Body mass index and adverse cardiovascular events in individuals with atrial fibrillation taking oral anticoagulants: a prospective, observational, long-term follow-up cohort study
Faculty of Medicine, Jan Kochanowski University, Kielce, Poland
Introduction
Atrial fibrillation (AF) is the most common persistent cardiac arrhythmia worldwide, affecting approximately 44 million people [1, 2], and its prevalence is expected to double in the coming decades [3]. This arrhythmia leads to adverse cardiovascular outcomes [4]. Numerous studies have linked obesity to an enhanced risk of AF [5, 6]; however, the influence of body mass index (BMI) on clinical events in individuals with established AF taking oral anticoagulants (OACs) remains unclear [4, 7].
The “obesity paradox” describes an intriguing phenomenon wherein overweight or obese individuals may experience better cardiovascular outcomes than those with normal BMI [8]. Although some studies support this in individuals with AF [9–13], other studies suggest no protective effect or even an enhanced risk of complications associated with a higher BMI [8, 14–16]. Additionally, evidence regarding the impact of BMI on cardiac thrombogenesis [2, 17, 18] and long-term cardiovascular events in individuals with AF taking OACs remains sparse and inconsistent.
Aim of the research
Given the importance of identifying factors influencing AF prognosis, we aimed to explore the association between BMI categories (normal weight, overweight, and obesity) and adverse cardiovascular outcomes, including left atrial appendage thrombus (LAAT) and other major events. By addressing these knowledge gaps, we hope to enhance our understanding of the complex relationship between BMI and cardiovascular risk in this high-risk population.
Material and methods
Study group
This prospective observational cohort study was conducted using data collected from the electronic medical database of the Provincial Combined Hospital in Kielce, Poland. Eligible participants were individuals with AF admitted to the Cardiology Department for electrical cardioversion guided by transoesophageal echocardiography (TEE) between December 2010 and March 2023. The inclusion and exclusion criteria are presented in Table 1. Consecutive recruitment ensured a representative cohort of individuals with AF.
This study adhered to the ethical principles of the Declaration of Helsinki from 1989. Ethical approval was granted by the Committee on Ethics of the Jan Kochanowski University of Humanities and Sciences in Kielce, Poland (ratification document code: 21/2010; date of agreement: 28 January 2010). Informed consent was obtained from all study participants. To ensure high-quality reporting, our study followed the Strengthening of Reporting Observational Studies in Epidemiology (STROBE) recommendations.
Oral anticoagulants
Patients receiving OACs were eligible for inclusion if they fulfilled the following criteria: vitamin K antagonist therapy with dose adjustment and international normalised ratio monitoring, maintaining a therapeutic range (international normalised ratio ≥ 2.0), or uninterrupted anticoagulation with apixaban, rivaroxaban, or dabigatran for at least 3 weeks before enrolment [19–22]. For dabigatran therapy, the standard full dose was 150 mg twice daily; however, a reduced dose of 110 mg twice daily was also permitted if any of the following applied: concomitant use of verapamil, age ≥ 80 years, “hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile international normalised ratio, elderly (> 65 years), drugs/alcohol concomitantly” (HAS-BLED) score ≥ 3, or estimated glomerular filtration rate (eGFR) 30–49 ml/min/1.73 m2 [20]. For rivaroxaban therapy, the standard full dose was 20 mg once daily; however, a reduced dose of 15 mg once daily was also permitted if any of the following applied: HAS-BLED score ≥ 3 or eGFR 15–49 ml/min/1.73 m2. For apixaban therapy, the standard full dose was 5 mg twice daily; however, a reduced dose of 2.5 mg twice daily was also permitted if two out of three of the following applied: serum creatinine level ≥ 1.5 mg/dl, body weight ≤ 60 kg, or age ≥ 80 years. For individuals on vitamin K antagonist therapy, the international normalised ratio was checked weekly for 3 weeks before enrolment, with all values required to be within the therapeutic range. eGFR was evaluated using the Modification of Diet in Renal Disease method [23].
The inclusion and exclusion criteria for the study were clear and unambiguous and were adhered to throughout the recruitment period. However, the quality of anticoagulant regimens in relation to the current guidelines for AF was always monitored and, if necessary, adjusted at discharge during the index hospitalisation.
Echocardiographic examination
Cardiac ultrasound measurements were performed by certified cardiac sonographers using the GE Vivid E95 and GE Vivid E9 ultrasound systems (GE Vingmed Ultrasound AS, Horten, Norway). The examinations followed established protocols and current guidelines [24]. The left atrial appendage (LAA) was imaged using a multiplanar ultrasound transducer from the mid-oesophageal view on TEE. The LA diameter was assessed at the end of ventricular systole using transthoracic echocardiography in the parasternal long-axis view, measured perpendicular to the long axis of the aortic root. The left ventricular ejection fraction was evaluated using the biplane Simpson method as per echocardiographic guidelines [25]. Cardiac blood clots (thrombi) were defined as echodense intracardiac masses with well-defined margins, clearly separated from the endocardial border, visualised in at least two imaging planes throughout the cardiac cycle, and distinguishable from the pectinate muscles on echocardiographic examination [26]. All measurements were documented and archived for further analysis to ensure reproducibility and compliance with clinical standards.
