COVID-19 prevention methods such as masking and social distancing also suppressed the circulation of common respiratory diseases, leaving young children lacking immunity to pathogens they otherwise would have been exposed to, a new multicenter clinical research study reveals. The investigators say their findings help explain the large post-pandemic rebound in these diseases and enable more accurate predictions for the future.
The study, published Aug. 6 in The Lancet Infectious Diseases and funded by the National Institutes of Health, followed 174 children under the age of 10 from 2022-23 across four academic medical centers across the country: Weill Cornell Medicine; University of Colorado Anschutz Medical Campus and Children’s Hospital Colorado; University of North Carolina; and the University of Alabama, Birmingham. Through repeat blood sampling and respiratory sampling during illness, the investigators gauged the children’s level of immunity to many common and emerging respiratory viruses, such as RSV (respiratory syncytial virus), influenza and enterovirus D68 (EV-D68), which can cause the polio-like illness acute flaccid myelitis.
The findings, among the first from the National Institutes of Health’s PREMISE (Pandemic Response Repository through Microbial and Immune Surveillance and Epidemiology) Program, showed that most young children lacked immunity to many normal respiratory viruses during the pandemic, suggesting they had not been exposed, as they typically would have, due to prevention measures in place. Enrolled children received routine medical care while participating in the observational study. Following the lifting of pandemic measures, the level of immunity rose across all pathogens studied, reflective of the unprecedented widespread resurgence of these viruses in children post-pandemic.
“PREMISE is a one-of-a-kind study as we followed very young children, with their parents’ consent, over a year for longitudinal sample collection, affording us the unique opportunity to assess immunity due to primary infection, re-exposure and even vaccination, during a time when mask requirements and other nonpharmaceutical interventions were lifted,” said co-first author Dr. Perdita Permaul, section chief of pediatric allergy and immunology, associate professor of clinical pediatrics and trial principal investigator at Weill Cornell Medicine.
The data allowed experts to recreate past circulation patterns and model predictions for future outbreaks with greater accuracy and precision. They showed that PREMISE data from 2022-23 could be used to accurately predict the subsequent wave of disease of the emerging pathogen EV-D68 that occurred in 2024.
“Findings from our study successfully demonstrate the utility of longitudinal immunologic surveillance in children, particularly young immunologically naïve unexposed children, to help model the behavior of endemic viruses,” said Permaul, who is also an Englander Clinical Scholar at Weill Cornell Medicine and a pediatric allergist and immunologist at NewYork-Presbyterian Komansky Children’s Hospital of Children’s Hospital of New York.
Investigators have so far evaluated nearly 1,000 children through PREMISE, based at NIH’s Vaccine Research Center, providing a treasure trove of sampling and data that can be used to learn which parts of viruses the human immune system attacks to develop immunity. This information may enable teams to better design new antibody treatments and effective vaccines to mimic this response.
“This approach allows for the rapid development of vaccine and monoclonal antibody therapeutics for pathogens of interest in children,” Permaul said. “Future analysis of blood samples collected from almost 1,000 children enrolled in PREMISE includes pathogen-specific T and B cell responses. Longitudinal immune surveillance in young children is an important tool for informing public health planning, assessing the effectiveness of pharmacologic and non-pharmacological interventions, developing ‘on the shelf’ therapeutics and mitigating overall disease burden.”
This study was funded by a subcontract with Frederick National Laboratory for Cancer Research (FNLCR), currently operated by Leidos Biomedical Research, Inc. through Agreement 21X192QT1. FNLCR funding was provided by the NIH’s Vaccine Research Center. The total project funding is $7.98 million over five years. No financing for this project is supplied by nongovernmental sources.
A version of this story first appeared on Children’s Hospital Colorado’s Newsroom.
Alyssa Sunkin-Strube is assistant director of editorial at Weill Cornell Medicine.
After first emerging in Wuhan, China, a pandemic was swiftly turned into a novel coronavirus (SARS-CoV-2) toward the end of 2019 and caused severe impacts on health and economic systems worldwide. SARS-CoV-2 is also named COVID-19 and affects the respiratory system most, but the disease effects are not limited to the lungs. Venous thromboembolism, acute kidney and liver damage, the release of cytokines, sepsis, disseminated intravascular coagulation, complications of pregnancy, and cardiac and neurological issues are all possible outcomes of a COVID-19 infection, in addition to pulmonary involvement.1
According to a report published in Wuhan, China, arrhythmia was found in 16.7% of hospitalized patients with COVID-19 and 44.4% of those monitored in intensive care.2 Although some studies conducted to date have revealed some clues about the potential for arrhythmia in individuals who have active disease, as of today, we are far from being able to explain why individuals who have completely recovered from the disease apply to outpatient clinics with complaints of palpitations.3,4
Heart rate turbulence (HRT) originates from the principle of accelerating sinus rhythm, which occurs as a reflex due to the short diastole period during ventricular premature beat in patients with sinus rhythm. In a healthy heart, there is an acceleration in ventricular rate and there is a degree of this acceleration. HRT indicates this degree of acceleration. In other words, it shows the autonomic activity of the heart. For an healthy HRT both the sympathetic and parasympathetic pathways of the heart must be intact.5 Abnormal HRT, which can occur due to many diseases, indicates decreased baroreflex sensitivity and autonomic dysfunction. It is well established that individuals with blunted HRT are more likely to die suddenly and from all causes.6
It has been revealed by the recent research on holter and pace that HRT is also impaired after atrial premature stimulation. Impaired HRT values, suggesting that the spontaneous emergence of clinical atrial fibrillation is associated with a brief increase in vagal outflow following early atrial excitement.7,8
Conditions where a range of symptoms persist for more than three months after recovery from acute COVID-19 are called Long-COVID.9 Long-COVID-19 may manifest itself with symptoms, such as chest pain, palpitations, cognitive disorders, breath shortness, fatigue, attention deficit, hair loss, headache, myalgia, and arthralgia.9–12
Recently, there has been an increase in the admission of patients who recovered from COVID-19 to the clinic complaining of palpitations and that these patients are referred to another departments with the preliminary diagnosis of somatization or panic disorder. Could a more sensitive assessment be made for these individuals? Could SARS-CoV-2 cause permanent damage to the autonomic nervous system (ANS) and predisposition to atrial fibrillation? This study utilized HRT to analyze the persistent impacts of SARS-CoV-2 on cardiac autonomic function in individuals recovered from COVID-19.
