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.

Objectives. Many studies have confirmed the existence of a relationship between SARS-CoV-2 virus infection and an increased incidence of arrhythmia in the population of adults, children and adolescents. It is believed that one of the potential side effects of COVID-19 vaccination is arrhythmia. However, large-scale studies confirming the relationship between COVID-19 vaccination and cardiac arrhythmia are currently lacking. The objective of this study was to analyze the occurrence of arrhythmias in 24 h Holter ECG monitoring among patients who had experienced COVID-19, comparing those who were vaccinated against SARS-CoV-2 with those who were unvaccinated. Methods. The study was performed on a study group of 237 patients, who underwent 24 h Holter monitoring. Results. Ventricular extrasystoles (VEs) were distinctively more common in patients, who had COVID-19 infection and were not vaccinated for COVID-19 comparing to the control group. Similarly, research has shown that supraventricular extrasystoles (SVEs) occurred remarkably more frequently in both unvaccinated and vaccinated patients after COVID-19 infection in relation to control groups. Multivariable regression analysis demonstrates that, in the whole study group, obesity, arterial hypertension, previous myocardial infarction and lack of vaccination against COVID-19 are independent risk factors for higher VE rates. Obesity, diabetes type 2 and lack of vaccination against COVID-19 are independent risk factors for higher SVE rates. The use of β-blockers is an independent protective factor against higher VE and SVE rates, and the use of ACE inhibitors against higher SVE rates. Conclusions. In this study, the authors obtained promising results for the future, facilitating further discussion and research on the topic of the antiarrhythmic advantages of COVID-19 vaccination. Moreover, the knowledge acquired in this study serves as a valuable tool for effectively promoting COVID-19 vaccination among patients.

Inadequate information exists regarding physiological changes post-COVID-19 infection. We used smart beds to record biometric data following COVID-19 infection in nonhospitalized patients. Recordings of daily biometric signals over 14 weeks in 59 COVID-positive participants' homes in 2020 were compared with the same participants' data from 2019. Participants completed a survey of demographic information, health conditions, COVID exposure and testing, and symptom prevalence/subjective severity. Mean age was 47.5 years (standard deviation [SD] 9.5), mean body mass index was 30.1 kg/m2 (SD 7.1), and 46% were men. During acute infection, 64% exhibited 5-6 h increased sleep duration, 51% had increased movement, and 64% had increased breathing rate (BR). Nearly 34% had paradoxical bradycardia (decreased heart rate by ~ 10 BPM concomitant with elevated BR and/or fever), with more-severe symptoms. Smart beds can detect physiological changes during COVID-19. A subtype of acute response (paradoxical bradycardia) may predict delay recovery from COVID-19.

Arrhythmia is one of the important cardiac manifestations of SARS-CoV-2 disease with possible mechanisms such as direct damage to the myocardium, hypoxia, myocardial damage, cytokine storm, and electrolyte imbalances. Bradyarrhythmia is a manifestation of conduction system involvement, which is associated with an unfavorable prognosis and sometimes requires treatments such as implanting a pacemaker. Whether bradycardia in the acute phase of the COVID pandemic is a transient complication of the virus or whether it will be permanent can affect the treatment approach.Is the effect of SARS-CoV-2 on the conduction system of the heart temporary or permanent, and in the one-year follow-up, how many patients will need a pacemaker?

The study population was among patients with symptomatic bradyar-rhythmias who were referred to Chamran Heart Center, Isfahan, Iran, from the outbreak of SARS-CoV-2 (February 2020) until February 2022 and were diagnosed with COVID-19 based on the polymerase chain reaction (PCR) test. They underwent permanent pacemaker implantation and were monitored for 1 month and 12 months after device implantation.

The most common comorbid disease was hypertension. Systolic blood pressure and respiratory rate in hospitalized patients decreased significantly during discharge. Also, oxygen saturation and heart rate increased significantly during discharge (P < 0.001). In this study, high-degree atrioventricular block remained permanent in most patients and was not transient.

Based on the experiences gained from this study, the implantation of a permanent pacemaker for the treatment of bradyarrhythmia should be done based on the existing guidelines, regardless of the status of COVID-19.

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.

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).

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

The coronavirus disease 2019 (COVID-19) is an infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that produces respiratory symptoms and has serious consequences for people's cardiovascular systems (CVS). It is a severe issue and a major task not only for health care experts but also for governments to contain this pandemic. SARS-CoV-2 is the seventh member of the human coronavirus family to be implicated in this zoonotic outbreak. COVID-19's CV interactions are comparable to those of SARS-CoV, Middle East respiratory syndrome (MERS-CoV), and influenza. Those who have COVID-19 and underlying cardiovascular diseases (CVDs) are at a higher risk of serious illness and mortality, and disease has been linked to several direct and indirect CV consequences. COVID-19 causes CVDs such as arrhythmias, cardiac arrest, cardiogenic shock, myocarditis, stress-cardiomyopathy, and acute myocardial damage (AMD) as a consequence of acute coronary syndrome. The provision of CV care may expose health care professionals to risk as they become hosts or vectors of viral transmission. It binds to the angiotensin-converting enzyme receptor, causing constitutional and pulmonary signs in the beginning, and then as the infection advances, it affects other organs such as the gastrointestinal tract, CVS, neurological system, and so on. COVID-19 mortality is increased by underlying CVDs comorbidities.

