. Patients with COVID-19 and CVDs are at higher mortality risk and they should be given high priority when receiving the treatment and intensive care during hospitalization.

Impaired physical functional status is one of the typical long-term sequelae of COVID-19 infection that significantly affects the quality of life and work capacity. Minor changes in cardiac structure and function that are unable to cause the manifestation of overt heart failure may remain undetected in COVID-19 convalescents, at the same time potentially contributing to the persistence of symptoms and development of long COVID syndrome.

To study the typical features and short-term dynamics of cardiac remodeling and possible signs of cardiac dysfunction following hospitalization for COVID-19.

This is a combined cross-sectional and longitudinal cohort study in which 176 hospitalized patients (93 female and 83 male, mean age 53.4 ± 13.6 years) with COVID-19 infection underwent comprehensive transthoracic echocardiography pre-discharge (22.6 ± 7.1 days from the onset of symptoms) with repeated evaluation after 1 month. The control group included 88 age-, sex-, height- and weight-matched healthy individuals, with a subset of those (n = 53) matched to the subset of non-hypertensive study participants (n = 106).

Concentric left ventricular geometry was revealed in 59% of participants, including 43% of non-hypertensive subjects; predominantly Grade I diastolic dysfunction was found in 35 and 25% of patients, respectively. Other findings were naturally following from described phenotype of the left venticle and included a mild increase in the absolute and relative wall thickness (0.45 ± 0.07 vs. 0.39 ± 0.04, p < 0.001), worsening of diastolic indices (e' velocity 9.2 ± 2.2 vs. 11.3 ± 2.6 cm/s, p < 0.001, E/e' ratio 7.5 ± 1.8 vs. 6.8 ± 1.7, p = 0.002) and global longitudinal strain (17.5 ± 2.4 vs. 18.6 ± 2.2, p < 0.001). No significant improvement was found on re-evaluation at 1 month.

Hospitalized patients recovering from COVID-19 were characterized by a high prevalence of left ventricular concentric remodeling, predominantly Grade I diastolic dysfunction, and a mild decrease in the longitudinal systolic function. These changes were less frequent but still prevalent in the non-hypertensive subgroup and largely persisted throughout the 1-month follow-up.

One of the most common complications of coronavirus disease 2019 (COVID-19) is myocardial injury, and although its cause is unclear, it can alter the heart's contractility. This study aimed to characterize the ventricular and atrial strain in patients who recovered from COVID-19 using cardiovascular magnetic resonance feature-tracking (CMR-FT).

In this single-center study, we assessed left ventricle (LV) and right ventricular (RV) global circumferential strain (GCS), global longitudinal strain (GLS), global radial strain (GRS), left atrial (LA) and right atrial (RA) longitudinal strain (LS) parameters by CMR-FT. The student's t-test and Wilcoxon rank-sum test were used to compare the variables.

We compared seventy-two patients who recovered from COVID-19 (49 ± 16 years) to fifty-four controls (49 ± 12 years, p = 0.752). The patients received a CMR examination 48 (34 to 165) days after the COVID-19 diagnosis. 28% had LGE. Both groups had normal LV systolic function. Strain parameters were significantly lower in the COVID-19 survivors than in controls.

Patients who recovered from COVID-19 exhibited significantly lower strain in the left ventricle (through LVGCS, LVGLS, LVGRS), right ventricle (through RVGLS and RVGRS), left atrium (through LALS), and right atrium (through RALS) than controls.

In this study, we aimed to identify the causes, predictors and gender disparities of 30-day and 90-day cardiovascular readmissions after COVID-19-related hospitalisations using National Readmission Database (NRD) 2020.

We used the NRD from 2020 to identify hospitalised adults with a principal diagnosis of COVID-19 infection.

We included subjects who were readmitted within 30 days and 90 days after index admission. We excluded subjects with elective and traumatic admissions. We used a multivariate Cox regression model to identify independent predictors of readmission.

Our outcomes were inpatient mortality, 30-day and 90-day cardiovascular readmission rates following COVID-19 infection.

During the study period, there were 1 024 492 index hospitalisations with a primary diagnosis of COVID-19 infection in the 2020 NRD database, 644 903 (62.9%) were included for 30-day readmission analysis, and 418 122 (40.8%) were included for 90-day readmission analysis. Of patients involved in the 30-day analysis, 7140 (1.1%) patients had a readmission within 30 days; of patients involved in the 90-day analysis, 8379 (2.0%) had a readmission within 90 days due to primarily cardiovascular causes. Cox regression analysis revealed that the female sex (aHR 0.89; 95% CI 0.82 to 0.95; p=0.001) was associated with a lower hazard of 30-day cardiovascular readmissions; however, congestive heart failure (aHR 2.45; 95% CI 2.2 to 2.72; p<0.001), arrhythmias (aHR 2.45; 95% CI 2.2 to 2.72; p<0.001) and valvular disease (aHR 2.45; 95% CI 2.2 to 2.72; p<0.001) had a higher hazard. The most common causes of cardiovascular readmissions were heart failure (34.3%), deep vein thrombosis/pulmonary embolism (22.5%) and atrial fibrillation (9.5%).