This retrospective study analyzed the records of 10,081 participants who visited the cardiology outpatient clinics at Elazığ Fethi Sekin City Hospital between June 1, 2022, and December 31, 2024, and underwent a 24-hour ECG Holter monitoring.
A total of 328 patients with a history of positive SARS-CoV-2 test results by at least one Real-Time (RT)-PCR test on nasopharyngeal swabs (Bio-Rad CFX96 RT PCR Detection System, Bio-Rad Laboratories, Inc., Hercules, CA, USA) were included in the Recovered COVID-19 group. A total of 407 individuals with no history of positive (RT)-PCR test results for SARS-CoV-2 during the same time period and no cardiac or systemic disease (other than hypertension) detected by physical examination, laboratory tests, or anamnesis were included in the control group (Figure 1).
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Figure 1 The Subjects inclusion flowchart diagram.
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Subjects with inadequate data in their files, were under 17 years old, those with atrial fibrillation, electrolyte imbalance, structural heart disease, heart valve disease, or systemic disease (apart from hypertension), individuals using anti-arrhythmic medications or agents that may lead to arrhythmia (such as terfenadine, probucol, erythromycin, amiodarone, antidepressants, clarithromycin, and antipsychotics), professional athletes, patients with a body mass index (BMI) above than 35, and pregnant women were excluded.
SARS-CoV-2 was caught at least once and no more than three times by the subjects in the COVID-19 recovery group. Individuals in the recovered COVID-19 group had a minimum of 4 weeks and a maximum of 204 weeks between 24-hour ECG-Holter evaluation and their most recent positive RT-PCR test.
The recovered COVID-19 group was given a semi-quantitative chest CT severity score for each of the five lung lobes (two on the left and three on the right). Visual assessment was used to determine each lobe’s percentage of involvement. The chest severity score was obtained by adding the scores corresponding to the percentage of involvement of each lobe (Table 1).5
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Table 1 Semi-Quantitative Chest Computed Tomography (CT) Severity Score and Chest CT Severity Index
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Since COVID-19, which accompanies conditions such as chronic obstructive pulmonary disease and myocardial infarction, can cause severe respiratory distress and arterial blood values <90%, patients with concomitant systemic diseases were excluded from the study before their chest tomography was analyzed. Depending on their chest CT severity score, the recovered COVID-19 group was separated into three subgroups. Mild, moderate, and severe were the classifications assigned to group II (155 instances), group III (56 patients), and group IV (42 patients). Group II (modest): The CT severity score was classified as modest (<8). Group III (Moderate): The CT severity score fell within the moderate range.8–15 Group IV (Severe): According to Table 1, the CT severity score was rated as severe.16–25
The current research was carried out in compliance with the Declaration of Helsinki’s tenets. The Ethics Committee of T.C. Fırat University granted the ethical permission (No: 2021/12-45). In compliance with the confidentiality and compliance of patient data, patient consent was waived by the ethics committee due to the retrospective nature of the study and therefore patient consent was not obtained.
To describe supraventricular ectopic beats, R-R interval tachograms and 4-lead Holter recordings were simultaneously examined. If, in addition to the presence of definitive evidence of abnormal atrial depolarization, the R-R interval was shortened by at least 20%, an ectopic beat was classified as a supraventricular premature beat. Only isolated premature supraventricular ectopic beats with a significant post-ectopic pause were evaluated.7
To evaluate HRT, 24 hour electrocardiography (ECG)-Holter data were evaluated using a 4-lead Holter device (Digitrak XT, Philips Medical Systems, Andover, USA) and Cardioscan II premier software (firmware version C.2). HRT parameters were measured by the method reported by Bauer et al.6 Turbulence onset (TO), which represents the beginning the sinus rhythm acceleration phase, and turbulence slope (TS) which describes the deceleration phase, were the two numerical IDs employed for the measurement. The start of heart rate turbulence (HRT) was defined as the difference, expressed as a percentage, between the mean of the last 2 sinus rhythm RR intervals before the supraventricular ectopic beat and the mean of the first two sinus rhythm RR intervals following the compensatory pause following the supraventricular ectopic beat. HRT onset was computed with the help of the formula below:
RR −1 and RR-2 refer to the 2 RR intervals immediately before the supraventricular ectopic beat, and RR1 and RR2 refer to the 2 RR intervals immediately after the compensatory pause (Figure 2). The highest positive slope of a regression line assessed across any five consecutive sequences in the first fifteen consecutive sinus intervals following a supraventricular ectopic beat was defined as the turbulence slope (TS), expressed in milliseconds per beat. An HRT Slope of ≤2.5 ms/beat and an HRT Onset of ≥0% were considered abnormal.7
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Figure 2 Measurement of the interval between RR1, RR2 and RR −1, RR-2 for supraventricular ectopic beats from 24 Hour ECG-Holter.
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SPSS software (SPSS Inc., Chicago, IL, USA) version 27.0 was used for statistical analysis. The Kolmogorov–Smirnov test was employed to examine the ability of continuous variables to follow a normal distribution. Since all of the continuous variables showed abnormal distribution, for the one-way ANOVA test, Tamhane’s T2 correction was employed to analyze these parameters and the variables were shown as median with 25th–75th. For categorical variables, using the chi-square test, variations between groups in baseline characteristics were evaluated and were presented as numbers and percentages. Spearman’s Rho and Pearson’s correlation analysis were used to analyze the correlation between continuous variables. Binary logistic regression analysis was conducted to detect which variables would independently predict the presence of abnormal atrial HRT onset. Results were presented as hazard ratios and 95% CI. Linear regression analysis was utilized to detect which variables would independently affect atrial HRT onset value. Results were presented as unstandardized and standardized β coefficients. P values were always two-tailed, and statistical significance was defined as values below 0.05.
Of the 10081 cases whose 24-hour ECG Holter recordings were retrospectively examined, 735 (The controls: 407, The recovered COVID-19 group: 328) were taken in the research. All cases were separated into four groups (controls, recovered mild COVID-19, recovered moderate COVID-19, recovered severe COVID-19). Although the prevalence of abnormal atrial HRT Onset existence and atrial HRT Onset value were significantly higher in the recovered severe COVID-19 group compared to the other groups, no difference was found between the control and other Recovered COVID-19 groups (Table 2) (Figure 3). However, no difference was found among the control group and other Recovered COVID-19 groups in terms of abnormal atrial HRT Slope prevalence, atrial HRT Slope value, HT, smoking, age, and gender (Table 2).