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.

The cardiovascular complications of viral illnesses are often underestimated in clinical practice. The influenza virus, one of the most prevalent viral infections, has been associated with a wide spectrum of arrhythmias that are typically transient and self-resolving. We present the case of a 60-year-old female with no prior cardiac comorbidities who developed a complete heart block after an influenza infection. She presented to the clinic with flu-like symptoms and was found to have a complete heart block with a junctional escape rhythm. Polymerase chain reaction testing subsequently confirmed an influenza A infection. She was initially placed on a temporary pacemaker. However, a permanent dual-chamber pacemaker was implanted as bradycardia persisted. Later follow-ups in the cardiology clinic showed that the patient remained dependent on the pacemaker. While there are a few descriptions of influenza-induced transient atrioventricular block, cases of influenza-induced permanent complete heart block are extremely rare, particularly in the absence of severe myocardial inflammation.

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

The current COVID-19 pandemic has led to many studies examining its arrhythmogenic effects. However, there are many other viruses that are capable of inducing arrhythmias that have not received as much attention. The objective of this study was to review common viruses and identify studies highlighting their arrhythmogenic effects.

In this review, we examined 15 viruses and the literature regarding their arrhythmogenic effects. The common mechanisms of action appear to be direct invasion of myocytes leading to immune mediated damage, infection of vascular endothelium, and alteration of cardiac ion channels.

This review highlights the growing evidence that supports the involvement of other viral infections in the development of arrhythmia. Physicians should be aware of these potentially life-threatening effects when caring for patients with these viruses, some of which are very common. Additional studies are required to better understand the complex mechanism and risk factors of cardiac arrhythmias in patients suffered from viral infections to determine whether the processes can be reversed or even prevented.

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.

Various studies in the medical literature reported significant cardiovascular involvement in patients with coronavirus disease 2019 (COVID-19) pneumonia. Atrial fibrillation (AF) was identified as the most commonly observed arrhythmia complicating COVID-19 infection with an increased risk of short-term mortality. We used the National Inpatient Sample Database (NIS) of 2020 to conduct this retrospective cohort study. Our study's population consisted of adult patients hospitalized for COVID-19 Pneumonia with or without the presence of paroxysmal atrial fibrillation (PAF). Encounters with COVID-19 and co-existing PAF had higher adjusted odds of inpatient mortality (Adjusted odds ratio [aOR]: 1.19, 95% CI: 1.11-1.28, P < 0.001), longer mean length of hospital stay (LOS) of 1.17 days (95% confidence interval [CI]: 1.03-1.38, P < 0.001), and higher odds of different in-hospital complications. Based on these results, conducting more prospective/retrospective cohort studies with an emphasis on long-term follow-up on patients who develop PAF following COVID-19 infection is warranted.

Cardiovascular events, driven by endothelial dysfunction, are a recognised complication of COVID-19. SARS-CoV-2 infections remain a persistent concern globally, and an understanding of the mechanisms causing endothelial dysfunction, particularly the role of inflammation, nitric oxide, and whether sex differences exist in this response, is lacking. We have previously demonstrated important sex differences in the inflammatory response and its impact on endothelial function and separately that the ingestion of inorganic nitrate can protect the endothelium against this dysfunction. In this study, we will investigate whether sex or a dietary inorganic nitrate intervention modulates endothelial function and inflammatory responses after the COVID-19 vaccine.

DiNOVasc-COVID-19 is a double-blind, randomised, single-centre, placebo-controlled clinical trial. A total of 98 healthy volunteers (49 males and 49 females) will be recruited. Participants will be randomised into 1 of 2 sub-studies: part A or part B. Part A will investigate the effects of sex on vascular and inflammatory responses to the COVID-19 vaccine. Part B will investigate the effects of sex and dietary inorganic nitrate on vascular and inflammatory responses to the COVID-19 vaccine. In part B, participants will be randomised to receive 3 days of either nitrate-containing beetroot juice (intervention) or nitrate-deplete beetroot juice (placebo). The primary outcome for both sub-studies is a comparison of the change in flow-mediated dilatation (FMD) from baseline after COVID-19 vaccination. The study has a power of > 80% to assess the primary endpoint. Secondary endpoints include change from baseline in inflammatory and leukocyte counts and in pulse wave analysis (PWA) and pulse wave velocity (PWV) following the COVID-19 vaccination.