Our study demonstrates that male gender, heart failure, arrhythmias and valvular disease carry higher hazards of 30-day and 90-day cardiovascular readmissions. Identifying risk factors and common causes of readmission may assist with lowering the burden of cardiovascular disease in patients with COVID-19 infection.

At the beginning of 2020, coronavirus disease 2019 (COVID-19) emerged as a new pandemic, leading to a worldwide health crisis and overwhelming healthcare systems due to high numbers of hospital admissions, insufficient resources, and a lack of standardized therapeutic protocols. Multiple genetic variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have been detected since its first public declaration in 2020, some of them being considered variants of concern (VOCs) corresponding to several pandemic waves. Nevertheless, a growing number of COVID-19 patients are continuously discharged from hospitals, remaining symptomatic even months after their first episode of COVID-19 infection. Long COVID-19 or 'post-acute COVID-19 syndrome' emerged as the new pandemic, being characterized by a high variability of clinical manifestations ranging from cardiorespiratory and neurological symptoms such as chest pain, exertional dyspnoea or cognitive disturbance to psychological disturbances, e.g., depression, anxiety or sleep disturbance with a crucial impact on patients' quality of life. Moreover, Long COVID is viewed as a new cardiovascular risk factor capable of modifying the trajectory of current and future cardiovascular diseases, altering the patients' prognosis. Therefore, in this review we address the current definitions of Long COVID and its pathophysiology, with a focus on cardiovascular manifestations. Furthermore, we aim to review the mechanisms of acute and chronic cardiac injury and the variety of cardiovascular sequelae observed in recovered COVID-19 patients, in addition to the potential role of Long COVID clinics in the medical management of this new condition. We will further address the role of future research for a better understanding of the actual impact of Long COVID and future therapeutic directions.

We sought to examine a 1-year incidence of atrial fibrillation (AF) among patients with SARS-CoV-2 virus (COVID-19) in comparison to those with non-COVID-19 acute upper respiratory infection (AURI).

Patients with a diagnosis of COVID-19 (in any setting) between April 2020 and June 2021 were identified in Optum Clinformatics. Two comparator cohorts were constructed: an 'AURI pandemic' cohort (AURI diagnosis between April 2020 and June 2021) and an 'AURI prepandemic' cohort (AURI diagnosis between January 2018 and December 2018). One-year incidence of AF was compared among: COVID-19 versus AURI pandemic cohort; COVID-19 versus AURI prepandemic cohort; and AURI pandemic versus AURI prepandemic cohort. For each comparison, we applied a matching weights technique to balance covariates. Logistic regression was used to compare the odds of incident AF among the matched cohorts.

When comparing the matched COVID-19 (n=102 227) cohort with the AURI pandemic (n=102 101) cohort, higher incidence of AF was observed among the COVID-19 cohort (2.2% vs 1.2%; p<0.001; OR 1.83; 95% CI 1.72 to 1.95). Similar findings were observed for the COVID-19 (n=169 687) versus AURI prepandemic (n=169 486) comparison (2.7% vs 1.6%; p<0.001; OR 1.70; 95% CI 1.63 to 1.78). When comparing the AURI pandemic (n=1 26 392) versus AURI prepandemic (n=1 26 394) cohort, no significant differences in incident AF were observed (1.1% vs 1.2%; p=0.133; OR 0.95, 95% CI 0.90 to 1.01).

Patients diagnosed with COVID-19 were found to be at a higher risk of incident AF as compared with those with AURI. Timely diagnosis and appropriate treatment of AF may potentially mitigate the burden of AF conferred by COVID-19.

Cardiomyopathy is a leading cause of sudden out-of-hospital death after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and coronavirus disease 2019 (COVID-19) vaccination. Such unexpected COVID-19-related cardiomyopathies are challenging to diagnose as specific pathological findings are not always identified.

We reported the autopsy findings of two cases of sudden death due to COVID-19-related cardiomyopathies. In one case, death occurred after SARS-CoV-2 infection, while in the other, after COVID-19 vaccination. We found common pathological findings in both hearts: decreased staining intensity with special stains, loss of rhabdomeres, and multivacuolation in cardiomyocytes without inflammatory cell infiltration. The remaining organs showed no findings that could have contributed to the deaths.

In cases of sudden death after SARS-CoV-2 infection or COVID-19 vaccination, the decreased staining intensity with special stains may aid the diagnosis of sudden death due to COVID-19-related cardiomyopathy, even when H&E staining shows few findings.