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Table 2 Comparison of Atrial HRT Parameters Between Recovered COVID-19 Subgroups and the Control Group
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Figure 3 Comparison of Atrial HRT Onset values between the groups.
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Spearman’s rho and Pearson’s correlation analyses revealed a positive correlation between atrial HRT Onset and recovered COVID-19 subjects’ chest CT severity score and recovered COVID-19 subgroups, while no association was found between atrial HRT Onset and the Number of positive PCR tests for COVID-19 and time elapsed after COVID-19 (Table 3) (Figures 4 and 5).
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Table 3 Spearman’s Rho and Pearson’s Correlation Analyses Between Atrial HRT Onset Value and Some Other Variables
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Figure 4 Spearman’s rho correlation analyses between Atrial HRT Onset value and groups.
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Figure 5 Pearson’s correlation analyses between Atrial HRT Onset value and recovered COVID-19 subjects’ chest CT severity score.
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Regression analyses revealed that recovery from severe COVID −19, recovered COVID-19 subjects’ chest CT severity score, HT and smoking were predictors for abnormal atrial HRT onset existence and independently affected atrial HRT onset values (Table 4 and Table 5).
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Table 4 Model-1. Binary Logistic Regression for Variables (Dependent Variable: Abnormal Atrial HRT Onset Existence)
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Table 5 Model-2. Linear Regression for Variables (Dependent Variable: Atrial HRT Onset Value)
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It is clear from the table that the logistic model was developed to ascertain if the independent variables are useful in forecasting the existence of abnormalities. The model’s variables have a 19.7% explanatory power in predicting the existence of aberrant atrial HRT onset, and atrial HRT onset is significant (Model-1. p<0.001; Nagelke R2 = 0.197) (Table 4). As can be seen from the table, having a history of severe COVID-19 is a 3.851-fold risk factor for abnormal atrial HRT Onset existence compared to not having a history of severe COVID-19 (p=0.002).
The developed linear regression model is significant when Model-2 is analyzed, and its explanatory power for the impacts of its variables on the atrial HRT Onset value is 9.2% (p<0.001; Nagelke R2 = 0.092) (Table 5). The table shows that the recovered COVID-19 subjects’ chest CT severity value variable has a statistically significant effect on the abnormal HRT Onset value. In other words, a 1-point increase in chest severity scores of individuals recovering from COVID-19 increases the atrial HRT Onset value by 0.033 units (p<0.001).
This study revealed that atrial HRT values and the presence of abnormal atrial HRT onset were higher in individuals who had severe COVID-19 and recovered than in other individuals who did not have, while the atrial HRT slope value and the presence of abnormal atrial HRT slope did not differ between the groups (Table 2) (Figure 3). Although a positive connection was found among atrial HRT onset value/abnormal atrial HRT onset presence and subjects’ chest severity score and COVID-19 subgroups with correlation analyses, no association was detected between these parameters and having a positive PCR test record for SARS-CoV-2 and the time elapsed since COVID-19 (Table 3) (Figures 4 and 5). Furthermore, analyses of regression showed that recovered COVID-19 subjects’ chest CT severity score, recovering from severe COVID-19, smoking and HT were independent predictors of atrial HRT Onset value and abnormal atrial HRT onset presence (Table 4 and Table 5).
SARS-CoV-2 binds to cardiomyocytes, type 2 pneumocytes, macrophages, and perivascular pericytes by binding to transmembrane angiotensin-converting enzyme 2 (ACE2) following proteolytic cleavage of the S-protein by serine protease. ACE2 is required for viral invasion, and ACE2 protein is found in many tissues, including the myocardium and central nervous system (CNS).13,14 In addition to direct viral invasion of myocardial and coronary endothelial cells, systemic inflammation, inappropriate T helper cell response after cytokine storm, increased calcium in myocytes induced by hypoxia causing apoptosis, hypoxia due to cardiac and respiratory failure, increased adrenergic stimulation and increased endogenous stress hormones, electrolyte imbalance, and side effects of medications taken to treat COVID-19 may be shown among the causes of cardiac clinical pictures seen in COVID-19.15,16 Stromal edema in the heart, secondary to vasculitis resulting from monocyte and lymphocyte infiltration into arterial and venous endothelial cells, is considered another cause.17 It was thought that SARS-CoV-2 had neural invasion based on genomic sequencing from cerebrospinal fluid (CSF) obtained from patients diagnosed with encephalitis and the isolation of similar viruses in brain tissue during autopsy studies.18,19 Considering that ACE2 is found in the capillary endothelium, it is thought that COVID-19 can reach the CNS by damaging the blood-brain barrier in this way.20 Some studies suggest that SARS-CoV-2, like previously reported SARS-CoV, may pass through the cribriform plate of the ethmoid bone into the systemic circulation and the virus may perform central invasion through the microcapillary network between the blood circulation around the ethmoidal bone and the brain.21,22 According to another view, SARS-CoV-2 has the ability to invade peripheral nerve terminals and slowly progresses through the synapse-related pathway to reach the CNS. In this context, it has been previously shown that when SARS-CoV and MERS-CoV were administered to mice via the nasal route, the virus reached the brain through the olfactory nerves and then affected different brain regions, including the thalamus and brainstem.20,21 Apart from the direct entry of the virus into the nervous system, COVID-19 infection may cause neurological problems due to widespread cardiopulmonary failure and metabolic abnormalities triggered by infection of SARS-CoV-2 or as a result of autoimmune mechanisms.23 In particular, by producing more inflammatory cytokines, the cytokine storm that takes place during the illness stimulates T cells, macrophages, and endothelial cells. Then, by triggering vascular leakage, complement activity, and the coagulation cascade, elevated interleukin (IL)-6 release damages neurons and the brain.24
Turbulent in heart rate is a phenomena seen in electrocardiograms that reflects momentary hemodynamic disturbances resulting from ventricular premature beats and describes the short-term baroreflex-mediated variations in the duration of the sinus cycle that occur after spontaneous ventricular premature beats. When compared to the rate before the ventricular premature beats, the sinus rate in healthy persons temporarily increases, then decelerates, and finally returns to the basal rate.25 A momentary drop in blood pressure due to a ventricular premature beat activates baroreceptors, which in turn causes a decrease in the RR interval cycle lengths as determined by TO and an increase in heart rate brought on by vagal inhibition. Meanwhile, the ANS’s sympathetic arc is stimulated by temporary relative hypotension.26 Vascular resistance and systolic blood pressure gradually rise due to increased sympathetic activity. As a result, vagal activity rises once again and cycle durations are extended which is indicated as TS.26–29 Heart rate turbulence, therefore, requires a robust interaction of both the vagal and sympathetic systems. A change in either of these systems can result in the absence of normal heart rate turbulence.29 Some recent studies have shown that the HRT evaluation results performed by evaluating atrial premature beats in patients with supraventricular premature beats indicate blunted HRT and that these patients are prone to atrial fibrillation.7,8