This study aims to evaluate whether sex or dietary influences endothelial function and inflammatory responses in healthy volunteers after receiving the COVID-19 vaccine.

ClinicalTrials.gov NCT04889274. Registered on 5 May 2023. The study was approved by the South Central - Oxford C Research Ethics Committee (21/SC/0154).

Although a novel oral antiviral agent can improve short-term COVID-19 outcomes, its effects on the long-term outcomes, namely the risk of major adverse cardiovascular events (MACEs), remains unknown. This retrospective cohort study used the TriNetX research network to identify nonhospitalized adult patients with COVID-19 between March 1, 2020, and January 1, 2022. A propensity score matching method was used to form two matched cohorts with and without receiving nirmatrelvir-ritonavir (NMV-r) or molnupiravir. The primary outcome was the incidence of MACEs within a 30-day to 1-year period following a diagnosis of COVID-19. Two cohorts of each 80 888 patients with balanced baseline characteristics were formed using propensity score matching. During the follow-up period, 976 patients in the study group and 1609 patients in the control group developed MACE. Overall, the study group had a significantly lower risk of MACE than the control group (hazard ratio [HR], 0.683; 95% confidence interval: 0.630-0.739). The significantly lower HRs of overall MACEs were consistently observed in most subgroup analyses (age: >41-≤64 years: 0.60 [0.52-0.89]; age: ≥65 years: 0.68 [0.62-0.76]; women: 0.63 [0.57-0.71]; men: 0.62 [0.55-0.70]; vaccinated: 0.74 [0.63-0.88]; unvaccinated: 0.66 [0.60-0.73]; NMV-r; 0.65 [0.59-0.71]; and molnupiravir: 0.75 [0.61-0.92]). In conclusion, novel oral antiviral agents, namely NMV-r and molnupiravir, were effective in reducing long-term MACEs among nonhospitalized patients with COVID-19, particularly when treated with NMV-r or in patients aged ≥40 years. These findings suggest the potential role of novel antiviral agents as a preventive measure to reduce further adverse cardiovascular outcomes.

The Brugada syndrome is an uncommon inherited condition associated with increased risk of ventricular tachyarrhythmias and sudden cardiac death. Different triggers including fever are well known to precipitate the Brugada pattern on electrocardiogram. We report a patient who presents with syncope, two days after the first dose of the BNT162b2 vaccine due to fever-related unmasking of Brugada syndrome.

Cardiotoxicity from first-generation H1-antihistamines has been debated since the 1990s. However, large-scale studies on this topic in a general pediatric population are lacking. This study aimed to assess the association between first-generation H1-antihistamine use and cardiovascular events in a nationwide pediatric population. In this case-crossover study, the main cohort included children with cardiovascular events from the National Health Insurance Service database (2008-2012 births in Korea) until 2018. The second cohort excluded children with specific birth histories or underlying cardiovascular diseases from the main cohort. Cardiovascular events of interest included cardiac arrhythmia and ischemic heart disease. Odds ratios (ORs) of cardiovascular events were estimated using conditional logistic regression models, comparing first-generation H1-antihistamine use during 0-15 days before cardiovascular events (hazard period) with use during 45-60 and 75-90 days before events (control periods). Among the participants, 1194 (59.9%) were aged 24 months to 6 years, and 1010 (50.7%) were male. Cardiovascular event risk was increased among users of first-generation H1-antihistamines (adjusted OR [aOR], 1.201; 95% confidence interval, 1.13-1.27). Significant odds of cardiovascular events persisted within 10 and 5 days (aOR, 1.25 and 1.25). In the second cohort, the association was comparable with that in the main cohort. Our findings indicate that cardiovascular event risk is increased in children who are administered first-generation H1-antihistamines.

