Outcomes of Anticoagulation Initiation in Critically Ill Patients with New-Onset Atrial Fibrillation: A Multicenter Retrospective Cohort Study

Outcomes of Anticoagulation Initiation in Critically Ill Patients with New-Onset Atrial Fibrillation: A Multicenter Retrospective Cohort Study | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Outcomes of Anticoagulation Initiation in Critically Ill Patients with New-Onset Atrial Fibrillation: A Multicenter Retrospective Cohort Study Raghad A. Alasmari, Khalid H. Alghamdi, Nouf M. Bahri, Ghida A. Bawaked, and 13 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7596772/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 11 Apr, 2026 Read the published version in BMC Cardiovascular Disorders → Version 1 posted 12 You are reading this latest preprint version Abstract Introduction: New-onset atrial fibrillation (NOAF) in intensive care units (ICU) carries a high risk of recurrence and atrial fibrillation (AF) related complications. However, evidence on the safety of anticoagulation (AC) in critically ill patients with NOAF is limited. This study aimed to evaluate the impact of AC initiation on clinical outcomes in this population. Methods A multicentre, retrospective cohort study was conducted across four hospitals in Saudi Arabia from January 1, 2018, to February 28, 2024. Adult ICU patients (≥ 18 years) with documented NOAF were included and categorized into two groups: those who received anticoagulation (AC group) and those who did not (non-AC group). The Study outcomes were the incidence of bleeding or thrombotic events during a 1-year follow-up. Results A total of 179 patients were included, with 52.5% in the AC group and 47.4% in the non-AC group. The mean age was 68.1 ± 13.4 years. The median CHA2DS2-VASc and HAS-BLED scores were 3 [2–4] and 2 [2–4], respectively. The mean APACHE II score was significantly lower in the AC group compared to the non-AC group (19.1 ± 6.8 vs. 23.8 ± 9.4; P = 0.0002). The incidence of bleeding events was similar between groups (21.3% vs. 21.2%; P = 0.9869), as was the incidence of thrombotic events (2.1% vs. 5.9%; P = 0.2592). Conclusions In critically ill patients with NOAF, anticoagulation did not significantly alter the risk of bleeding or thrombotic events within 1 year of follow-up. These findings highlight the need for further prospective studies to guide anticoagulation decisions in this high-risk population. Anticoagulation New-onset Atrial Fibrillation Bleeding Thromboembolism Critical Illness Figures Figure 1 Figure 2 Figure 3 Introduction Atrial fibrillation (AF) is considered one of the most common types of cardiac arrhythmia in critically ill patients ( 1 , 2 ). Newly diagnosed AF occurs in approximately 14% of critically ill patients ( 3 ). Recent evidence suggests that patients who developed AF during acute illness (e.g., postoperatively, sepsis) have high long-term risks for AF recurrence and AF-associated complications, such as stroke, heart failure, longer intensive care unit (ICU) and hospital stays, and mortality ( 4 , 5 ). Even though a reversible condition often drives new onset Atrial fibrillation (NOAF), it is unclear whether AF persists after managing the primary condition, increasing the risk of subsequent stroke ( 6 ). NOAF developed during critical illness presents challenges for both short- and long-term management and is associated with a poor prognosis ( 4 ). Currently, the data are insufficient regarding estimates of stroke risk reduction or rates of severe bleeding with systemic anticoagulation during critical illness. A retrospective study of 38,582 patients with sepsis and AF found that 35.3% were given anticoagulants during admission. In this study, the use of therapeutic parenteral anticoagulation during hospitalization with sepsis and AF showed a potentially higher bleeding risk. They were not associated with a reduction in ischemic stroke ( 4 ). Another retrospective cohort study of 2,304 hospitalized critically ill patients with a primary diagnosis of acute coronary syndromes (ACS), acute pulmonary disease, or sepsis, and a complication of NOAF during admission. This study reported ischemic stroke and bleeding rates after three years of follow-up. There is no association between anticoagulation and a lower incidence of ischemic stroke in patients with NOAF occurring with acute pulmonary disease, sepsis, or ACS. However, anticoagulation was associated with a higher risk of bleeding in patients with AF associated with acute pulmonary disease, but not in sepsis or ACS ( 7 ). Few studies have addressed the safety of initiating anticoagulation in ICU patients who developed NOAF during admission. Our study aims to determine the impact of initiating AC versus no AC in critically ill patients with NOAF on patients’ clinical outcomes. Methods Study design and setting A Multicentre, retrospective cohort study was conducted between January 01, 2018, and February 28, 2024, in four hospitals in Saudi Arabia, including King Faisal Specialist Hospital and research centre– Jeddah (KFSHRC-J), King Faisal Specialist Hospital and research centre– Riyadh (KFSHRC-R), King Fahad Medical City (KFMC), and King Saud University Medical City (KSUMC). The institutional review board approved the study at all participating centres. The study included all critically ill adult patients 18 years and older, admitted to the medical ICU, who had a documented diagnosis of new onset of AF during ICU admission and received antiarrhythmic drugs. Patients under 18 years old, patients who were admitted to the ICU post-cardiac surgery, patients on treatment doses of anticoagulants for another indication, and patients with Pre-existing AF were excluded. Patients were followed for one year post-NOAF occurrence. Study outcomes The primary outcome was the incidence of bleeding events. The secondary outcomes include the incidence of thrombotic events, documented recurrent AF episodes within one year of follow-up, Length of ICU and hospital stay, and 30-day mortality. Data collection Data were collected retrospectively from the hospital's electronic health records using REDCap (version 10.8.0 - © 2021 Vanderbilt University). The data were extracted for all patients admitted to the medical ICU who were started on oral or intravenous (IV) amiodarone boluses or infusion, oral or IV metoprolol, or oral or IV digoxin. Patients who had documented NOAF were included in the study. Patients were divided into two groups: those who received anticoagulation (AC group) and those who did not (non-AC group) post NOAF. Variables extracted from the medical record will include demographics, comorbidities, APACHE II Score, underlying cause for AF, HAS bleed score, and CHAVSC score on the day of NOAF. Additional data extracted, including 30-day mortality, date of hospital admission and discharge, date of ICU admission and discharge, date of NOAF, date of documented bleeding, date of documented thrombosis, and date of documented recurrent AF episode (time to subsequent AF onset). Definitions NOAF was defined as detecting at least one episode of atrial fibrillation (AF) during the ICU stay, identified by a physician via electrocardiogram (ECG) and documented as AF in the patient profile. We defined recurrent AF as any documented detection of an AF rhythm on ECG, as noted by the physician in the patient profile, following the initial episode of new-onset atrial fibrillation (NOAF) up to 1 year of follow-up. Initiation of full anticoagulation following NOAF episode was defined as prescription for parenteral AC, warfarin, or direct oral anticoagulants (DOACs) within ICU stay and after the NOAF episode. The definitions of major and nonmajor bleeds were based on the International Society on Thrombosis and Hemostasis definitions and criteria. Major bleeding is defined as bleeding that is associated with hemodynamic compromise, occurs in an anatomically critical site, requires transfusion (2 units of packed red blood cells [RBCs]), or results in a haemoglobin drop of 2 g/dL. All other bleeding is categorized as non-major (minor) ( 8 ). Time of bleeding was determined based on documentation of the first clinical recognition of bleeding in physicians' or nursing notes. Thrombotic events were defined as any venous thrombosis, including deep vein thrombosis (DVT) or pulmonary embolism (PE), or other confirmed thromboses (e.g., catheter-associated or atypical site thrombosis) that are confirmed by imaging. Statistical analysis The outcomes of interest in this study included bleeding and thrombotic events within one year of NOAF, as well as mortality within 30 days of NOAF. The primary exposure was the status of initiating treatment doses of AC post-NOAF. Descriptive statistics were generated for all patients according to their AC initiation status. Normality assessment for continuous variables included the Shapiro-Wilk and Kolmogorov-Smirnov tests, as well as the observation of each variable's mean, median, skewness, kurtosis, and graphical results. Frequencies were reported for categorical variables. The associations between outcomes, exposure, predictor variables, and AC treatment status were observed using Student’s t-test, Kruskal-Wallis test, Chi-square, and Fisher’s exact tests. Data with a P-value of less than 0.05 was considered significant. Data that was significant in the univariate analysis was included in the multivariable analysis. Univariate and multivariable logistic models were constructed to predict mortality within 30 days of NOAF and a bleeding event within one year of NOAF, adjusting for full AC treatment status and other predictor variables. Kaplan-Meier curves were generated to examine the time to event of bleeding and thrombosis within one year of NOAF in patients according to AC treatment status. SAS software version 9.4 was used for statistical analyses. Results Baseline Characteristics Among 1968 patients screened, 179 were considered for inclusion (Fig. 1). The mean and standard deviation (SD) age was 68.1 ± 13.4 years. Just over half (54.8%) of the patients were male, and almost three-fourths (72.6%) of them had hypertension. In addition, nearly two-thirds (64.3%) of the patients had diabetes, and over one-fourth (27.4%) had chronic kidney disease. Forty-three percent of the participants had received anticoagulant prophylaxis three months before experiencing NOAF, and just under one-fifth (19.0%) of the patients had a history of a bleeding event within the same three-month period. The mean ± SD APACHE II score for all patients was 21.4 ± 8.4, and the