A triggering focal activator and alterations in the atrial electrophysiologic characteristics that might sustain AF are both components of the pathophysiology of AF.30 According to experimental research, parasympathetic activation significantly reduces the atrial effective refractory period, which makes it easier for AF to start and continue.31,32 Premature beats are necessary in HR turbulence analysis, which examines changes in autonomic control over time. Therefore, by examining the changes in the HR turbulence measurements before the onset of AF, we attempted to test the hypothesis that modified vagal reactions to atrial premature beats might start before the onset of paroxysmal AF.7 A brief initial acceleration followed by a lengthier period of sinus rhythm slowdown characterizes the considered normal HRT response. This results in a negative TO in individuals with an intact HRT response and a higher TS response than those with an impaired HRT response. Therefore, both TO and TS parameters are considered to be related to the balanced functioning of the ANS and baroreflex sensitivity.33
If symptoms and signs persist for more than 12 weeks after COVID-19 infection and other causes are excluded, it is considered Long-COVID-19 syndrome.9 Although the pathogenesis of this period is not clear, persistent hyperinflammatory process, ongoing viral activity within the viral reservoir of the host, inadequate antibody response and enduring effects of tissue tropism are held responsible for the Long-COVID-19 syndrome. However, the presence and extent of organ damage, the variability in the time required for recovery of all organ systems, the severe acute disease period, intensive care syndromes, complications related to COVID-19 in the acute period, and the side effects of drugs used during the acute disease process are also factors.34 Long-COVID syndrome, the incidence of which varies between 10% and 60%, may include symptoms that concern many systems, such as fatigue, chest pain, shortness of breath, cough, decreased exercise intolerance, headache, and loss of taste and smell. In addition, palpitations, joint pain, muscle pain and weakness, insomnia, diarrhea, rash or hair loss, issues with balance and movement, issues with memory and focus, and cognitive problems, including deteriorating quality of life, can be observed.35 In COVID-19 individuals, sinus tachycardia is often the most prevalent arrhythmia.36 Nonetheless, the most likely pathogenic arrhythmias are ventricular tachycardia, atrial fibrillation, or atrial flutter.37,38 The pathophysiology of COVID-19-associated AF is not well understood, but some hypotheses that have been proposed include electrolyte and acid-base balance abnormalities that may occur in the acute phase of severe disease, increased adrenergic activation, decreased angiotensin-converting enzyme 2 (ACE2) receptor count, sialic acid-spike protein and CD147 interaction, and myocardial and endothelial damage caused by inflammatory cytokine storm.39 In the initial phase of severe COVID-19 illness, hypoxia and deficiencies in electrolytes have been commonly documented. These conditions are believed to lead to the emergence of abrupt arrhythmias.40 An arrhythmia occurring at this stage may persist in the post-COVID period and cause a feeling of palpitations. Several survey-based studies have reported that patients who had COVID-19 reported more complaints of palpitations than patients who had never had COVID-19.36,41 However, patients’ explanations of palpitations are subjective interpretations, differ based on how the questionnaire is designed, and are not supported by concrete electrocardiographic data. A recent study based on an online survey, in which no concrete electrocardiographic data were documented, suggested that the cause of these complaints reported by the participants was postural orthostatic tachycardia syndrome.36 As of today, objective ECG and Holter-ECG data are needed to show that subjective palpitation complaints described in the post-COVID-19 period indicate specific cardiac arrhythmias. A recently published study analyzing HRT of ventricular extrasystoles suggests that individuals who have recovered from severe COVID-19 may be more likely to develop malignant ventricular arrhythmia than individuals who have never had severe COVID-19.42 Another recent study examining the effects of the post-COVID-19 period on HRT reported that HRT values were blunted in the group with positive current COVID-19 test results compared to the group with negative test results.43 Both studies were based on ventricular extrasystoles. The current study analyzes the HRT of supraventricular ectopic beats and whether individuals who have recovered from COVID-19 are predisposed to developing AF in the future.
Compared to the control group and other recovered COVID-19 subgroups, the recovered severe COVID-19 subgroup in the current investigation had a substantially lower atrial HRT Onset value and a significantly greater prevalence of aberrant atrial HRT Onset (Table 2) (Figure 3). Correlation analyzes revealed that abnormal atrial HRT Onset values were associated with the severity of recovered COVID-19 and chest severity score, but not with the time after recovery or history of positive PCR test results (Table 3) (Figures 4 and 5). Presence of abnormal atrial HRT onset using regression analyses and the atrial HRT Onset value was independently predicted by smoking, HT, recovery from severe COVID-19, and the chest CT severity level of recovered COVID-19 participants. The fact that atrial HRT values in group IV were blunted compared to other groups can be linked to the invasive and medicinal procedures used in the treatment plan for individuals with severe COVID-19 (the use of agents known to have harmful effects on the immune system and myocardium, such as steroids, in high doses eg, Prednisolone 1 gram/day, intubation), prolonged profound hypoxia, as well as to the being infected with high doses of SARS-CoV-2, which is believed to harm the ANS when a patient is unwell. The findings suggest that those have recovered from severe COVID-19 are more likely than those who have not had severe COVID-19 to have blunted atrial HRT and, thus, a greater risk of developing AF.
This investigation demonstrates that the HRT Onset responses to atrial premature impulses are blunted in recovered severe COVID-19 individuals compared with the other groups. ANS dysfunction may be brought on by the neurological, cardiac, and systemic symptoms of COVID-19 and the medications used to treat it, particularly corticosteroids and an ANS dysfunction may result in deviant autonomic reflexes, such as the temporary augmentation of vagal outflow that lessens heart rate variations in response to premature impulses, which explains these deviating HRT reactions to atrial premature beats.