Introduction: While acute Coronavirus disease 2019 (COVID-19) affects the cardiovascular (CV) system according to recent data, an increased CV risk has been reported also during long-term follow-up (FU). In addition to other CV pathologies in COVID-19 survivors, an enhanced risk for arrhythmic events and sudden cardiac death (SCD) has been observed. While recommendations on post-discharge thromboprophylaxis are conflicting in this population, prophylactic short-term rivaroxaban therapy after hospital discharge showed promising results. However, the impact of this regimen on the incidence of cardiac arrhythmias has not been evaluated to date. Methods: To investigate the efficacy of this therapy, we conducted a single center, retrospective analysis of 1804 consecutive, hospitalized COVID-19 survivors between April and December 2020. Patients received either a 30-day post-discharge thromboprophylaxis treatment regimen using rivaroxaban 10 mg every day (QD) (Rivaroxaban group (Riva); n = 996) or no thromboprophylaxis (Control group (Ctrl); n = 808). Hospitalization for new atrial fibrillation (AF), new higher-degree Atrioventricular-block (AVB) as well as incidence of SCD were investigated in 12-month FU [FU: 347 (310/449) days]. Results: No differences in baseline characteristics (Ctrl vs Riva: age: 59.0 (48.9/66.8) vs 57 (46.5/64.9) years, p = n.s.; male: 41.5% vs 43.7%, p = n.s.) and in the history of relevant CV-disease were observed between the two groups. While hospitalizations for AVB were not reported in either group, relevant rates of hospitalizations for new AF (0.99%, n = 8/808) as well as a high rate of SCD events (2.35%, n = 19/808) were seen in the Ctrl. These cardiac events were attenuated by early post-discharge prophylactic rivaroxaban therapy (AF: n = 2/996, 0.20%, p = 0.026 and SCD: n = 3/996, 0.30%, p < 0.001) which was also observed after applying a logistic regression model for propensity score matching (AF: χ ²-statistics = 6.45, p = 0.013 and SCD: χ ²-statistics = 9.33, p = 0.002). Of note, no major bleeding complications were observed in either group. Conclusion: Atrial arrhythmic and SCD events are present during the first 12 months after hospitalization for COVID-19. Extended prophylactic Rivaroxaban therapy after hospital discharge could reduce new onset of AF and SCD in hospitalized COVID-19 survivors.

Since the pandemic in 2019, coronavirus 2019 (COVID-19) has continued to be linked with a variety of organ systems and complications. While it is generally considered a respiratory disease, its link with the heart is widely discussed in the literature. This article focuses on the acute cardiovascular complications of COVID-19 and the possible predictors of these complications. Our study included 97 articles (58 case reports, eight case series, 23 retrospective cohort studies, five prospective cohort studies, and three cross-sectional studies). Several mechanisms have been proposed to explain COVID-19-induced cardiovascular complications, with cytokine-induced inflammation and direct cardiac damage noted as the significant focus. Patients with underlying cardiovascular complications such as hypertension and diabetes were noted to be at increased risk of acute cardiovascular complications, as well as an increased risk of severe disease and death. Also, acute myocardial infarction and arrhythmias were two of the most common acute cardiovascular complications noted in our review. Other acute cardiovascular complications are myocarditis, takotsubo syndrome, acute thromboembolic events, and pericardial complications. This article provides an updated review of acute cardiovascular complications of COVID-19, its pathogenesis, and risk stratification and emphasizes the need for high suspicion in patients with underlying cardiovascular risk factors.

Background: Atrial fibrillation (AF) has been described as a common cardiovascular manifestation in patients suffering from coronavirus disease 2019 (COVID-19) and has been suggested to be a potential risk factor for a poor clinical outcome. Methods: In this observational study, all patients hospitalized due to COVID-19 in 2020 in the Cantonal Hospital of Baden were included. We assessed clinical characteristics, in-hospital outcomes as well as long-term outcomes with a mean follow-up time of 278 (±90) days. Results: Amongst 646 patients diagnosed with COVID-19 (59% male, median age: 70 (IQR: 59-80)) in 2020, a total of 177 (27.4%) patients were transferred to the intermediate/intensive care unit (IMC/ICU), and 76 (11.8%) were invasively ventilated during their hospitalization. Ninety patients (13.9%) died. A total of 116 patients (18%) showed AF on admission of which 34 (29%) had new-onset AF. Patients with COVID-19 and newly diagnosed AF were more likely to require invasive ventilation (OR: 3.5; p = 0.01) but did not encounter an increased in-hospital mortality. Moreover, AF neither increased long-term mortality nor the number of rehospitalizations during follow-up after adjusting for confounders. Conclusions: In patients suffering from COVID-19, the new-onset of AF on admission was associated with an increased risk of invasive ventilation and transfer to the IMC/ICU but did not affect in-hospital or long-term mortality.

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality, imposing an increasing global health burden. Cardiac ion channels (voltage-gated Na_V, Ca_V, K_Vs, and others) synergistically shape the cardiac action potential (AP) and control the heartbeat. Dysfunction of these channels, due to genetic mutations, transcriptional or post-translational modifications, may disturb the AP and lead to arrhythmia, a major risk for CVD patients. Although there are five classes of anti-arrhythmic drugs available, they can have varying levels of efficacies and side effects on patients, possibly due to the complex pathogenesis of arrhythmias. As an alternative treatment option, Chinese herbal remedies have shown promise in regulating cardiac ion channels and providing anti-arrhythmic effects. In this review, we first discuss the role of cardiac ion channels in maintaining normal heart function and the pathogenesis of CVD, then summarize the classification of Chinese herbal compounds, and elaborate detailed mechanisms of their efficacy in regulating cardiac ion channels and in alleviating arrhythmia and CVD. We also address current limitations and opportunities for developing new anti-CVD drugs based on Chinese herbal medicines.