underlying cause of NOAF was sepsis in 54.8% of cases. For the 98 patients with sepsis as the underlying cause of NOAF, almost half (49.0%) were taking vasopressors 24 hours before experiencing NOAF (Table 1). Over half (52.5%) of the patients were in the AC group after experiencing NOAF. Compared to the non-AC group, patients in the AC group were significantly older (70.2 ± 13.8 years vs. 65.7 ± 12.7 years, p = 0.0275) (Table 1). There was also a significant association between full AC treatment status and patients with oncology/hematology malignancies, where 29.4% of patients in the non-AC group had this type of comorbidity, compared to 13.8% of patients in the AC group with an oncology/hematology malignancy (p = 0.0109). The mean APACHE II score was also significantly higher for patients in the non-AC group than those in the AC group (23.8 ± 9.4 vs. 19.1 ± 6.8, p = 0.0002). Among the patients who experienced sepsis as the underlying cause of NOAF (n = 98), 49% received vasopressors (66.7% vs 29.8%, p = 0.0003) in the non-AC group and the AC group, respectively (Table 1). Outcomes and Regression Analysis More than half (54.2%) of the patient population in this study died within 30 days of experiencing NOAF, with 68.2% of the patients in the non-AC group compared to 41.5% of the patients in the AC group having this outcome (p=-0.0003) (Table 2). For most of the patients (92.7%) who died, the cause of death was not related to bleeding or thrombosis. Seven patients (3.9%) had a thrombotic event within 1 year of experiencing NOAF (Supplementary appendix, Table e1), and 38 patients (21.2%) had a bleeding event within 1 year of NOAF. The median time to the first bleeding event for the 38 patients was 14.5 days (range, 4–31), compared to 7.0 days (range, 5–10) for the time to the first thrombotic event among patients experiencing this outcome. The median (length of stay in the ICU was 14.0 (7–28) days for all patients. (Table 2) After adjusting for all predictors in the univariate analysis, taking anticoagulant prophylaxis medication three months before experiencing NOAF and a history of a bleeding event three months before experiencing NOAF remained as significant predictors of a bleeding event within 1 year following NOAF in this patient population (Tables 3 and 4). The multivariable regression found that having a bleeding event within 1 year following NOAF was 3.36 times more likely for patients that had taken anticoagulant prophylaxis three months before having NOAF (AOR = 3.36, 95% CI = 1.54–7.33, p = 0.0023) and 3.75 times more likely for patients that had a history of bleeding three months before having NOAF (AOR = 3.75, 95% CI = 1.58–8.86, p = 0.0026) (Table 4). Table 3 Univariate association of predictor variables and the event of bleeding within one year of NOAF Predictor OR 95% CI p-value Age (years) 1.01 (0.98–1.04) 0.4079 Gender (female) 0.74 (0.36–1.54) 0.4210 Apache II score 1.03 (0.99–1.07) 0.2130 Taking full anticoagulation treatment post NOAF 1.01 (0.49–2.06) 0.9869 History of bleeding event three months prior to NOAF 3.53 (1.57–7.94) 0.0023 Medications taken three months prior to NOAF Single antiplatelet Dual antiplatelet Anticoagulant prophylaxis None 0.87 1.99 3.29 0.77 (0.40–1.91) (0.64–6.20) (1.55–6.99) (0.35–1.67) 0.7263 0.2383 0.0019 0.5019 OR, odds ratio; CI, confidence interval; NOAF, new-onset atrial fibrillation Table 4 Multivariable association of predictor variables and event of bleeding within one year of NOAF Predictor OR 95% CI p-value Age (years) 1.02 (0.99–1.05) 0.1700 History of bleeding event three months prior to NOAF 3.75 (1.58–8.86) 0.0026 Taking anticoagulant prophylaxis three months prior to NOAF 3.36 (1.54–7.33) 0.0023 OR, odds ratio; CI, confidence interval; NOAF, new-onset atrial fibrillation Univariate regression analysis revealed that, for every one-unit increase in APACHE II score, the odds of mortality increase by 7% [odds ratio (OR) and 95% confidence interval (CI) = 1.07 (1.03–1.11), p = 0.0011] (Table 5). The outcome of mortality was 0.33 times as likely for patients in the AC group after experiencing NOAF (OR and 95% CI = 0.33 [0.18–0.61], p = 0.0004). In addition, taking vasopressors 24 hours before NOAF increased the likelihood of mortality within 30 days by 3.59 times (OR = 3.59, 95% CI 1.56–8.28, p = 0.0027). (Table 5) Table 5 Univariate association of predictor variables and 30-day mortality in NOAF patients Predictor OR 95% CI p-value Age (years) 1.00 (0.99–1.03) 0.5149 Gender (female) 1.01 (0.56–1.82) 0.9745 Apache II score 1.07 (1.03–1.11) 0.0011 Taking full anticoagulation treatment 0.33 (0.18–0.61) 0.0004 NOAF underlying cause of sepsis 0.90 (0.50–1.63) 0.7390 Taking vasopressors 24 hours prior to NOAF 1 3.59 (1.56–8.28) 0.0027 History of stroke/TIA 0.92 (0.37–2.29) 0.8591 OR, odds ratio; CI, confidence interval; NOAF, new-onset atrial fibrillation; TIA, transient ischemic attack; 1 includes n = 98 patients with NOAF as underlying cause of sepsis A multivariable model for all patients (n = 179) revealed that an increase in APACHE II score and AC treatment status remained significant predictors of mortality within 30 days, after adjusting for all other predictors (Table 6). In a multivariable model predicting mortality within 30 days in the patients with sepsis as the underlying cause of NOAF (n = 98), taking AC treatment remained protective, adjusting for the other predictors in the model [adjusted odds ratio (AOR) = 0.30, 95% CI = 0.11–0.81, p = 0.0171] (Table 7). Table 6 Multivariable analysis of association between predictor variables and 30-day mortality (n = 179) Predictor OR 95% CI p-value Age (years) 1.01 (0.99–1.04) 0.3153 Apache II score 1.05 (1.01–1.09) 0.0159 Taking full anticoagulation treatment post-NOAF 0.37 (0.19–0.72) 0.0031 OR, odds ratio; CI, confidence interval Table 7 Multivariable analysis of association between predictor variables and 30-day mortality for patients with sepsis as the underlying cause of NOAF (n = 98) Predictor OR 95% CI p-value Age (years) 1.01 (0.98–1.04) 0.6029 Apache II score 1.05 (0.99–1.11) 0.1334 Taking full anticoagulation treatment post-NOAF 0.30 (0.11–0.81) 0.0171 Taking vasopressors 24 hours prior to NOAF 0.48 (0.19–1.20) 0.1151 OR, odds ratio; CI, confidence interval The probability of not experiencing a bleeding event after NOAF was 0.8849 for patients on the AC group and 0.8490 for patients on the non-AC group. (Fig. 2) The difference in patient event experience according to full AC treatment status was insignificant [Log-Rank Chi-sq = 1.43, degrees of freedom (df) = 1, p-value = 0.2309]. Similarly, the probability of not experiencing a thrombotic event after NOAF was 0.9772 for patients on AC group and 0.9318 for patients on non AC group and the difference in event experience for patients according to full AC treatment status was not significant [Log-Rank Chi-sq = 2.40, degrees of freedom (df) = 1, p-value = 0.1209] (Fig. 3). Discussion Our study adds to a growing body of literature exploring the impact of AC initiation in critically ill patients with NOAF. This condition remains poorly addressed in current clinical guidelines. As a recent international survey has demonstrated, the significant variation in NOAF management across regions highlights the lack of standardized protocols. It highlights the need for context-specific data to guide therapy.( 9 ). One might expect patients who are on AC to be more prone to bleeding. However, this was not the case in our study; Bleeding complications, though infrequent, remain a key concern. In our cohort, the bleeding rate was similar between the two groups, at 21%. Of these, 47.4% were major bleeding events, and 54.6% were minor bleeding events. In contrast to the study conducted by Darwish et al., our study observed a higher bleeding rate (8.6% vs. 21%) ( 3 ). This can be further explained by the fact that one-third of our patient population (27%) had chronic kidney disease (CKD). Chronic kidney disease is considered a risk factor for both bleeding and thrombosis. Our findings contradict the observations made in previous studies regarding bleeding. For instance, Walkey et al. conducted a retrospective cohort study to evaluate the risk of stroke and bleeding associated with AC administration for NOAF during sepsis. Clinically significant bleeding occurred more often among patients who received parenteral AC (1163 of 13,505 [8.6%]) than among patients who did not receive parenteral AC (979 of 13,505 [7.2%]; RR, 1.21; 95% CI, 1.10–1.32) ( 4 ). Our study, as well as the survey conducted by Walkey et al., utilized the HAS-BLED score to assess bleeding risk. However, it has not been validated for estimating bleeding risk in critically ill patients with NOAF ( 5 ). However, our findings were consistent with prior systematic reviews and observational data, which report that the bleeding risk often offsets the theoretical thromboembolic benefit of AC during critical illness, specifically among patients with sepsis. This population frequently overlaps with NOAF( 10 ). As expected, in our study, the initiation of AC resulted in a non-significantly lower rate of thrombotic events, 2.1% versus 5.9%. The 2014 ACC/AHA atrial fibrillation guidelines and the subsequent 2019 focused update both acknowledge that the role of AC in acute non-cardiac illness remains to be elucidated ( 11 , 12 ). Studies conducted to observe the benefit of AC in reducing the risk of thromboembolism in NOAF in critically ill patients showed no significant difference. Notably, thromboembolism in the available literature is defined as the incidence of stroke development after NOAF ( 7 , 12 , 13 ). In a retrospective cohort study conducted by Quon et al., which overlooked 2,304 critically ill patients who were 65 years or older and hospitalized for ACS, acute pulmonary disease or sepsis and a complication of NOAF, anticoagulation administration didn’t result in a lower incidence of ischemic stroke in ACS, acute pulmonary disease and sepsis with the following odds ratio OR respectively OR: 1.22 [95% confidence interval (CI): 0.65 to 2.27], OR: 0.97 [95% CI: 0.53 to 1.77], and OR: 1.98 [95% CI: 0.29 to 13.47])( 7 ). Additionally, a post hoc analysis of the AFTER-ICU study (Atrial Fibrillation Treatment Evaluation Registry in the ICU) was conducted by Sakuraya et al. in 2021. It was a prospective multicentre cohort study of NOAF in the general ICU population. The study aimed to describe the efficacy of AC initiation (within 48 hours of NOAF) according to the CHA2DS2-VASc score in critically ill patients. The study