There is a significant increase in the applications of recovered from COVID-19 individuals to psychiatric outpatient clinics with complaints of palpitations. In recently published articles on this subject, a parallel treatment protocol is introduced to the daily routine when palpitations are related to sadness, anxiety, or panic disorder.44–48 The COVID-19 process, medical and invasive treatment processes may lead to irreversible damage to the heart muscle itself, internal conduction pathways or ANS. It should be kept in mind any potential harm to the heart’s tissue, the ANS, or the intrinsic conduction pathways may cause supraventricular arrhythmia and therefore palpitation.
Limitations of the study include the long-term effects of COVID-19 vaccines on the myocardium are not yet known and these vaccines were ignored when evaluating the cases, as well as the retrospective nature of the study.
This study demonstrated that abnormal atrial HRT independently was associated with recovering from severe COVID-19. In this context, this research offers verifiable proof of persistent palpitation complaints months after COVID-19 treatment, and it recommends a thorough 24-hour ECG-Holter examination for individuals who have recovered from severe COVID-19 to identify abnormal atrial HRT presence early and prevent AF.
The ethical approval was taken from the Ethics Committee of T.C. Fırat University (2021/12–45).
This article’s research, authoring, and/or publishing were all done without any financial assistance to the author/authors.
Regarding the research, authorship, and/or publishing of this paper, the authors have no possible conflicts of interest to report.
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26. Segerson NM, Wasmund SL, Abedin M, et al. Heart rate turbulence parameters correlate with post-premature ventricular contraction changes in muscle sympathetic activity. Hear Rhythm. 2007;4(3):284–289. doi:10.1016/j.hrthm.2006.10.020
27. Berkowitsch A, Zareba W, Neumann T, et al. Risk stratification using heart rate turbulence and ventricular arrhythmia in MADIT II: usefulness and limitations of a 10-minute holter recording. Ann Noninvasive Electrocardiol. 2004;9(3):270–279. doi:10.1111/j.1542-474X.2004.93600.x
28. Zuern CS, Barthel P, Bauer A. Heart rate turbulence as risk-predictor after myocardial infarction. Front Physiol. 2011;2:99. doi:10.3389/fphys.2011.00099
29. Wichterle D, Melenovsky V, Simek J, Malik J, Malik M. Hemodynamics and autonomic control of heart rate turbulence. J Cardiovasc Electrophysiol. 2006;17(3):286–291. doi:10.1111/j.1540-8167.2005.00330.x
30. Markides V, Schilling RJ. Atrial fibrillation: classification, pathophysiology, mechanisms and drug treatment. Heart. 2003;89(8):939–943. doi:10.1136/heart.89.8.939
31. Liu L, Nattel S. Differing sympathetic and vagal effects on atrial fibrillation in dogs: role of refractoriness heterogeneity. Am J Physiol. 1997;273:805–816 doi:10.1152/ajpheart.1997.273.2.H805
32. Geddes LA, Hinds M, Babbs CF, et al. Maintenance of atrial fibrillation in anesthetized and unanesthetized sheep using cholinergic drive. Pacing Clin Electrophysiol. 1996;19(2):165–175. doi:10.1111/j.1540-8159.1996.tb03308.x
33. Iwasaki M, Yuasa F, Yuyama R, et al. Correla-tion of heart rate turbulence with sympathovagal balance in patients with acute myocardial infarction. Clin Exp Hypertens. 2005;27(2–3):251–257. doi:10.1081/CEH-48872
34. Nikki N. Long covid: how to define it and how to manage it. BMJ. 2020;370:m3489. doi:10.1136/bmj.m3489
35. Sudre CH, Murray B, Varsavsky T, et al. Attributes and predictors of Long-COVID: analysis of COVID cases and their symptoms collected by the covid symptoms study app. medRxiv. 2020. doi:10.1101/2020.10.19.20214494
36. Davis HE, Assaf GS, McCorkell L, et al. Characterizing long COVID in an international cohort: 7 months of symptoms and their impact. EClin Med. 2021;38:101019. doi:10.1016/j.eclinm.2021.101019
37. Ingul CB, Grimsmo J, Mecinaj A, et al. Cardiac dysfunction and arrhythmias 3 months after hospitalization for COVID-19. J Am Heart Assoc. 2022;11(3):e023473. doi:10.1161/JAHA.121.023473
38. Spinoni EG, Mennuni M, Rognoni A, et al. Contribution of atrial fibrillation to in-hospital mortality in patients with COVID-19. Circ Arrhythm Electrophysiol. 2021;14(2):e009375. doi:10.1161/CIRCEP.120.009375
39. Gawałko M, Kapłon-Cieślicka A, Hohl M, Dobrev D, Linz D. COVID-19 associated atrial fibrillation: incidence, putative mechanisms and potential clinical implications. Int J Cardiol Heart Vasc. 2020;30:100631. doi:10.1016/j.ijcha.2020.100631
40. Guo T, Fan Y, Chen M, et al. Cardiovascular Implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19). JAMA Cardiol. 2020;5(7):1–8. doi:10.1001/jamacardio.2020.1017
41. Huang C, Huang L, Wang Y, et al. 6-month consequences of COVID-19 in patients discharged from hospital: a cohort study. Lancet. 2023;401(10393):e21–e33. doi:10.1016/S0140-6736(23)00810-3
42. Yılmaz M, Mirzaoğlu Ç. Retrospective cohort study: severe COVID-19 leads to permanent blunted heart rate turbulence. Diagnostics. 2025;15(5):621. doi:10.3390/diagnostics15050621
43. Taş S, Taş Ü. Effects of COVID-19 on the autonomic cardiovascular system: heart rate variability and turbulence in recovered patients. Tex Heart Inst J. 2023;50(4):e227952. doi:10.14503/THIJ-22-7952
44. Huang B, Yan H, Hu L, et al. The contribution of psychological distress to resting palpitations in patients who recovered from severe COVID-19. Int J Gen Med. 2021;14:9371–9378. doi:10.2147/IJGM.S334715
45. Keshtkar A, Bahrami B. Relationship between COVID-19 anxiety and hypochondriasis in retirees aged 60 to 70 years in Shiraz. J Environ Treat Tech. 2021;9(4):737–740. doi:10.47277/JETT/9(4)739
46. Kasi LS, Moorthy B. A case report on care-seeking type illness anxiety disorder after COVID-19 infection. Case Rep Psychiatry. 2023;2023:3003499. doi:10.1155/2023/3003499
47. Kumar A, Cohen C. Post-COVID-19 panic disorder in older adults: two case reports. Am J Geriatric Psychiatry. 2021;29(4):58–59. doi:10.1016/j.jagp.2021.01.050
48. Javelot H, Weiner L. Panic and pandemic: narrative review of the literatüre on the links and risks of panic disorder as a consequence of the SARS-CoV-2 pandemic. Encephale. 2021;47(1):38–42. doi:10.1016/j.encep.2020.08.001
Lung cancer: © Crystal Light – stock.adobe.com
New, long-term follow-up data from the phase 3 GEMSTONE-302 trial (NCT03789604) confirm that the addition of sugemalimab (Cejemli) to first-line platinum-based chemotherapy provides a significant and durable overall survival (OS) benefit for patients with metastatic non–small cell lung cancer (NSCLC) who lack common genomic alterations. The 4-year follow-up, published in The Lancet Oncology, demonstrates that this combination therapy doubles the 4-year OS rate compared to chemotherapy alone, establishing it as a compelling standard of care option.1,2
The multicenter, double-blind study enrolled 479 patients with metastatic squamous or nonsquamous NSCLC without known sensitizing EGFR, ALK, ROS1, or RET genomic alterations. Patients were randomized in a 2:1 ratio to receive either sugemalimab plus platinum-based chemotherapy (n = 320) or a placebo plus chemotherapy (n = 159). The primary analysis previously demonstrated significant improvements in both progression-free survival (PFS) and OS. This latest report, with a median follow-up of over 43 months, reinforces those initial findings with extended survival data.