Background: The risk for worse outcomes of COVID-19 (Coronavirus 2019 disease) is higher in patients with cardiac conditions. In this study, we aim to investigate the risks of COVID-19-induced conditions in cases with underlying heart failure. Methods: We systematically searched PubMed, Scopus, Ovid, ProQuest, Web of Science, and the Cochrane library, to collect the English language articles that investigated patients with underlying heart failure who get infected by COVID-19. The second version of comprehensive meta-analysis (CMA.2) software was used to conduct the meta-analysis. Results: From 5997 publications, our eligibility criteria were met by 27 studies. Overall, outcomes investigated in all studies include but are not limited to mortality rate, length of hospitalization, need for Intensive care unit (ICU) admission, need for mechanical ventilation, and major cardiovascular conditions. Regarding mortality heart failure patients were more susceptible to death (OR:2.570, 95%CI: 2.085 to 3.169; p-value:<0.001). Also in heart failure patients, the risk of mechanical ventilation was higher (OR:1.707, 95%CI: 1.113 to 2.617; p-value: 0.014). Conclusion: Pre-existing heart failure is associated with the increased risk of mortality and the need for mechanical ventilation while getting infected with COVID-19. Finding an answer to determine the risk of hospitalization, length of stay, readmission rate, and multiorgan failure is necessary for further development of preventive care and making a plan for providing optimal healthcare facilities for these patients.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), is known to affect the cardiovascular system. Cardiac manifestations in COVID-19 can be due to direct damage to the myocardium and conduction system as well as by the disease's effect on the various organ systems. These manifestations include acute coronary syndrome, ST- segment elevations, cardiomyopathy, and dysrhythmias. Some of these dysrhythmias can be detrimental to the patient. Therefore, it is important for the emergency physician to be aware of the different arrhythmias associated with COVID-19 and how to manage them. This narrative review discusses the pathophysiology underlying the various arrhythmias associated with COVID-19 and their management considerations.

A 28-year-old G2P0010 woman with a history of COVID infection during her current pregnancy treated with monoclonal antibodies and benign gestational thrombocytopenia presented for routine prenatal care at 33 weeks' gestation. The patient was asymptomatic, but incidental tachycardia was noted on the physical exam with an irregular rhythm. An electrocardiogram (ECG) was performed and was consistent with multifocal atrial tachycardia at a rate of 144 beats per minute. The patient was started on labetalol 50 mg daily and was referred to cardiology for consultation. An echocardiogram was performed and showed dilated left ventricular cavity with a moderately reduced ejection fraction of 40%. No previous echocardiogram was available for comparison; the patient had no history of cardiac disease. The dose of labetalol was increased to 50 mg twice daily and she was admitted for digoxin loading and titration. Though fetal tolerance was excellent, her heart rate was not controlled. Digoxin was switched to flecainide and labetalol was switched to metoprolol which improved her heart rate and repeat echocardiogram showed an ejection fraction of 50%. The patient was admitted for induction of labor at 39 weeks of gestation and continued intrapartum flecainide. Metoprolol was continued intra and postpartum. Flecainide was resumed at three days postpartum due to the recurrence of atrial tachycardia and has been maintained. A repeat echocardiogram is scheduled six weeks postpartum to evaluate left ventricular function and wean off antiarrhythmics.

Brugada syndrome (BRS) is a channelopathy with three characteristic electrocardiogram patterns and an increased risk of sudden cardiac death (SCD), in the absence of gross structural heart disease. Fever is shown to precipitate ventricular arrhythmias in patients with BRS. Here, we report a rare case of Brugada pattern in a patient with Coronavirus Disease 2019 (COVID-19) without fever. A baseline ECG should be considered for patients with COVID-19, even in the absence of fever. COVID-19 by itself may be a factor that can induce Brugada pattern ECGs.

Activin A has been linked to cardiac dysfunction in aging and disease, with elevated circulating levels found in patients with hypertension, atherosclerosis, and heart failure. Here, we investigated whether Activin A directly impairs cardiomyocyte (CM) contractile function and kinetics utilizing cell, tissue, and animal models. Hydrodynamic gene delivery-mediated overexpression of Activin A in wild-type mice was sufficient to impair cardiac function, and resulted in increased cardiac stress markers (N-terminal pro-atrial natriuretic peptide) and cardiac atrophy. In human-induced pluripotent stem cell-derived (hiPSC) CMs, Activin A caused increased phosphorylation of SMAD2/3 and significantly upregulated SERPINE1 and FSTL3 (markers of SMAD2/3 activation and activin signaling, respectively). Activin A signaling in hiPSC-CMs resulted in impaired contractility, prolonged relaxation kinetics, and spontaneous beating in a dose-dependent manner. To identify the cardiac cellular source of Activin A, inflammatory cytokines were applied to human cardiac fibroblasts. Interleukin -1β induced a strong upregulation of Activin A. Mechanistically, we observed that Activin A-treated hiPSC-CMs exhibited impaired diastolic calcium handling with reduced expression of calcium regulatory genes (SERCA2, RYR2, CACNB2). Importantly, when Activin A was inhibited with an anti-Activin A antibody, maladaptive calcium handling and CM contractile dysfunction were abrogated. Therefore, inflammatory cytokines may play a key role by acting on cardiac fibroblasts, causing local upregulation of Activin A that directly acts on CMs to impair contractility. These findings demonstrate that Activin A acts directly on CMs, which may contribute to the cardiac dysfunction seen in aging populations and in patients with heart failure.