hypothesized that early AC initiation would have a positive effect on neurological outcomes. The primary outcome was a composite outcome of mortality and ischemic stroke. After adjusting for confounders, the study concluded that there was no statistically significant difference between the two groups in terms of the primary outcome. However, in the early AC initiation group, there was a numerically lower incidence of ischemic stroke when compared to no AC. Ischemic stroke until hospital discharge occurred in 10 (4.7%) vs 3 (3.1%), p = 0.112. During ICU stay, 5 (2.4%) vs 1 (1.1%), p = 0.448. After ICU discharge, 5 (2.8%) vs 0 (0%), p = 0.1 ( 13 ). Similar to the studies mentioned above, our findings indicate that there was no statistically significant difference, but numerically lower thrombotic events within one year of NOAF [2 (2.1) vs 5 (5.9), p = 0.2592]. It should be noted that we had a broader definition of thromboembolism as we captured not only stroke but also deep venous thrombosis and pulmonary embolism. We propose several theories to explain the findings in our study. Firstly, we had a smaller sample size compared to other studies. This may have led to no difference being shown. Secondly, like the studies mentioned, the CHA2DS2-VASc score of our patient population was 3 [2–4], indicating a moderate risk of thrombosis. Furthermore, the CHA2DS2-VASc score has not yet been validated to assess thrombotic risk in NOAF in the critically ill population ( 14 , 15 ). Moreover, 50% of patients who didn’t receive treatment doses of AC received prophylactic AC. Lastly, the incidence of stroke post-NOAF in critically ill patients is much lower than in the general population with atrial fibrillation ( 16 ) Only a few observational studies have overlooked the relationship between anticoagulation and mortality in patients who are deemed critically ill and presenting with NOAF. For instance, a research study conducted by Darwish et al. on 115 patients with NOAF and sepsis showed no statistically significant difference in survival rates during hospitalization (66.2% for the non-anticoagulated group vs. 74.3% for the anticoagulated group, P = .392) ( 3 ). Sakuraya et al. examined early versus late administration of AC in critically ill patients presenting with NOAF. Early AC administration was defined as AC initiation within 48 hours of the onset of NOAF. The 30-day mortality rate was numerically lower in those who received early AC (13.7%) compared to those who received late AC (24.4%) ( 13 ). Our analysis revealed a statistically significantly lower 30-day mortality rate in those who received AC, 41.5%, compared to 68.2% in those who didn’t receive treatment doses of AC, with a p-value of 0.0003. There was a statistically significant difference between the two groups in terms of age, APACHE II score and the recipient of vasopressors 24 hours before NOAF however, when multivariable analysis was performed in all patients with NOAF only age, increased of APACHE II score, and the administration of complete AC treatment were determined to be predictors of 30 days mortality. Notably, the cause of death in 92.7% of the patient population was not related to thrombosis or bleeding. Although the multivariable analysis adjusted for APACHE II score and vasopressor use, these factors may not fully capture the extent of bleeding risk or coagulopathy at the time of NOAF. The study’s strength lies in its multicentre design, and multivariable analysis was conducted to detect any potential bias from confounders. The study’s limitations include the following: the study included only patients who received pharmacologic intervention, which may have excluded untreated NOAF cases and thereby limited the external validity of the findings. The observational chart review nature prevented us from documenting whether the patients who received parenteral AC had their laboratory activated partial thromboplastin time in the therapeutic range. The role of direct oral anticoagulants (DOACs) has not been examined to prevent stroke in NOAF in critically ill patients. Also, the majority of our patients’ underlying cause of NOAF was sepsis. Thus, it is difficult to extrapolate our findings to other critically ill populations, such as surgical patients. Moreover, a significant limitation of this study is the potential for immortal time bias due to the variable timing of anticoagulation initiation; patients who survived long enough to receive anticoagulation may have had an inherent survival advantage over those who died earlier and were classified as non-anticoagulated. A key limitation is that death may act as a competing risk for bleeding and thrombotic events, potentially leading to an overestimation of their incidence, as the survival analysis was performed without conducting competing risk analysis. A potential limitation is the possibility of confounding by indication in the comparison of bleeding rates between anticoagulated and non-anticoagulated patients, as those at higher bleeding risk may have been selectively excluded from receiving anticoagulation, potentially masking actual differences in bleeding risk. The observed association between lack of anticoagulation and higher 30-day mortality may be influenced by residual confounding related to illness severity. Patients with coagulopathy, active bleeding, or hemodynamic instability—who are less likely to receive anticoagulation—are also inherently at higher risk of death. Lastly, our study is not powered to detect differences between groups. Conclusions The study showed no statistically significant differences in bleeding and thrombotic events between critically ill patients with NOAF who received anticoagulation and those who did not receive anticoagulation within one year of follow-up. However, 30-day mortality was lower in patients who received full anticoagulation post-NOAF. These findings, combined with growing international evidence, support the adoption of an individualized strategy. Given the variability in practice, uncertain benefits during acute illness, and emerging data supporting stroke prevention in select high-risk patients, we advocate for selective AC initiation based on bleeding risk and thromboembolic profile, and follow-up for survivors with NOAF. Future trials are urgently needed to determine the optimal timing and duration of anticoagulation for this population. Abbreviations ACS: Acute Coronary Syndromes AC: Anticoagulation AF: Atrial Fibrillation DVT: Deep Vein Thrombosis ECG: Electrocardiogram ICU: Intensive Care Units IV: Intravenous IQR: Interquartile Ranges KFSHRC-J: King Faisal Specialist Hospital and Research Centre-Jeddah ( KFSHRC-R: King Faisal Specialist Hospital and Research Centre– Riyadh KFMC: King Fahad Medical City KSUMC: King Saud University Medical City LMWH: Low Molecular Weight Heparin. NOAF: New Onset Atrial Fibrillation n: Frequencies PE: Pulmonary Embolism SD: Standard Deviation Declarations Ethics approval and consent to participate The study was reviewed and approved by the Institutional Review Board (IRB) at King Faisal Specialist Hospital and Research Centre in Jeddah and Riyadh, King Fahad Medical City in Riyadh, and King Saud University Medical City in Riyadh (Reference numbers IRB 2023-31, 24-185, and 3/0797/IRB, respectively). The data were kept confidential; only the research team had access to the files. Written informed consent was waived due to the retrospective nature of the study. This study was conducted in accordance with Good Clinical Research Practice (Declaration of Helsinki) and the rules and guidelines of the Ethics Committee at KFSHRC. Consent for publication Not applicable Availability of data and materials The datasets used and/or analysed during the current study are available from the corresponding author upon reasonable request. Competing interests The authors declare that they have no competing interests Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Declaration of generative AI and AI-assisted technologies in the writing process During the preparation of this work, the authors used [Grammarly] to [enhance grammatical accuracy and improve clarity of expression for the readers]. After using this tool/service, the authors reviewed and edited the content as needed and take full responsibility for the content of the publication. Authors’ contributions Raghad ALASMARI contributed to conceptualization, manuscript writing, data acquisition, and proposal writing. Namareq Aldardeer and Khalid Alghamdi conceptualized, supervised, and critically reviewed the manuscript; Awatif Hafiz performed data acquisition and manuscript writing; Emily HEAPHY performed data analysis and manuscript writing; Nouf Bahiri, Ghida Bawaked, Abdullah Alhammad, Marwa Amer, Turkiah Alkhaldi, Raghad Alshhri, Firas Kseibi, Amro Hajja, Noran Abouobaid, Ghassan Bagazi, Raghad Bajaba, and Hanadi Shaheen performed data acquisition. All authors read and approved the final manuscript. Clinical Trial Number Not applicable Acknowledgments Not applicable References Korelitz BI, Sommers SC. Responses to drug therapy in ulcerative colitis. Evaluation by rectal biopsy and histopathological changes. Am J Gastroenterol. 1975 Nov;64(5):365–70. Artucio H, Pereira M. Cardiac arrhythmias in critically ill patients: Epidemiologic study. Crit Care Med. 1990 Dec;18(12):1383–8. Darwish OS, Strube S, Nguyen HM, Tanios MA. 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Available from: https://www.ahajournals.org/doi/10.1161/CIR.0000000000000665 Sakuraya M, Yoshida T, Sasabuchi Y, Yoshihiro S, Uchino S. Clinical prediction scores and early anticoagulation therapy for new-onset atrial fibrillation in critical illness: a post-hoc analysis. BMC Cardiovasc Disord. 2021 Dec;21(1):423. Lip GYH, Frison L, Halperin JL, Lane DA. Identifying Patients at High Risk for Stroke Despite Anticoagulation: A Comparison of Contemporary Stroke Risk Stratification Schemes in an Anticoagulated Atrial Fibrillation Cohort. Stroke. 2010 Dec;41(12):2731–8. Lip GYH, Nieuwlaat R, Pisters R, Lane DA, Crijns HJGM. Refining Clinical Risk Stratification for Predicting Stroke and Thromboembolism in Atrial Fibrillation Using a Novel Risk Factor-Based Approach. Chest. 2010 Feb;137(2):263–72. Butt JH, Xian Y, Peterson ED, Olsen PS, Rørth R, Gundlund A, et al. Long-term Thromboembolic Risk in Patients With Postoperative Atrial Fibrillation After Coronary Artery Bypass Graft Surgery and Patients With Nonvalvular Atrial Fibrillation. JAMA Cardiol. 