At the data cutoff in May 2023, the median OS for the sugemalimab group was 25.2 months (95% CI, 20.1–30.2), a substantial improvement over the 16.9 months (95% CI, 12.8–20.7) observed in the control group. This translated to a hazard ratio (HR) of 0.68 (95% CI, 0.54–0.85), indicating a 32% reduction in the risk of death. The survival benefit was particularly striking at the 4-year mark, with an OS rate of 32.1% in the sugemalimab arm compared with just 17.3% in the placebo arm. This long-term benefit was observed across different histological subtypes, with 4-year OS rates of 27.6% vs 11.7% in squamous NSCLC and 35.5% vs 20.2% in nonsquamous NSCLC.
The initial benefit in PFS also remained robust over the extended follow-up. The median PFS was 9.0 months (95% CI, 7.4–10.9 months) with the addition of sugemalimab, a significant increase from the 4.9 months (95% CI, 4.8–5.2 months) in the control group (HR, 0.49; 95% CI, 0.39–0.60). This earlier finding highlighted the combination’s ability to delay disease progression effectively.
In terms of safety, the long-term data from the GEMSTONE-302 trial did not introduce any new safety signals. The rates of treatment-related grade 3 or 4 adverse events were similar between the sugemalimab and control groups (56% vs 57%). The most common high-grade adverse events included decreased neutrophils (33% vs 33%), decreased white blood cells (15% vs 17%), and anemia (14% vs 11%). The incidence of treatment-related serious adverse events was 26% in the sugemalimab group and 20% in the control group. No new treatment-related deaths were reported since the previous interim analysis, which showed a treatment-related death rate of 3% versus 1%.
The extended outcomes from the GEMSTONE-302 trial underscore the long-term efficacy and manageable safety profile of sugemalimab in combination with platinum-based chemotherapy.
“These results underscore the efficacy of sugemalimab plus platinum-based chemotherapy as a standard first-line treatment option for both squamous and nonsquamous metastatic NSCLC while maintaining a manageable safety profile,” the study authors wrote. Findings support the continued use of this regimen as a potent first-line treatment for patients with metastatic NSCLC who do not have common driver mutations, offering clinicians a valuable tool to improve patient outcomes and survival duration.
A new study reveals how Lactococcus lactis (L. lactis), a common food bacterium, regulates the production of a key precursor in vitamin K₂ (menaquinone) biosynthesis. The bacteria produce enough of this precursor to support their growth while preventing toxic buildup.
Engineering microbes to overproduce vitamins provides a greener and more cost-effective alternative to chemical synthesis or extraction from plants and animals. However, bacterial cells typically limit their production to self-sustaining levels. By dissecting the control system for the vitamin K₂ precursor, researchers have identified how substrate availability and genetic architecture impose a production ceiling as well as how those limits can be lifted.
Vitamin-producing microbes could transform nutrition and medicine, but we must first decode their inherent checks and balances. Our work shows how L. lactis finely tunes its internal supply of the K₂ precursor, allowing us to rewire it with precision.”
Caroline Ajo‑Franklin, co-corresponding author of the study, the Ralph and Looney Professor of Biosciences, director of the Rice Synthetic Biology Institute and a Cancer Prevention and Research Institute of Texas (CPRIT) Scholar
The study, published in the mBio journal Aug. 11, focuses on the unstable intermediate compound that channels all forms of vitamin K₂.
Researchers employed a three-pronged approach: biosensing, genetic engineering and mathematical modeling. Because the precursor is difficult to detect, the team built a custom biosensor in a different bacterium. This sensor is thousands of times more sensitive than conventional methods and requires minimal lab equipment.
Next, the researchers used genetic tools to alter the levels of enzymes in the biosynthetic pathway. By measuring precursor output under different conditions, they fed the results into a mathematical model of the pathway. Initially, the model assumed an unlimited precursor supply, but predictions did not align with laboratory results.
“Once we allowed for depletion of the starting substrate, the model output matched our experimental data,” said Oleg Igoshin, co-corresponding author and professor of bioengineering and biosciences. “It became clear that cells hit a natural production ceiling when the substrate runs low.”
Data and modeling indicated that L. lactis maintains precursor levels at an optimal balance, high enough for its own needs but low enough to avoid toxicity. Simply overexpressing pathway enzymes did not increase output beyond the threshold because precursor materials became limited, much like attempting to bake more cookies with extra baking sheets but without enough flour.
The order of enzyme-encoding genes on DNA also influenced precursor levels: Rearranging these genes altered how much intermediate the cell produced. This suggests an additional layer of evolutionary regulation that has not been well understood.
“By tuning substrate supply, enzyme expression and gene order simultaneously, we can push production above the natural ceiling,” said Siliang Li, the first author of the study and a former graduate student who is now a postdoctoral fellow at Rice.
This insight opens the door to engineering L. lactis or other food-grade bacteria to produce more vitamin K₂ in fermentation processes or even in probiotic formulations.
“Enhanced production could reduce the need for feedstocks and lab space, ultimately lowering costs and bringing fortified foods and supplements closer to reality,” said Jiangguo Zhang, co-first author and a Rice graduate student.