Statistical analysis
Categorical variables are summarised as frequencies and percentages. Continuous variables are summarised as means, SDs, medians, and interquartile ranges. The normality of continuous variables was evaluated using the Shapiro–Wilk test. For all continuous variables, the Kruskal–Wallis test was performed because of their non-normal distribution. For categorical variables, the Fisher exact test (when the expected frequency was < 5) or the c2 test was applied. To evaluate the differences between the subgroups presented in Tables 2 and 3, the Fisher exact test was performed for variables such as prior transient ischaemic attack, stroke, systemic thromboembolism, chronic obstructive pulmonary disease, previous myocardial infarction, and peripheral artery disease, and c2 tests were applied to other categorical variables. Kaplan–Meier survival curves for cardiovascular death and hospitalisation for heart failure were created according to BMI categories (normal weight, overweight, and obese). For the multiple-sample survival analysis, the Mantel procedure was used to assign a score to each survival time. Then, a c2 value was computed on the basis of the sums of these scores for each group.
Statistical analysis
Statistical significance was defined as a two-tailed p-value < 0.05. Survival data analyses were performed using Statistica (data analysis software system, version 13; TIBCO Software Inc.), where the described survival analysis method is the default test in multiple-sample survival analysis. Other statistical analyses were conducted using R (version 4.0.3; R Foundation for Statistical Computing, Vienna, Austria).
Results
In total, 500 consecutive individuals with AF, who were taking OACs, were included in this study. Follow-up data were collected for a median duration of 1927.5 days (interquartile range: 1004–2643 days), beginning on the day of the TEE procedure. Follow-up was completed for all participants. Endpoint information was collected from the hospital database and directly from participants or their relatives during the first evaluation and 12 months after study enrolment and was reassessed annually. The proportion of women was significantly lower in the overweight group than in the normal-weight and obese groups (p = 0.035). Diastolic blood pressure was significantly lower in the normal-weight group than in the other groups (p = 0.006). The LA diameter was smaller in the normal-weight group than in the other groups (p < 0.001). Arterial hypertension and diabetes mellitus were less prevalent in the normal-weight group than in the other groups (p < 0.001 and < 0.001, respectively). Angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers were prescribed less frequently in the normal-weight group (p < 0.001) (Table 2).
During the index hospitalisation, a rate control strategy was applied without electrical cardioversion in 82 individuals (16.4%) due to either LAAT (65 [13%]) or recurrent arrhythmia (17 [3.4%]) in patients unlikely to maintain sinus rhythm. Among the 418 (83.6%) individuals who underwent electrical cardioversion, 365 (87.3%) achieved sinus rhythm. No periprocedural complications were observed. LAAT rates were similar across different BMI categories (p = 0.25), and no significant differences were observed in the rates of hospitalisation for heart failure, myocardial infarction, transient ischaemic attack, stroke, systemic thromboembolism, cardiovascular death, or all-cause mortality among the BMI groups (Table 3).
Kaplan–Meier survival curves for cardiovascular death and hospitalisation for HF in the normal, overweight, and obese groups are presented in Figures 1 and 2. Survival distributions showed no significant differences in cardiovascular death and hospitalisation for HF among the BMI groups (p = 0.06 for both analyses).
In summary, although there were notable differences in baseline characteristics, such as lower comorbidity rates and more favourable echocardiographic measurements in the normal-weight group, no significant differences were found in long-term cardiovascular outcomes or LAAT across the BMI categories.
Discussion
This study aimed to evaluate the effects of BMI on adverse cardiovascular outcomes in individuals with AF taking OACs. Our findings revealed that BMI status, stratified into normal-weight, overweight, and obese categories, did not significantly influence cardiovascular outcomes. Normal-weight individuals exhibited fewer comorbidities and had more favourable echocardiographic measurements; however, these differences in baseline characteristics did not translate into improved long-term outcomes or LAAT formation. Our findings suggest that BMI is not a predictor of adverse outcomes in individuals with AF taking OACs.
Previous studies have shown inconsistent associations between BMI and cardiovascular outcomes in individuals with AF. Some studies suggest that obesity negatively impacts prognosis and increases cardiovascular mortality and morbidity [8, 14–16], whereas others indicate the opposite [9–13]. This inverse relationship between obesity and improved long-term cardiovascular outcomes has been described as the “obesity paradox”. Previous trials addressing this issue have shown varying representations of individuals receiving OAC therapy.
Overall, BMI has increased significantly in recent decades in adults, children, and adolescents [6], and obesity is a major risk factor for cardiovascular morbidity and mortality [27, 28]. It is well established that obesity increases AF susceptibility [29]. In a meta-analysis by Wanahita et al. [30], obesity was associated with a 49% increased risk of developing AF in the general population, and the risk increased in parallel with greater BMI. Similarly, a meta-analysis by Asad et al. [31] found that obesity was associated with an enhanced risk of new-onset AF in susceptible patients, which appeared consistent in men and women.