2018 May 1;3(5):417. Table 1 and 2 Table 1 and 2 are available in the Supplementary Files section. Additional Declarations No competing interests reported. Supplementary Files 6.SupplementaryAppendix.docx Table12.docx Cite Share Download PDF Status: Published Journal Publication published 11 Apr, 2026 Read the published version in BMC Cardiovascular Disorders → Version 1 posted Editorial decision: Revision requested 28 Oct, 2025 Reviews received at journal 15 Oct, 2025 Reviews received at journal 12 Oct, 2025 Reviewers agreed at journal 08 Oct, 2025 Reviews received at journal 06 Oct, 2025 Reviewers agreed at journal 06 Oct, 2025 Reviewers agreed at journal 06 Oct, 2025 Reviewers invited by journal 05 Oct, 2025 Editor assigned by journal 02 Oct, 2025 Editor invited by journal 23 Sep, 2025 Submission checks completed at journal 19 Sep, 2025 First submitted to journal 19 Sep, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7596772","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":528410994,"identity":"b6d2a752-1466-4e95-998a-a4f8ebb9fe31","order_by":0,"name":"Raghad A. 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02:24:27","extension":"html","order_by":13,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":122025,"visible":true,"origin":"","legend":"","description":"","filename":"earlyproof.html","url":"https://assets-eu.researchsquare.com/files/rs-7596772/v1/669bd0cbbd058bdcec118920.html"},{"id":93731920,"identity":"4653f080-6fe6-4222-8cd2-c18ff0c3bcc8","added_by":"auto","created_at":"2025-10-17 02:24:26","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":373852,"visible":true,"origin":"","legend":"\u003cp\u003ePatient Screening Flowchart\u003c/p\u003e\n\u003cp\u003eFlow diagram illustrating the screening and inclusion process of critically ill patients with new-onset atrial fibrillation (NOAF). Patients were assessed for eligibility based on predefined criteria, including ICU admission, absence of prior atrial fibrillation, and data availability.\u003cbr\u003e\n \u003cstrong\u003eAbbreviations:\u003c/strong\u003e ICU = Intensive Care Unit; IV = Intravenous\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-7596772/v1/9fbc8a6fb16c570217838a7b.png"},{"id":93731943,"identity":"1465ead4-2856-4ff2-86fa-2f147b43bc8d","added_by":"auto","created_at":"2025-10-17 02:24:27","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":129685,"visible":true,"origin":"","legend":"\u003cp\u003eTime to First Bleeding Event after NOAF, Stratified by Anticoagulation Type\u003c/p\u003e\n\u003cp\u003eKaplan–Meier survival curve showing time to first bleeding event within 1 year following NOAF diagnosis. Patients are stratified by the type of anticoagulation administered (e.g., AC, or no anticoagulation).\u003cbr\u003e\n \u003cstrong\u003e\u0026nbsp;Abbreviations\u003c/strong\u003e: NOAF = New-Onset Atrial Fibrillation; DOAC = Direct Oral Anticoagulant; LMWH = Low Molecular Weight Heparin.\u003c/p\u003e","description":"","filename":"floatimage2.png","url":"https://assets-eu.researchsquare.com/files/rs-7596772/v1/7f9b72795ce0ca5591ef8f35.png"},{"id":93732542,"identity":"0b307365-f5a0-435a-a082-3977ce44ab44","added_by":"auto","created_at":"2025-10-17 02:32:26","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":12060,"visible":true,"origin":"","legend":"\u003cp\u003eTime to First Thrombotic Event after NOAF, Stratified by Anticoagulation Type\u003c/p\u003e\n\u003cp\u003eKaplan–Meier survival curve depicting the time to first thrombotic event (e.g., ischemic stroke, systemic embolism, DVT, or PE) during the 1-year follow-up period after NOAF. Groups are stratified by anticoagulation treatment type.\u003cbr\u003e\n\u003cstrong\u003eAbbreviations\u003c/strong\u003e: NOAF = New-Onset Atrial Fibrillation; DVT = Deep Vein Thrombosis; PE = Pulmonary Embolism.\u003c/p\u003e","description":"","filename":"floatimage3.png","url":"https://assets-eu.researchsquare.com/files/rs-7596772/v1/3aa0fd69271c456e4e7decfb.png"},{"id":106809295,"identity":"858718f0-ea41-4670-b362-d8adf726509d","added_by":"auto","created_at":"2026-04-13 16:09:14","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1328558,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-7596772/v1/83a58178-6d5f-4d4e-85e1-a15a2f5f7bb7.pdf"},{"id":93732543,"identity":"f3e9a081-d1ad-4aab-ba9f-aba77d9d0a7e","added_by":"auto","created_at":"2025-10-17 02:32:27","extension":"docx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":17228,"visible":true,"origin":"","legend":"","description":"","filename":"6.SupplementaryAppendix.docx","url":"https://assets-eu.researchsquare.com/files/rs-7596772/v1/24a97799a718546d0fa6debb.docx"},{"id":93731933,"identity":"4bfc75a9-d389-41cb-9ea3-b12a9c880865","added_by":"auto","created_at":"2025-10-17 02:24:27","extension":"docx","order_by":2,"title":"","display":"","copyAsset":false,"role":"supplement","size":23249,"visible":true,"origin":"","legend":"","description":"","filename":"Table12.docx","url":"https://assets-eu.researchsquare.com/files/rs-7596772/v1/d7f1983530fb421e07ef401a.docx"}],"financialInterests":"No competing interests reported.","formattedTitle":"Outcomes of Anticoagulation Initiation in Critically Ill Patients with New-Onset Atrial Fibrillation: A Multicenter Retrospective Cohort Study","fulltext":[{"header":"Introduction","content":"\u003cp\u003eAtrial fibrillation (AF) is considered one of the most common types of cardiac arrhythmia in critically ill patients (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). Newly diagnosed AF occurs in approximately 14% of critically ill patients (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). Recent evidence suggests that patients who developed AF during acute illness (e.g., postoperatively, sepsis) have high long-term risks for AF recurrence and AF-associated complications, such as stroke, heart failure, longer intensive care unit (ICU) and hospital stays, and mortality (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). Even though a reversible condition often drives new onset Atrial fibrillation (NOAF), it is unclear whether AF persists after managing the primary condition, increasing the risk of subsequent stroke (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). NOAF developed during critical illness presents challenges for both short- and long-term management and is associated with a poor prognosis (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). Currently, the data are insufficient regarding estimates of stroke risk reduction or rates of severe bleeding with systemic anticoagulation during critical illness. A retrospective study of 38,582 patients with sepsis and AF found that 35.3% were given anticoagulants during admission. In this study, the use of therapeutic parenteral anticoagulation during hospitalization with sepsis and AF showed a potentially higher bleeding risk. They were not associated with a reduction in ischemic stroke (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). Another retrospective cohort study of 2,304 hospitalized critically ill patients with a primary diagnosis of acute coronary syndromes (ACS), acute pulmonary disease, or sepsis, and a complication of NOAF during admission. This study reported ischemic stroke and bleeding rates after three years of follow-up. There is no association between anticoagulation and a lower incidence of ischemic stroke in patients with NOAF occurring with acute pulmonary disease, sepsis, or ACS. However, anticoagulation was associated with a higher risk of bleeding in patients with AF associated with acute pulmonary disease, but not in sepsis or ACS (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eFew studies have addressed the safety of initiating anticoagulation in ICU patients who developed NOAF during admission. Our study aims to determine the impact of initiating AC versus no AC in critically ill patients with NOAF on patients\u0026rsquo; clinical outcomes.\u003c/p\u003e"},{"header":"Methods","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e\u003ch2\u003eStudy design and setting\u003c/h2\u003e\u003cp\u003eA Multicentre, retrospective cohort study was conducted between January 01, 2018, and February 28, 2024, in four hospitals in Saudi Arabia, including King Faisal Specialist Hospital and research centre\u0026ndash; Jeddah (KFSHRC-J), King Faisal Specialist Hospital and research centre\u0026ndash; Riyadh (KFSHRC-R), King Fahad Medical City (KFMC), and King Saud University Medical City (KSUMC). The institutional review board approved the study at all participating centres. The study included all critically ill adult patients 18 years and older, admitted to the medical ICU, who had a documented diagnosis of new onset of AF during ICU admission and received antiarrhythmic drugs. Patients under 18 years old, patients who were admitted to the ICU post-cardiac surgery, patients on treatment doses of anticoagulants for another indication, and patients with Pre-existing AF were excluded. Patients were followed for one year post-NOAF occurrence.\u003c/p\u003e\u003c/div\u003e\n\u003ch3\u003eStudy outcomes\u003c/h3\u003e\n\u003cp\u003eThe primary outcome was the incidence of bleeding events. The secondary outcomes include the incidence of thrombotic events, documented recurrent AF episodes within one year of follow-up, Length of ICU and hospital stay, and 30-day mortality.\u003c/p\u003e\n\u003ch3\u003eData collection\u003c/h3\u003e\n\u003cp\u003eData were collected retrospectively from the hospital's electronic health records using REDCap (version 10.8.0 - \u0026copy; 2021 Vanderbilt University). The data were extracted for all patients admitted to the medical ICU who were started on oral or intravenous (IV) amiodarone boluses or infusion, oral or IV metoprolol, or oral or IV digoxin. Patients who had documented NOAF were included in the study. Patients were divided into two groups: those who received anticoagulation (AC group) and those who did not (non-AC group) post NOAF. Variables extracted from the medical record will include demographics, comorbidities, APACHE II Score, underlying cause for AF, HAS bleed score, and CHAVSC score on the day of NOAF. Additional data extracted, including 30-day mortality, date of hospital admission and discharge, date of ICU admission and discharge, date of NOAF, date of documented bleeding, date of documented thrombosis, and date of documented recurrent AF episode (time to subsequent AF onset).