This study was supported by CPRIT and the National Science Foundation and facilitated by the Rice Synthetic Biology Institute.
Source:
Journal reference:
Li, S., et al. (2025)The growth benefits and toxicity of quinone biosynthesis are balanced by a dual regulatory mechanism and substrate limitations. mBio. doi.org/10.1128/mbio.00887-25.
The Khyber Pakhtunkhwa Home Department on Monday announced that a three-day curfew was being imposed from today until August 14 (Thursday) amid an operation against militants in the areas.
At the end of July, security forces backed by gunship helicopters and artillery launched ‘Operation Sarbakaf’ against terrorists in Lowi Mamund tehsil and imposed a three-day curfew in the region.
The operation was paused after both sides agreed to a ceasefire until the conflict was completely resolved through dialogue; however, peace talks between militant commanders and the Bajaur peace jirga fell through.
Today’s statement said that the curfew would be imposed from 11am today until 11am on August 14, in order to ensure the safety of the public during the anti-terror operation.
“A complete curfew will be imposed … in which movement on the roads and leaving houses will be prohibited,” the statement read.
It listed Laghari, Guati, Ghanam Shah, Bad Siya, Kamar, Amanta, Zagai, Gut, Gunde, Gadigal, Niag Kali, Rigi, Daag, Damadola, Sultan Beg, Chautra, Shenkot, Gang, Jeewar, Inam Khoro, Chengai, Anga, Safri, Bar Gatki, Kharki, Shukro and Bakro as areas in which the curfew would be in effect in Bajaur.
Khar Munda Road, Khar Navagi Road, Khar Pusht Salarzai Road and Khar Sadiqabad Inayat Kalay Road were also listed as off limits under the curfew.
“The public is requested to end their activities by 10:30am and return to their homes during the curfew; otherwise, they will be at risk of any untoward incident,” the statement added.
Meanwhile, Adviser to the KP Chief Minister on Information Barrister Mohammad Ali Saif said in a statement that the curfew was limited only to Bajaur and Miranshah, rubbishing rumours that it had been imposed across KP.
“Rumours of a curfew across Khyber Pakhtunkhwa are completely false,” the statement read. “Life in the province is going on as usual. There is no curfew except for specific areas in Bajaur and Miranshah.
“News of a curfew is political propaganda and an attempt to mislead the public,” Saif was quoted as saying. “The rumour-mongering mafia wants to spoil the province’s journey of peace and development.”
Saif urged people to avoid listening to rumours and implored them to only pay attention to information from official sources, reiterating that movement in the province was normal.
“Those who create fear by lying about the curfew are enemies of the people,” the statement read. “Action will be taken against those spreading false information on social media. The people of KP know that propaganda will fail.”
Meanwhile, according to Khar Assistant Commissioner Dr Sadiq Ali, people displaced by the operation have been housed in 100 government schools and colleges.
“Right now, we have 435 schools. More than 100 private schools are also vacant,” he told Dawn.com. “A form has been issued for the registration of victims, and it is also being done through Nadra (National Database and Registration Authority).
In a speech in the KP assembly today, Awami National Party Member of the Provincial Assembly (MPA) Nisar Baz Khan raised questions about whether the home department was under the control of the provincial government.
“At midnight, the provincial home department ordered that curfew be imposed across Bajaur. Is the home department under the provincial government or not? If so, who imposed this curfew and under what authority?” he asked.
“On the one hand, millions of people are homeless and on the streets, with no place to hide, and on the other hand, the government is blocking their routes by imposing a curfew. If there is no transport arrangement, how will people leave?”
Nisar said appeals were made and jirgas were held to halt the operation, but it started anyway.
“Now, it should be clarified whether this operation is being carried out with the permission of the chief minister or with the permission of the prime minister,” Nisar said. “I clearly say that the operation in Bajaur should be stopped and the curfew should be lifted immediately. Emergency relief should also be provided for IDPs (internally displaced persons).”
Lung cancer—a tumor in the parenchyma or within the bronchi—is divided into 2 types: non-small cell lung cancer (NSCLC) and small cell lung cancer.1 NSCLC accounts for around 85% to 90% of lung cancers. NSCLC with epidermal growth factor receptor (EGFR) exon 20 insertion mutations (exon20ins) represents an especially common type of NSCLC, with experts noting that these mutations are particularly difficult to treat due to their unique makeup and heightened heterogeneity.2,6
Image Credit: © patsuda – stock.adobe.com
Guidelines published by the National Comprehensive Cancer Network (NCCN) are recognized as the standard of cancer care; they are updated at least annually. The most recent version of the NCCN Guidelines for NSCLC was updated at the beginning of July 2025.
Revisions in the 7th version of the 2025 NCCN Guidelines for NSCLC include the medication sunvozertinib (Zegfrovy; Dizal Pharmaceuticals), which was recently granted accelerated approval by the FDA.3 Approval was based on the efficacy results—specifically, a robust overall response rate (ORR)—from the WU-KONG1B study, a multinational, open-label, dose randomization trial.3
Sunvozertinib demonstrated an ORR of 46% when treating locally advanced or metastatic NSCLC with EGFR exon20ins.3 Critically, these robust efficacy rates were observed across patients with varying demographics and differing EGFR subtypes, with most patients achieving a sustained response.5 This evidence demonstrates that sunvozertinib can successfully treat NSCLC that has progressed during or after platinum-based chemotherapy.3 It is important to note continued approval of this medication is dependent on confirmatory trials.4
Amy C. Nieto is a 2026 PharmD Candidate at the University of Connecticut School of Pharmacy in Storrs, CT.
Based on the NCCN guidelines, patients should receive amivantamab-vmjw (Rybrevant; Johnson & Johnson) plus carboplatin-pemetrexed or systemic therapy as a first-line treatment (based on if an adenocarcinoma or squamous cell carcinoma is present). If the patient progresses from initial therapy, sunvozertinib is now recommended during subsequent lines of therapy. Table 1 details the treatment options for NSCLC (note sunvozertinib’s place in therapy).