Cardiovascular complications of severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) infection are well-described in the general population but remain limited among pregnant patients. This review summarizes data from case reports, case series, and observational studies of cardiovascular manifestations of corona virus disease 2019 (COVID-19) in pregnant patients and provides recommendations to the cardiovascular clinician regarding management considerations in this vulnerable population. Pregna is an immunocompromised state in which cardiovascular demands are increased. Cardiovascular complications of COVID-19 that have been described in pregnancy include myocardial injury, cardiomyopathy, thromboembolism, pre-eclampsia and arrhythmia. Physiologic and cardiovascular changes in pregnancy predispose pregnant patients with COVID-19 to more severe illness than the general population. Black or Hispanic race, obesity, diabetes, hypertension and lung disease are risk factors for more severe infection, maternal death and adverse perinatal outcomes. Pregnant patients with severe COVID-19 disease compared with non-pregnant age-matched women with COVID infection are more likely to be admitted to the intensive care unit (ICU), receive mechanical ventilation and require advanced mechanical circulatory support. Cardiovascular complications of COVID-19 in pregnant patients requires further attention, particularly given the anticipated increase in birth volume and ongoing nature of COVID-19 pandemic with novel variants. Clinicians should have a lower threshold for cardiac testing and multidisciplinary management in pregnant women with severe COVID-19 disease. Given the persistence of COVID-19 within our communities, diagnostic laboratory and imaging testing for high-risk pregnant patients hospitalized with COVID-19 infection should be routine. We strongly urge the implementation of a cardio-obstetric multidisciplinary team in individually managing these high-risk patients in an effort to improve maternal and fetal outcomes.

603,711,760 confirmed cases of COVID-19 have been reported throughout the world and 6,484,136 individuals have died from complications of COVID-19 as of September 7, 2022. Significantly, the Omicron variant has produced the largest number of COVID-19 associated hospitalizations since the beginning of the pandemic. Cardiac injury occurs in ≥20% of the hospitalized patients with COVID-19 and is associated with cardiac dysrhythmias in 17 to 44%, cardiac injury with increases in blood troponin in 22 to 40%, myocarditis in 2 to 7%, heart failure in 4 to 21%, and thromboembolic events in 15 to 39%. Risk factors for cardiac complications include age >70 years, male sex, BMI ≥30 kg/m2, diabetes, pre-existing cardiovascular disease, and moderate to severe pneumonia at hospital presentation. Patients with prior cardiovascular disease who contract COVID-19 and experience a significant increase in their blood troponin concentration are at risk for mortality rates as high as 69%. This review focuses on the prevalence, the pathophysiologic mechanisms of CoV-2 injury to the cardiovascular system and the current recommended treatments in hospitalized patients with COVID-19 in order that medical personnel can decrease the morbidity and mortality of patients with COVID-19 and effectively treat patients with Covid and post Covid syndrome.

Diagnosing COVID-19 accurately and rapidly is vital to control its quick spread, lessen lockdown restrictions, and decrease the workload on healthcare structures. The present tools to detect COVID-19 experience numerous shortcomings. Therefore, novel diagnostic tools are to be examined to enhance diagnostic accuracy and avoid the limitations of these tools. Earlier studies indicated multiple structures of cardiovascular alterations in COVID-19 cases which motivated the realization of using ECG data as a tool for diagnosing the novel coronavirus. This study introduced a novel automated diagnostic tool based on ECG data to diagnose COVID-19. The introduced tool utilizes ten deep learning (DL) models of various architectures. It obtains significant features from the last fully connected layer of each DL model and then combines them. Afterward, the tool presents a hybrid feature selection based on the chi-square test and sequential search to select significant features. Finally, it employs several machine learning classifiers to perform two classification levels. A binary level to differentiate between normal and COVID-19 cases, and a multiclass to discriminate COVID-19 cases from normal and other cardiac complications. The proposed tool reached an accuracy of 98.2% and 91.6% for binary and multiclass levels, respectively. This performance indicates that the ECG could be used as an alternative means of diagnosis of COVID-19.