\u003c/p\u003e\n\u003ch3\u003eDefinitions\u003c/h3\u003e\n\u003cp\u003eNOAF was defined as detecting at least one episode of atrial fibrillation (AF) during the ICU stay, identified by a physician via electrocardiogram (ECG) and documented as AF in the patient profile. We defined recurrent AF as any documented detection of an AF rhythm on ECG, as noted by the physician in the patient profile, following the initial episode of new-onset atrial fibrillation (NOAF) up to 1 year of follow-up. Initiation of full anticoagulation following NOAF episode was defined as prescription for parenteral AC, warfarin, or direct oral anticoagulants (DOACs) within ICU stay and after the NOAF episode. The definitions of major and nonmajor bleeds were based on the International Society on Thrombosis and Hemostasis definitions and criteria. Major bleeding is defined as bleeding that is associated with hemodynamic compromise, occurs in an anatomically critical site, requires transfusion (2 units of packed red blood cells [RBCs]), or results in a haemoglobin drop of 2 g/dL. All other bleeding is categorized as non-major (minor) (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e). Time of bleeding was determined based on documentation of the first clinical recognition of bleeding in physicians' or nursing notes. Thrombotic events were defined as any venous thrombosis, including deep vein thrombosis (DVT) or pulmonary embolism (PE), or other confirmed thromboses (e.g., catheter-associated or atypical site thrombosis) that are confirmed by imaging.\u003c/p\u003e\u003cdiv id=\"Sec7\" class=\"Section2\"\u003e\u003ch2\u003eStatistical analysis\u003c/h2\u003e\u003cp\u003eThe outcomes of interest in this study included bleeding and thrombotic events within one year of NOAF, as well as mortality within 30 days of NOAF. The primary exposure was the status of initiating treatment doses of AC post-NOAF. Descriptive statistics were generated for all patients according to their AC initiation status. Normality assessment for continuous variables included the Shapiro-Wilk and Kolmogorov-Smirnov tests, as well as the observation of each variable's mean, median, skewness, kurtosis, and graphical results. Frequencies were reported for categorical variables. The associations between outcomes, exposure, predictor variables, and AC treatment status were observed using Student\u0026rsquo;s t-test, Kruskal-Wallis test, Chi-square, and Fisher\u0026rsquo;s exact tests.\u003c/p\u003e\u003cp\u003eData with a P-value of less than 0.05 was considered significant. Data that was significant in the univariate analysis was included in the multivariable analysis. Univariate and multivariable logistic models were constructed to predict mortality within 30 days of NOAF and a bleeding event within one year of NOAF, adjusting for full AC treatment status and other predictor variables. Kaplan-Meier curves were generated to examine the time to event of bleeding and thrombosis within one year of NOAF in patients according to AC treatment status. SAS software version 9.4 was used for statistical analyses.\u003c/p\u003e\u003c/div\u003e"},{"header":"Results","content":"\u003cdiv id=\"Sec9\"\u003e\n \u003ch2\u003eBaseline Characteristics\u003c/h2\u003e\n \u003cp\u003eAmong 1968 patients screened, 179 were considered for inclusion (Fig. 1). The mean and standard deviation (SD) age was 68.1 ± 13.4 years. Just over half (54.8%) of the patients were male, and almost three-fourths (72.6%) of them had hypertension. In addition, nearly two-thirds (64.3%) of the patients had diabetes, and over one-fourth (27.4%) had chronic kidney disease. Forty-three percent of the participants had received anticoagulant prophylaxis three months before experiencing NOAF, and just under one-fifth (19.0%) of the patients had a history of a bleeding event within the same three-month period. The mean ± SD APACHE II score for all patients was 21.4 ± 8.4, and the underlying cause of NOAF was sepsis in 54.8% of cases. For the 98 patients with sepsis as the underlying cause of NOAF, almost half (49.0%) were taking vasopressors 24 hours before experiencing NOAF (Table 1).\u003c/p\u003e\n \u003cp\u003eOver half (52.5%) of the patients were in the AC group after experiencing NOAF. Compared to the non-AC group, patients in the AC group were significantly older (70.2 ± 13.8 years vs. 65.7 ± 12.7 years, p = 0.0275) (Table\u0026nbsp;1). There was also a significant association between full AC treatment status and patients with oncology/hematology malignancies, where 29.4% of patients in the non-AC group had this type of comorbidity, compared to 13.8% of patients in the AC group with an oncology/hematology malignancy (p = 0.0109). The mean APACHE II score was also significantly higher for patients in the non-AC group than those in the AC group (23.8 ± 9.4 vs. 19.1 ± 6.8, p = 0.0002). Among the patients who experienced sepsis as the underlying cause of NOAF (n = 98), 49% received vasopressors (66.7% vs 29.8%, p = 0.0003) in the non-AC group and the AC group, respectively (Table\u0026nbsp;1).\u003c/p\u003e\n\u003c/div\u003e\n\u003ch3\u003eOutcomes and Regression Analysis\u003c/h3\u003e\n\u003cp\u003eMore than half (54.2%) of the patient population in this study died within 30 days of experiencing NOAF, with 68.2% of the patients in the non-AC group compared to 41.5% of the patients in the AC group having this outcome (p=-0.0003) (Table 2). For most of the patients (92.7%) who died, the cause of death was not related to bleeding or thrombosis. Seven patients (3.9%) had a thrombotic event within 1 year of experiencing NOAF (Supplementary appendix, Table e1), and 38 patients (21.2%) had a bleeding event within 1 year of NOAF. The median time to the first bleeding event for the 38 patients was 14.5 days (range, 4–31), compared to 7.0 days (range, 5–10) for the time to the first thrombotic event among patients experiencing this outcome. The median (length of stay in the ICU was 14.0 (7–28) days for all patients. (Table 2)\u003c/p\u003e\n\u003cp\u003eAfter adjusting for all predictors in the univariate analysis, taking anticoagulant prophylaxis medication three months before experiencing NOAF and a history of a bleeding event three months before experiencing NOAF remained as significant predictors of a bleeding event within 1 year following NOAF in this patient population (Tables\u0026nbsp;3 and 4). The multivariable regression found that having a bleeding event within 1 year following NOAF was 3.36 times more likely for patients that had taken anticoagulant prophylaxis three months before having NOAF (AOR = 3.36, 95% CI = 1.54–7.33, p = 0.0023) and 3.75 times more likely for patients that had a history of bleeding three months before having NOAF (AOR = 3.75, 95% CI = 1.58–8.86, p = 0.0026) (Table\u0026nbsp;4).\u003c/p\u003e\n\u003cdiv\u003e\n \u003ctable id=\"Tab3\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 3\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eUnivariate association of predictor variables and the event of bleeding within one year of NOAF\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ePredictor\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eOR\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e95% CI\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ep-value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.01\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.98–1.04)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.4079\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eGender (female)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.74\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.36–1.54)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.4210\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eApache II score\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.03\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.99–1.07)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.2130\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTaking full anticoagulation treatment post NOAF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.01\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.49–2.06)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.9869\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHistory of bleeding event three months prior to NOAF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e3.53\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(1.57–7.94)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.0023\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eMedications taken three months prior to NOAF\u003c/p\u003e\n \u003cp\u003eSingle antiplatelet\u003c/p\u003e\n \u003cp\u003eDual antiplatelet\u003c/p\u003e\n \u003cp\u003eAnticoagulant prophylaxis\u003c/p\u003e\n \u003cp\u003eNone\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.87\u003c/p\u003e\n \u003cp\u003e1.99\u003c/p\u003e\n \u003cp\u003e3.29\u003c/p\u003e\n \u003cp\u003e0.77\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e(0.40–1.91)\u003c/p\u003e\n \u003cp\u003e(0.64–6.20)\u003c/p\u003e\n \u003cp\u003e(1.55–6.99)\u003c/p\u003e\n \u003cp\u003e(0.35–1.67)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.7263\u003c/p\u003e\n \u003cp\u003e0.2383\u003c/p\u003e\n \u003cp\u003e0.0019\u003c/p\u003e\n \u003cp\u003e0.5019\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eOR, odds ratio; CI, confidence interval; NOAF, new-onset atrial fibrillation\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cdiv\u003e\n \u003ctable id=\"Tab4\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 4\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eMultivariable association of predictor variables and event of bleeding within one year of NOAF\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ePredictor\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eOR\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e95% CI\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ep-value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.02\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.99–1.05)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.1700\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHistory of bleeding event three months prior to NOAF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e3.75\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(1.58–8.86)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.0026\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTaking anticoagulant prophylaxis three months prior to NOAF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e3.36\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(1.54–7.33)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.0023\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eOR, odds