The recommended dosing of sunvozertinib, a kinase inhibitor, for NSCLC is 200 mg by mouth once daily taken with food. Common adverse reactions possible with sunvozertinib include diarrhea, rash, and decreased appetite, among others. Furthermore, the prescribing information for sunvozertinib describes several warnings and precautions, including:4
The recently published data from WU-KONG1 Part B demonstrated the strong efficacy of sunvozertinib in treating progression of NSCLC with EGFR exon 20 insertion mutations. This evidence enabled the FDA to grant the medication priority review, followed by an accelerated approval, making it the world’s first and only approved treatment for patients in this population. The NCCN, as of July 2025, updated their guidelines accordingly to reflect the evidence and approval.5 Oncology is an ever-changing field; it is important as pharmacists and technicians to stay up-to-date on current drug approvals and guideline updates. As the treatment paradigm of NSCLC continues to shift, pharmacists will be essential in communicating updates in standard-of-care treatment options and counseling patients on key management strategies.6
Serendipitously and for the first time, an international research team led by scientists at the U.S. Department of Energy’s SLAC National Accelerator Laboratory formed solid binary gold hydride, a compound made exclusively of gold and hydrogen atoms.
The researchers were studying how long it takes hydrocarbons, compounds made of carbon and hydrogen, to form diamonds under extremely high pressure and heat. In their experiments at the European XFEL (X-ray Free-Electron Laser) in Germany, the team studied the effect of those extreme conditions in hydrocarbon samples with an embedded gold foil, which was meant to absorb the X-rays and heat the weakly absorbing hydrocarbons. To their surprise, they not only saw the formation of diamonds, but also discovered the formation of gold hydride.
“It was unexpected because gold is typically chemically very boring and unreactive — that’s why we use it as an X-ray absorber in these experiments,” said Mungo Frost, staff scientist at SLAC who led the study. “These results suggest there’s potentially a lot of new chemistry to be discovered at extreme conditions where the effects of temperature and pressure start competing with conventional chemistry, and you can form these exotic compounds.”
The results, published in Angewandte Chemie International Edition, provide a glimpse of how the rules of chemistry change under extreme conditions like those found inside certain planets or hydrogen-fusing stars.
Studying dense hydrogen
In their experiment, the researchers first squeezed their hydrocarbon samples to pressures greater than those within Earth’s mantle using a diamond anvil cell. Then, they heated the samples to over 3,500 degrees Fahrenheit by hitting them repeatedly with X-ray pulses from the European XFEL. The team recorded and analyzed how the X-rays scattered off the samples, which allowed them to resolve the structural transformations within.
As expected, the recorded scattering patterns showed that the carbon atoms had formed a diamond structure. But the team also saw unexpected signals that were due to hydrogen atoms reacting with the gold foil to form gold hydride.
Under the extreme conditions created in the study, the researchers found hydrogen to be in a dense, “superionic” state, where the hydrogen atoms flowed freely through the gold’s rigid atomic lattice, increasing the conductivity of the gold hydride.
Hydrogen, which is the lightest element of the periodic table, is tricky to study with X-rays because it scatters X-rays only weakly. Here, however, the superionic hydrogen interacted with the much heavier gold atoms, and the team was able to observe hydrogen’s impact on how the gold lattice scattered X-rays. “We can use the gold lattice as a witness for what the hydrogen is doing,” Mungo said.
The gold hydride offers a way to study dense atomic hydrogen under conditions that might also apply to other situations that are experimentally not directly accessible. For example, dense hydrogen makes up the interiors of certain planets, so studying it in the lab could teach us more about those foreign worlds. It could also provide new insights into nuclear fusion processes inside stars like our sun and help develop technology to harness fusion energy here on Earth.
Exploring new chemistry
In addition to paving the way for studies of dense hydrogen, the research also offers an avenue for exploring new chemistry. Gold, which is commonly regarded as an unreactive metal, was found to form a stable hydride at extremely high pressure and temperature. In fact, it appears to be only stable at those extreme conditions as when it cools down, the gold and hydrogen separate. The simulations also showed that more hydrogen could fit in the gold lattice at higher pressure.
“These results suggest there’s potentially a lot of new chemistry to be discovered at extreme conditions where the effects of temperature and pressure start competing with conventional chemistry, and you can form these exotic compounds.” Mungo Frost SLAC staff scientist
The simulation framework could also be extended beyond gold hydride. “It’s important that we can experimentally produce and model these states under these extreme conditions,” said Siegfried Glenzer, High Energy Density Division director and professor for photon science at SLAC and the study’s principal investigator. “These simulation tools could be applied to model other exotic material properties in extreme conditions.”
The team also included researchers from Rostock University, DESY, European XFEL, Helmholtz-Zentrum Dresden-Rossendorf, Frankfurt University and Bayreuth University, all in Germany; the University of Edinburgh, UK; the Carnegie Institution for Science, Stanford University and the Stanford Institute for Materials and Energy Sciences (SIMES). Parts of this work were supported by the DOE Office of Science.
IHSE USA, the global provider of KVM solutions, introduces its latest innovation: the Draco XStreme series. This new product line is “based on a next-generation hardware platform and represents a fundamental shift in design, combining cutting-edge performance with maximum flexibility and long-term sustainability,” says the company. The new extender series supports video resolutions ranging from Full HD up to 8K and is engineered for seamless integration with both proprietary and future IP-based transmission technologies.
At the heart of this platform lies the JPEG XS codec co-developed with the Fraunhofer Institute for Integrated Circuits. The first of its kind in KVM, the Draco XStreme series enables visually lossless video without any frame drops, up to 16-bits of deep color, HDR support, less than 1 millisecond per frame of video transmission latency, and frame rates of up to 480 fps all on JPEG XS, a widely accepted codec standard in AV and broadcasting.
“With the introduction of the Draco XStreme series, IHSE sets a new benchmark for the industry,” says Gregory Lenczycki, COO of IHSE USA. “The new series features the latest hardware components, delivering exceptional performance while maintaining low power consumption, which is an essential factor for long-term availability and future-proof video and signal transmission.”
Key advantages of the new Draco XStreme series include the ability to transmit high-resolution, low-latency video signals with reduced infrastructure requirements. For instance, users can transmit 4K60 signals over a standard 1 GB network without visible loss in image quality. This not only reduces energy consumption but also simplifies system architecture, resulting in total project cost savings.
The Draco XStreme series introduces several industry-first features. Notably, IHSE is launching its first Dual-Head 4K60 Extender, capable of transmitting two 4K60 video signals over a single cable. Additionally, the company is releasing a Single-Head 4K60 Extender that operates over a 1 GB link for even greater video transmission efficiency.
The series establishes a future-ready foundation for hybrid environments. By bridging proprietary and IP-based systems, it enables interoperability and scalability, paving the way for next-generation KVM applications, the company says.