Throughout 2021, the medical and scientific communities have focused on managing the acute morbidity and mortality caused by the coronavirus disease 2019 (COVID-19) pandemic. With the approval of multiple vaccines, there is a light at the end of this dark tunnel and an opportunity to focus on the future, including managing the long-term sequelae in patients who have survived acute COVID-19. In this Perspectives article, we highlight what is known about the cardiovascular sequelae in survivors of COVID-19 and discuss important questions that need to be addressed in prospective studies to understand and mitigate these lasting cardiovascular consequences, including in post-acute COVID-19 syndrome. To provide the greatest benefit to these survivors, prospective studies should begin now, with resources made available to monitor and study this population in the coming years.

The clinical characteristics of COVID-19 are diverse from a simple common cold symptom to acute respiratory distress syndrome (ARDS). In the present study, we attempted to identify the associated factors in surviving COVID-19 intensive care unit (ICU) patients based on their clinical characteristics.

This retrospective study was performed on 114 laboratory-confirmed COVID-19 patients admitted to the intensive care units of Hormozgan University of Medical Sciences, Iran. Demographic, medical, clinical manifestations at admission time, and outcome data were obtained from the patient's medical records.

Of 114 participants included in this study, 64.9% were men. Their mean age was approximately 54 years old, 69.3% of them died and 30.7% of them were discharged. The mortality rate was 2.96 times higher in people who had ARDS compared to their counterparts, 1.37 times higher in people under non-invasive ventilation, and 3.56 times higher in people under invasive mechanical ventilation.Three common underlying diseases among them were hypertension in 34.2%, diabetes in 23.7%, and cardiovascular diseases in 17.5% of them. Alive and dead patients significantly differed only in the following laboratory tests: D-dimer, urea, troponin, Procalcitonin, and ferritin.

The mortality rate among COVID-19 patients admitted to ICU is generally high. Dyspnea, as the initial presentation and comorbidity, especially hypertension, diabetes, and cardiovascular diseases, may be associated with a higher risk of developing severe disease and consequent mortality. Therefore, D-dimer, urea, troponin, Procalcitonin, and ferritin at the time of hospital admission could predict the severity of the disease and its probable mortality.

COVID-19 is a dynamic disease and may affect different tissues and organs as it progresses. Therefore, the impact generated by the disease in all its stages and organs requires a functional and versatile imaging technique able to detect particularities or artifacts dynamically. Ultrasonography fulfills all these requirements and exhibit several advantages relative to other imaging modalities, including portability, lower cost and biosafety. Throughout the COVID-19 pandemic, ultrasonography displayed a crucial role in the triage, monitoring, indicating organ damages and enabling individualized therapeutical decisions in COVID-19 patients. This review is dedicated to highlight the main pathological effects correlated with ultrasound changes caused by COVID-19 in the lungs, heart and liver.

Arrhythmia is a very common complication of coronavirus disease 2019 (COVID-19); however, the prevalence of ventricular arrhythmia and associated outcomes are not well-explored. Here, we conducted a systematic review and meta-analysis to determine the prevalence and associated death of ventricular arrhythmia and sudden cardiac death (SCD) in patients with COVID-19.

Databases of PubMed, Cochrane Library, Embase, and MdeRxiv were searched. Studies that could calculate the prevalence of ventricular arrhythmia/SCD during hospital admission or associated death in patients with COVID-19 were included. The study was registered with the PROSPERO (CRD42021271328).

A total of 21 studies with 13,790 patients were included. The pooled prevalence of ventricular arrhythmia was 5% (95% CI: 4-6%), with a relatively high-SCD prevalence (1.8% in hospitalized COVID-19 and 10% in deceased cases of COVID-19). Subgroup analysis showed that ventricular arrhythmia was more common in patients with elevated cardiac troponin T [ES (effect size): 10%, 95% CI: -0.2 to 22%] and in European (ES: 20%, 95% CI: 11-29%) populations. Besides, ventricular arrhythmia was independently associated with an increased risk of death in patients with COVID-19 [odds ratio (OR) = 2.83; 95% CI: 1.78-4.51].

Ventricular arrhythmia and SCD resulted as a common occurrence with a high prevalence in patients with COVID-19 admitted to the hospital. Furthermore, ventricular arrhythmia significantly contributed to an increased risk of death in hospitalized patients with COVID-19. Clinicians might be vigilant of ventricular arrhythmias for patients with COVID-19, especially for severe cases.

www.york.ac.uk/inst/crd, identifier: CRD42021271328.

Many types of cardiac arrhythmias can occur in people with COVID-19, and these arrhythmias can affect the patient's outcomes. We have experienced paroxysmal complete atrioventricular block in a patient with COVID-19 and would like to share the course of treatment.