ratio; CI, confidence interval; NOAF, new-onset atrial fibrillation\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003eUnivariate regression analysis revealed that, for every one-unit increase in APACHE II score, the odds of mortality increase by 7% [odds ratio (OR) and 95% confidence interval (CI) = 1.07 (1.03–1.11), p = 0.0011] (Table\u0026nbsp;5). The outcome of mortality was 0.33 times as likely for patients in the AC group after experiencing NOAF (OR and 95% CI = 0.33 [0.18–0.61], p = 0.0004). In addition, taking vasopressors 24 hours before NOAF increased the likelihood of mortality within 30 days by 3.59 times (OR = 3.59, 95% CI 1.56–8.28, p = 0.0027). (Table\u0026nbsp;5)\u003c/p\u003e\n\u003cdiv\u003e\n \u003ctable id=\"Tab5\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 5\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eUnivariate association of predictor variables and 30-day mortality in NOAF patients\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ePredictor\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eOR\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e95% CI\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ep-value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.00\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.99–1.03)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.5149\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eGender (female)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.01\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.56–1.82)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.9745\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eApache II score\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.07\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(1.03–1.11)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.0011\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTaking full anticoagulation treatment\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.33\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.18–0.61)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.0004\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNOAF underlying cause of sepsis\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.90\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.50–1.63)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.7390\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTaking vasopressors 24 hours prior to NOAF\u003csup\u003e1\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e3.59\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(1.56–8.28)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.0027\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eHistory of stroke/TIA\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.92\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.37–2.29)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.8591\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eOR, odds ratio; CI, confidence interval; NOAF, new-onset atrial fibrillation; TIA, transient ischemic attack; \u003csup\u003e1\u003c/sup\u003eincludes n = 98 patients with NOAF as underlying cause of sepsis\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003eA multivariable model for all patients (n = 179) revealed that an increase in APACHE II score and AC treatment status remained significant predictors of mortality within 30 days, after adjusting for all other predictors (Table\u0026nbsp;6). In a multivariable model predicting mortality within 30 days in the patients with sepsis as the underlying cause of NOAF (n = 98), taking AC treatment remained protective, adjusting for the other predictors in the model [adjusted odds ratio (AOR) = 0.30, 95% CI = 0.11–0.81, p = 0.0171] (Table\u0026nbsp;7).\u003c/p\u003e\n\u003cdiv\u003e\n \u003ctable id=\"Tab6\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 6\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eMultivariable analysis of association between predictor variables and 30-day mortality (n = 179)\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ePredictor\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eOR\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e95% CI\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ep-value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.01\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.99–1.04)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.3153\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eApache II score\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.05\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(1.01–1.09)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.0159\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTaking full anticoagulation treatment post-NOAF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.37\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.19–0.72)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.0031\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eOR, odds ratio; CI, confidence interval\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cdiv\u003e\n \u003ctable id=\"Tab7\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 7\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eMultivariable analysis of association between predictor variables and 30-day mortality for patients with sepsis as the underlying cause of NOAF (n = 98)\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ePredictor\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eOR\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003e95% CI\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ep-value\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (years)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.01\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.98–1.04)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.6029\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eApache II score\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e1.05\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.99–1.11)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.1334\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTaking full anticoagulation treatment post-NOAF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.30\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.11–0.81)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.0171\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTaking vasopressors 24 hours prior to NOAF\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.48\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e(0.19–1.20)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e0.1151\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"4\"\u003eOR, odds ratio; CI, confidence interval\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003eThe probability of not experiencing a bleeding event after NOAF was 0.8849 for patients on the AC group and 0.8490 for patients on the non-AC group. (Fig.\u0026nbsp;2) The difference in patient event experience according to full AC treatment status was insignificant [Log-Rank Chi-sq = 1.43, degrees of freedom (df) = 1, p-value = 0.2309]. Similarly, the probability of not experiencing a thrombotic event after NOAF was 0.9772 for patients on AC group and 0.9318 for patients on non AC group and the difference in event experience for patients according to full AC treatment status was not significant [Log-Rank Chi-sq = 2.40, degrees of freedom (df) = 1, p-value = 0.1209] (Fig.\u0026nbsp;3).\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eOur study adds to a growing body of literature exploring the impact of AC initiation in critically ill patients with NOAF. This condition remains poorly addressed in current clinical guidelines. As a recent international survey has demonstrated, the significant variation in NOAF management across regions highlights the lack of standardized protocols. It highlights the need for context-specific data to guide therapy.(\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eOne might expect patients who are on AC to be more prone to bleeding. However, this was not the case in our study; Bleeding complications, though infrequent, remain a key concern. In our cohort, the bleeding rate was similar between the two groups, at 21%. Of these, 47.4% were major bleeding events, and 54.6% were minor bleeding events. In contrast to the study conducted by Darwish et al., our study observed a higher bleeding rate (8.6% vs. 21%) (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). This can be further explained by the fact that one-third of our patient population (27%) had chronic kidney disease (CKD). Chronic kidney disease is considered a risk factor for both bleeding and thrombosis. Our findings contradict the observations made in previous studies regarding bleeding. For instance, Walkey et al. conducted a retrospective cohort study to evaluate the risk of stroke and bleeding associated with AC administration for NOAF during sepsis. Clinically significant bleeding occurred more often among patients who received parenteral AC (1163 of 13,505 [8.6%]) than among patients who did not receive parenteral AC (979 of 13,505 [7.2%]; RR, 1.21; 95% CI, 1.10\u0026ndash;1.32) (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). Our study, as well as the survey conducted by Walkey et al., utilized the HAS-BLED score to assess bleeding risk. However, it has not been validated for estimating bleeding risk in critically ill patients with NOAF (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). However, our findings were consistent with prior systematic reviews and observational data, which report that the bleeding risk often offsets the theoretical thromboembolic benefit of AC during critical illness, specifically among patients with sepsis. This population frequently overlaps with NOAF(\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e).\u003c/p\u003e\u003cp\u003eAs expected, in our study, the initiation of AC resulted in a non-significantly lower rate of thrombotic events, 2.1% versus 5.9%. The 2014 ACC/AHA atrial fibrillation guidelines and the subsequent 2019 focused update both acknowledge that the role of AC in acute non-cardiac illness remains to be elucidated (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e). Studies conducted to observe the benefit of AC in reducing the risk of thromboembolism in NOAF in critically ill patients showed no significant difference. Notably, thromboembolism in the available literature is defined as the incidence of stroke development after NOAF (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). In a retrospective cohort study conducted by Quon et al., which overlooked 2,304 critically ill patients who were 65 years or older and hospitalized for ACS, acute pulmonary disease or sepsis and a complication of NOAF, anticoagulation administration didn\u0026rsquo;t result in a lower incidence of ischemic stroke in ACS, acute pulmonary disease and sepsis with the following odds ratio OR respectively OR: 1.22 [95% confidence interval (CI): 0.65 to 2.27], OR: 0.97 [95% CI: 0.53 to 1.77], and OR: 1.98 [95% CI: 0.29 to 13.47])(\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). Additionally, a post hoc analysis of the AFTER-ICU study (Atrial Fibrillation Treatment Evaluation Registry in the ICU) was conducted by Sakuraya et al. in 2021. It was a prospective multicentre cohort study of NOAF in the general ICU population. The study aimed to describe the efficacy of AC initiation (within 48 hours of NOAF) according to the CHA2DS2-VASc score in critically ill patients. The study hypothesized that early AC initiation would have a positive effect on neurological outcomes. The primary outcome was a composite outcome of mortality and ischemic stroke. After adjusting for confounders, the study concluded that there was no statistically significant difference between the two groups in terms of the primary outcome. However, in the early AC initiation group, there was a numerically lower incidence of ischemic stroke when compared to no AC. Ischemic stroke until hospital discharge occurred in 10 (4.7%) vs 3 (3.1%), p\u0026thinsp;=\u0026thinsp;0.112. During ICU stay, 5 (2.4%) vs 1 (1.1%), p\u0026thinsp;=\u0026thinsp;0.448. After ICU discharge, 5 (2.8%) vs 0 (0%), p\u0026thinsp;=\u0026thinsp;0.1 (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Similar to the studies mentioned above, our findings indicate that there was no statistically significant difference, but numerically lower thrombotic events within one year of NOAF [2 (2.1) vs 5 (5.9), p\u0026thinsp;=\u0026thinsp;0.2592]. It should be noted that we had a broader definition of thromboembolism as we captured not only stroke but also deep venous thrombosis and pulmonary embolism. We propose several theories to explain the findings in our study. Firstly, we had a smaller sample size compared to other studies. This may have led to no difference being shown. Secondly, like the studies mentioned, the CHA2DS2-VASc score of our patient population was 3 [2\u0026ndash;4], indicating a moderate risk of thrombosis. Furthermore, the CHA2DS2-VASc score has not yet been validated to assess thrombotic risk in NOAF in the critically ill population (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e, \u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e). Moreover, 50% of patients who didn\u0026rsquo;t receive treatment doses of AC received prophylactic AC. Lastly, the incidence of stroke post-NOAF in critically ill patients is much lower than in the general population with atrial fibrillation (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e)\u003c/p\u003e\u003cp\u003eOnly a few observational studies have overlooked the relationship between anticoagulation and mortality in patients who are deemed critically ill and presenting with NOAF. For instance, a research study conducted by Darwish et al. on 115 patients with NOAF and sepsis showed no statistically significant difference in survival rates during hospitalization (66.2% for the non-anticoagulated group vs. 74.3% for the anticoagulated group, P\u0026thinsp;=\u0026thinsp;.392) (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). Sakuraya et al. examined early versus late administration of AC in critically ill patients presenting with NOAF. Early AC administration was defined as AC initiation within 48 hours of the onset of NOAF. The 30-day mortality rate was numerically lower in those who received early AC (13.7%) compared to those who received late AC (24.4%) (\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e). Our analysis revealed a statistically significantly lower 30-day mortality rate in those who received AC, 41.5%, compared to 68.2% in those who didn\u0026rsquo;t receive treatment doses of AC, with a p-value of 0.0003. There was a statistically significant difference between the two groups in terms of age, APACHE II score and the recipient of vasopressors 24 hours before NOAF however, when multivariable analysis was performed in all patients with NOAF only age, increased of APACHE II score, and the administration of complete AC treatment were determined to be predictors of 30 days mortality. Notably, the cause of death in 92.7% of the patient population was not related to thrombosis or bleeding. Although the multivariable analysis adjusted for APACHE II score and vasopressor use, these factors may not fully capture the extent of bleeding risk or coagulopathy at the time of NOAF.\u003c/p\u003e\u003cp\u003eThe study\u0026rsquo;s strength lies in its multicentre design, and multivariable analysis was conducted to detect any potential bias from confounders. The study\u0026rsquo;s limitations include the following: the study included only patients who received pharmacologic intervention, which may have excluded untreated NOAF cases and thereby limited the external validity of the findings. The observational chart review nature prevented us from documenting whether the patients who received parenteral AC had their laboratory activated partial thromboplastin time in the therapeutic range. The role of direct oral anticoagulants (DOACs) has not been examined to prevent stroke in NOAF in critically ill patients. Also, the majority of our patients\u0026rsquo; underlying cause of NOAF was sepsis. Thus, it is difficult to extrapolate our findings to other critically ill populations, such as surgical patients. Moreover, a significant limitation of this study is the potential for immortal time bias due to the variable timing of anticoagulation initiation; patients who survived long enough to receive anticoagulation may have had an inherent survival advantage over those who died earlier and were classified as non-anticoagulated. A key limitation is that death may act as a competing risk for bleeding and thrombotic events, potentially leading to an overestimation of their incidence, as the survival analysis was performed without conducting competing risk analysis. A potential limitation is the possibility of confounding by indication in the comparison of bleeding rates between anticoagulated and non-anticoagulated patients, as those at higher bleeding risk may have been selectively excluded from receiving anticoagulation, potentially masking actual differences in bleeding risk. The observed association between lack of anticoagulation and higher 30-day mortality may be influenced by residual confounding related to illness severity. Patients with coagulopathy, active bleeding, or hemodynamic instability\u0026mdash;who are less likely to receive anticoagulation\u0026mdash;are also inherently at higher risk of death. Lastly, our study is not powered to detect differences between groups.\u003c/p\u003e"},{"header":"Conclusions","content":"\u003cp\u003eThe study showed no statistically significant differences in bleeding and thrombotic events between critically ill patients with NOAF who received anticoagulation and those who did not receive anticoagulation within one year of follow-up. However, 30-day mortality was lower in patients who received full anticoagulation post-NOAF. These findings, combined with growing international evidence, support the adoption of an individualized strategy. Given the variability in practice, uncertain benefits during acute illness, and emerging data supporting stroke prevention in select high-risk patients, we advocate for selective AC initiation based on bleeding risk and thromboembolic profile, and follow-up for survivors with NOAF. Future trials are urgently needed to determine the optimal timing and duration of anticoagulation for this population.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eACS: Acute Coronary Syndromes\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eAC: Anticoagulation\u003c/p\u003e\n\u003cp\u003eAF: Atrial Fibrillation\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eDVT: Deep Vein Thrombosis\u003c/p\u003e\n\u003cp\u003eECG: Electrocardiogram\u003c/p\u003e\n\u003cp\u003eICU: Intensive Care Units\u003c/p\u003e\n\u003cp\u003eIV: Intravenous\u003c/p\u003e\n\u003cp\u003eIQR: Interquartile Ranges\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eKFSHRC-J: King Faisal Specialist Hospital and Research Centre-Jeddah (\u003c/p\u003e\n\u003cp\u003eKFSHRC-R: King Faisal Specialist Hospital and Research Centre\u0026ndash; Riyadh\u003c/p\u003e\n\u003cp\u003eKFMC: King Fahad Medical City\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eKSUMC: King Saud University Medical City \u0026nbsp;\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eLMWH: Low Molecular Weight Heparin.\u003c/p\u003e\n\u003cp\u003eNOAF: New Onset Atrial Fibrillation\u0026nbsp;\u003c/p\u003e\n\u003cp\u003en: Frequencies\u003c/p\u003e\n\u003cp\u003ePE: Pulmonary Embolism\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eSD: Standard Deviation\u0026nbsp;\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe study was reviewed and approved by the Institutional Review Board (IRB) at King Faisal Specialist Hospital and Research Centre in Jeddah and Riyadh, King Fahad Medical City in Riyadh, and King Saud University Medical City in Riyadh (Reference numbers IRB 2023-31, 24-185, and 3/0797/IRB, respectively). The data were kept confidential; only the research team had access to the files. Written informed consent was waived due to the retrospective nature of the study. This study was conducted in accordance with Good Clinical Research Practice (Declaration of Helsinki) and the rules and guidelines of the Ethics Committee at KFSHRC.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe datasets used and/or analysed during the current study are available from the corresponding author upon reasonable request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eDeclaration of generative AI and AI-assisted technologies in the writing process\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eDuring the preparation of this work, the authors used [Grammarly] to [enhance grammatical accuracy and improve clarity of expression for the readers]. After using this tool/service, the authors reviewed and edited the content as needed and take full responsibility for the content of the publication.