The aim of this study is to develop and validate a scoring system as a tool for predicting the in-hospital mortality in COVID-19 patients in early stage of disease.

This retrospective cohort study, conducted on 893 COVID-19 patients in Tehran from February 18 to July 20, 2020. Potential factors were chosen via stepwise selection and multivariable logistic regression model. Cross-validation method was employed to assess the predictive performance of the model as well as the scoring system such as discrimination, calibration, and validity indices.

The COVID-19 patients' median age was 63 yrs (54.98% male) and 233 (26.09%) patients expired during the study. The scoring system was developed based on 8 selected variables: age ≥55 yrs (OR = 5.67, 95% CI: 3.25-9.91), males (OR = 1.51, 95% CI: 1.007-2.29), ICU need (OR = 16.32, 95% CI 10.13-26.28), pulse rate >90 (OR = 1.89, 95% CI: 1.26-2.83), lymphocytes <17% (OR = 2.33, 95%CI: 1.54-3.50), RBC ≤4, 10 6/L (OR = 2.10, 95% CI: 1.35-3.26), LDH >700 U/L (OR = 1.68, 95%CI: 1.13-2.51) and troponin I level >0.03 ng/mL (OR = 1.75, 95%CI: 1.17-2.62). The AUC and the accuracy of scoring system after cross-validation were 79.4% and 79.89%, respectively.

This study showed that developed scoring system has a good performance and can use to help physicians for identifying high-risk patients in early stage of disease .

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also known as COVID-19, emerged in late 2019 in Wuhan, China. The World Health Organization declared the virus a pandemic on March 11, 2020. Disease progression from COVID-19 infection has shown significant symptom manifestations within organ systems beyond the respiratory system. The literature has shown increasing evidence of cardiovascular involvement during disease course and an associated increase in mortality among infected patients. Although the understanding of this novel virus is continually evolving, it is currently proposed that the mechanism by which the SARS-CoV-2 virus contributes to cardiovascular manifestations involves the ACE2 transmembrane protein. The protein ACE2 is highly expressed in blood vessel pericytes, and infection can result in microvascular dysfunction and subsequent acute coronary syndromes. Complications involving the cardiovascular system include myocardial infarction, arrhythmias, shock, and heart failure. In this evidence-based review, we discuss risk factors of cardiovascular involvement in COVID-19 infection, pathophysiology of COVID-19-related cardiovascular infection, and injury, COVID-19 effects on the cardiovascular system and corresponding treatments, and hematologic effects of COVID-19 and COVID-19 in heart transplant patients. Clinicians managing COVID-19 patients should appreciate the potential cardiovascular effects related to the disease process.

The antiviral medication "favipiravir" should be considered as a possible cause of unexplained sinus bradycardia.

The emergence of the novel SARS coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has resulted in an unprecedented pandemic that has been accompanied by a global health crisis. Although the lungs are the main organs involved in COVID-19, systemic disease with a wide range of clinical manifestations also develops in patients infected with SARS-CoV-2. One of the major systems affected by this virus is the cardiovascular system. The presence of preexisting cardiovascular disease increases mortality in patients with COVID-19, and cardiovascular injuries, including myocarditis, cardiac rhythm abnormalities, endothelial cell injury, thrombotic events, and myocardial interstitial fibrosis, are observed in some patients with COVID-19. The underlying pathophysiology of COVID-19-associated cardiovascular complications is not fully understood, although direct viral infection of myocardium and cytokine storm have been suggested as possible mechanisms of myocarditis. In this Review, we summarize available data on SARS-CoV-2-related cardiac damage and discuss potential mechanisms of cardiovascular implications of this rapidly spreading virus.

COVID-19 has emerged as one of the most devastating and clinically significant infectious diseases of the last decade. It has reached global pandemic status at an unprecedented pace and has placed significant demands on health care systems worldwide. Although COVID-19 primarily affects the lungs, epidemiologic reports have shown that the disease affects other vital organs of the body, including the heart, vasculature, kidneys, brain, and the hematopoietic system. Of importance is the emerging awareness of the effects of COVID-19 on the cardiovascular system. The current state of knowledge regarding cardiac involvement in COVID-19 is presented in this article, with particular focus on the cardiovascular manifestations and complications of COVID-19 infection. The mechanistic insights of disease causation and the relevant pathophysiology involved in COVID-19 as they affect the heart are explored and described. Relevant practice essentials and clinical management implications for patients with COVID-19 with a cardiac pathology are presented in light of recent evidence.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 (COVID-19), has been associated with a broad spectrum of cardiac manifestations ranging from myocardial injury and heart failure to cardiac arrhythmias. In this report, we present a rare case of sinus node dysfunction/asystole in a young patient without any known history of coronary artery disease or cardiac arrhythmias, which necessitated pacemaker placement.