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026rsquo; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eRaghad ALASMARI contributed to conceptualization, manuscript writing, data acquisition, and proposal writing. Namareq Aldardeer and Khalid Alghamdi conceptualized, supervised, and critically reviewed the manuscript; Awatif Hafiz performed data acquisition and manuscript writing; Emily HEAPHY performed data analysis and manuscript writing; Nouf Bahiri, Ghida Bawaked, Abdullah Alhammad, Marwa Amer, Turkiah Alkhaldi, Raghad Alshhri, Firas Kseibi, Amro Hajja, Noran Abouobaid, Ghassan Bagazi, Raghad Bajaba, and Hanadi Shaheen performed data acquisition. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eClinical Trial Number\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgments\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable\u0026nbsp;\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eKorelitz BI, Sommers SC. Responses to drug therapy in ulcerative colitis. Evaluation by rectal biopsy and histopathological changes. Am J Gastroenterol. 1975 Nov;64(5):365\u0026ndash;70. \u003c/li\u003e\n\u003cli\u003eArtucio H, Pereira M. Cardiac arrhythmias in critically ill patients: Epidemiologic study. Crit Care Med. 1990 Dec;18(12):1383\u0026ndash;8. \u003c/li\u003e\n\u003cli\u003eDarwish OS, Strube S, Nguyen HM, Tanios MA. Challenges of Anticoagulation for Atrial Fibrillation in Patients With Severe Sepsis. Ann Pharmacother. 2013 Oct;47(10):1266\u0026ndash;71. \u003c/li\u003e\n\u003cli\u003eWalkey AJ, Quinn EK, Winter MR, McManus DD, Benjamin EJ. Practice Patterns and Outcomes Associated With Use of Anticoagulation Among Patients With Atrial Fibrillation During Sepsis. JAMA Cardiol. 2016 Sep 1;1(6):682. \u003c/li\u003e\n\u003cli\u003ePisters R, Lane DA, Nieuwlaat R, De Vos CB, Crijns HJGM, Lip GYH. A Novel User-Friendly Score (HAS-BLED) To Assess 1-Year Risk of Major Bleeding in Patients With Atrial Fibrillation. Chest. 2010 Nov;138(5):1093\u0026ndash;100. \u003c/li\u003e\n\u003cli\u003eHindricks G, Potpara T, Dagres N, Arbelo E, Bax JJ, Blomstr\u0026ouml;m-Lundqvist C, et al. 2020 ESC Guidelines for the diagnosis and management of atrial fibrillation developed in collaboration with the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2021 Feb 1;42(5):373\u0026ndash;498. \u003c/li\u003e\n\u003cli\u003eQuon MJ, Behlouli H, Pilote L. Anticoagulant Use and Risk of Ischemic Stroke and Bleeding in Patients With Secondary Atrial Fibrillation Associated With Acute Coronary Syndromes, Acute Pulmonary Disease, or Sepsis. JACC Clin Electrophysiol. 2018 Mar;4(3):386\u0026ndash;93. \u003c/li\u003e\n\u003cli\u003eTomaselli GF, Mahaffey KW, Cuker A, Dobesh PP, Doherty JU, Eikelboom JW, et al. 2020 ACC Expert Consensus Decision Pathway on Management of Bleeding in Patients on Oral Anticoagulants. J Am Coll Cardiol. 2020 Aug;76(5):594\u0026ndash;622. \u003c/li\u003e\n\u003cli\u003eJohnston BW, Udy AA, McAuley DF, Mogk M, Welters ID, Sibley S. An International Survey of the Management of Atrial Fibrillation in Critically Unwell Patients. Crit Care Explor. 2024 Mar 26;6(4):e1069. \u003c/li\u003e\n\u003cli\u003eTeixeira C, Tonietto TF. The quandary of anticoagulation for sepsis patients with new-onset atrial fibrillation. Crit Care Sci. 2025 Feb 28;37:e20250120. \u003c/li\u003e\n\u003cli\u003eJanuary CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation [Internet]. 2014 Dec 2 [cited 2025 Apr 14];130(23). Available from: https://www.ahajournals.org/doi/10.1161/CIR.0000000000000041\u003c/li\u003e\n\u003cli\u003eJanuary CT, Wann LS, Calkins H, Chen LY, Cigarroa JE, Cleveland JC, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society in Collaboration With the Society of Thoracic Surgeons. Circulation [Internet]. 2019 Jul 9 [cited 2025 Apr 18];140(2). Available from: https://www.ahajournals.org/doi/10.1161/CIR.0000000000000665\u003c/li\u003e\n\u003cli\u003eSakuraya M, Yoshida T, Sasabuchi Y, Yoshihiro S, Uchino S. Clinical prediction scores and early anticoagulation therapy for new-onset atrial fibrillation in critical illness: a post-hoc analysis. BMC Cardiovasc Disord. 2021 Dec;21(1):423. \u003c/li\u003e\n\u003cli\u003eLip GYH, Frison L, Halperin JL, Lane DA. Identifying Patients at High Risk for Stroke Despite Anticoagulation: A Comparison of Contemporary Stroke Risk Stratification Schemes in an Anticoagulated Atrial Fibrillation Cohort. Stroke. 2010 Dec;41(12):2731\u0026ndash;8. \u003c/li\u003e\n\u003cli\u003eLip GYH, Nieuwlaat R, Pisters R, Lane DA, Crijns HJGM. Refining Clinical Risk Stratification for Predicting Stroke and Thromboembolism in Atrial Fibrillation Using a Novel Risk Factor-Based Approach. Chest. 2010 Feb;137(2):263\u0026ndash;72. \u003c/li\u003e\n\u003cli\u003eButt JH, Xian Y, Peterson ED, Olsen PS, R\u0026oslash;rth R, Gundlund A, et al. Long-term Thromboembolic Risk in Patients With Postoperative Atrial Fibrillation After Coronary Artery Bypass Graft Surgery and Patients With Nonvalvular Atrial Fibrillation. JAMA Cardiol. 2018 May 1;3(5):417. \u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Table 1 and 2","content":"\u003cp\u003eTable 1 and 2 are available in the Supplementary Files section.\u003c/p\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-cardiovascular-disorders","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bcar","sideBox":"Learn more about [BMC Cardiovascular Disorders](http://bmccardiovascdisord.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bcar/default.aspx","title":"BMC Cardiovascular Disorders","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Anticoagulation, New-onset Atrial Fibrillation, Bleeding, Thromboembolism, Critical Illness","lastPublishedDoi":"10.21203/rs.3.rs-7596772/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7596772/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eIntroduction:\u003c/h2\u003e\u003cp\u003eNew-onset atrial fibrillation (NOAF) in intensive care units (ICU) carries a high risk of recurrence and atrial fibrillation (AF) related complications. However, evidence on the safety of anticoagulation (AC) in critically ill patients with NOAF is limited. This study aimed to evaluate the impact of AC initiation on clinical outcomes in this population.\u003c/p\u003e\u003ch2\u003eMethods\u003c/h2\u003e\u003cp\u003eA multicentre, retrospective cohort study was conducted across four hospitals in Saudi Arabia from January 1, 2018, to February 28, 2024. Adult ICU patients (\u0026ge;\u0026thinsp;18 years) with documented NOAF were included and categorized into two groups: those who received anticoagulation (AC group) and those who did not (non-AC group). The Study outcomes were the incidence of bleeding or thrombotic events during a 1-year follow-up.\u003c/p\u003e\u003ch2\u003eResults\u003c/h2\u003e\u003cp\u003eA total of 179 patients were included, with 52.5% in the AC group and 47.4% in the non-AC group. The mean age was 68.1\u0026thinsp;\u0026plusmn;\u0026thinsp;13.4 years. The median CHA2DS2-VASc and HAS-BLED scores were 3 [2\u0026ndash;4] and 2 [2\u0026ndash;4], respectively. The mean APACHE II score was significantly lower in the AC group compared to the non-AC group (19.1\u0026thinsp;\u0026plusmn;\u0026thinsp;6.8 vs. 23.8\u0026thinsp;\u0026plusmn;\u0026thinsp;9.4; P\u0026thinsp;=\u0026thinsp;0.0002). The incidence of bleeding events was similar between groups (21.3% vs. 21.2%; P\u0026thinsp;=\u0026thinsp;0.9869), as was the incidence of thrombotic events (2.1% vs. 5.9%; P\u0026thinsp;=\u0026thinsp;0.2592).\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e\u003cp\u003eIn critically ill patients with NOAF, anticoagulation did not significantly alter the risk of bleeding or thrombotic events within 1 year of follow-up. These findings highlight the need for further prospective studies to guide anticoagulation decisions in this high-risk population.\u003c/p\u003e","manuscriptTitle":"Outcomes of Anticoagulation Initiation in Critically Ill Patients with New-Onset Atrial Fibrillation: A Multicenter Retrospective Cohort Study","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-10-17 02:24:03","doi":"10.21203/rs.3.rs-7596772/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2025-10-28T08:23:40+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-10-16T01:56:44+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-10-12T19:38:44+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"78545199253128441117545955430695128741","date":"2025-10-08T23:00:45+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2025-10-06T23:40:38+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"57747539232636745767715009577760763593","date":"2025-10-06T23:32:34+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"136959045209747274440374442821656970366","date":"2025-10-06T16:25:42+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2025-10-06T02:31:26+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2025-10-02T19:38:53+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2025-09-23T05:19:31+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2025-09-19T16:36:16+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Cardiovascular Disorders","date":"2025-09-19T16:33:17+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-cardiovascular-disorders","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bcar","sideBox":"Learn more about [BMC Cardiovascular Disorders](http://bmccardiovascdisord.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bcar/default.aspx","title":"BMC Cardiovascular Disorders","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"4c6dfbd2-bc2f-4790-a61f-483cd5b7cd18","owner":[],"postedDate":"October 17th, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"published-in-journal","subjectAreas":[],"tags":[],"updatedAt":"2026-04-13T16:05:56+00:00","versionOfRecord":{"articleIdentity":"rs-7596772","link":"https://doi.org/10.1186/s12872-026-05826-5","journal":{"identity":"bmc-cardiovascular-disorders","isVorOnly":false,"title":"BMC Cardiovascular Disorders"},"publishedOn":"2026-04-11 15:57:50","publishedOnDateReadable":"April 11th, 2026"},"versionCreatedAt":"2025-10-17 02:24:03","video":"","vorDoi":"10.1186/s12872-026-05826-5","vorDoiUrl":"https://doi.org/10.1186/s12872-026-05826-5","workflowStages":[]},"version":"v1","identity":"rs-7596772","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-7596772","identity":"rs-7596772","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}