The association between BMI categories and adverse cardiovascular outcomes has been studied previously. Grymonprez et al. [32] conducted a meta-analysis of observational and randomised studies and found that the overweight and obese groups with AF taking anticoagulation therapy had significantly lower risks of systemic embolism, stroke, and all-cause mortality than the normal-weight group. Similarly, Zhou et al. [33] demonstrated a reduced risk of systemic embolism, stroke, and all-cause mortality in overweight or obese individuals with AF who received OAC therapy. Proietti et al. [34] conducted a meta-analysis of the ARISTOTLE, RE-LY, and ROCKET AF trials that revealed an obesity paradox in individuals with AF; the overweight and obese groups had a significantly lower risk of stroke/systemic embolic events than those with a normal BMI. Ardestani et al. [12] analysed individuals with AF, of whom 87% were taking warfarin anticoagulant therapy across all BMI categories. Their findings indicated that overweight individuals had a significantly reduced risk of cardiovascular death (hazard ratio [HR]: 0.47, p = 0.002), whereas obesity did not negatively affect cardiovascular (p = 0.15) or overall survival (p = 0.3). Similarly, Badheka et al. [9] conducted a post hoc analysis of the AFFIRM trial, comprising individuals with AF (approximately 87% taking warfarin across BMI groups), and found that those who were overweight and obese had significantly lower risks of cardiovascular and all-cause mortality than normal-weight individuals. In a prospective study by Wang et al. [10] involving 2016 participants with AF or atrial flutter followed up for a mean of 12 months (with only 20% receiving anticoagulation therapy [warfarin]), those with normal and low weights were associated with higher risks of cardiovascular and all-cause mortality than those who were overweight. Agarwal et al. [35] analysed a cohort of individuals hospitalised for AF, of whom 15.3% were obese, finding that obesity was associated with significantly lower rates of in-hospital mortality and stroke events, although anticoagulation status was not explored. Zhu et al. [36] performed a meta-analysis of nine studies (participants were not fully receiving anticoagulation therapy), reporting that individuals who were underweight (BMI < 18.5 kg/m²) faced higher risks of cardiovascular death, all-cause mortality, and systemic embolism/stroke than those who were overweight or obese.
Contrasting evidence exists regarding the positive effects of obesity and overweight status on cardiovascular outcomes. Overvad et al. [14] analysed a cohort of more than 3000 individuals with AF, of whom only 21.8% received anticoagulation therapy. They reported higher risks of composite endpoints in those who were overweight or obese. Nteli et al. [8] observed increased mortality and hospitalisation rates of AF, heart failure, or stroke in individuals across abnormal BMI categories, noting that anticoagulant use was consistent across groups but involved only 60% of the study population. In a retrospective study by Wang et al. [15] that included 1286 individuals with AF observed over a median of 2.1 years, 13.3% of the participants were anticoagulated with warfarin. The study found that being overweight was an independent risk factor for ischaemic stroke, obesity was an independent risk factor for thromboembolism, and being underweight was an independent risk factor for all-cause mortality. However, BMI did not significantly affect cardiovascular death, with normal weight serving as the reference category for all comparisons. Similarly, Patti et al. [16] examined the influence of BMI on clinical outcomes in individuals with established AF over a 1-year follow-up period, with the majority of participants receiving OACs. Without anticoagulant therapy, obesity was associated with a higher risk of thromboembolic events than a lower BMI; however, anticoagulant therapy effectively equalised the rates of thromboembolic events across all the BMI groups.
In our previous report [4], conducted on the same study population as the present study, we provided Cox proportional hazards regression analyses to correlate demographics and comorbidities with cardiovascular outcomes. They revealed that a lower left ventricular ejection fraction, lower eGFR, greater left atrial diameter, and the presence of LAAT, but not BMI, were associated with a poor prognosis in anticoagulated individuals with AF.
The present study evaluated the relationship between BMI and LAAT in individuals with AF treated with OACs. Findings from previous studies have been inconsistent, reflecting the complexity of this relationship. Uziębło-Życzkowska et al. [17] conducted a multicentre study involving 2816 individuals with AF or atrial flutter referred for TEE before cardioversion or ablation, most of whom were receiving anticoagulant therapy. LA/LAA thrombi were detected in 7.9% of the participants; abnormal BMI (overweight or obese) did not significantly increase the prevalence of thrombi compared to normal weight. Similarly, Turek et al. [2] analysed 296 individuals with AF taking anticoagulants and found that 14.5% had LAA thrombi, with no association between BMI and thrombus formation. In contrast, Tang et al. [18] examined 433 individuals with nonvalvular AF, 6% of whom had LA/LAA thrombi detected using TEE; the prevalence of thrombi was significantly higher in individuals with BMI 27.0 kg/m² (10.6%) than in those with BMI < 27.0 kg/m² (3.0%; p = 0.001), with BMI 27.0 kg/m² identified as an independent predictor of LA/LAA thrombus (odds ratio: 4.02, p = 0.025). In addition, 12 (2.8%) individuals received anticoagulant therapy. These findings underscore the need for further research to clarify the impact of BMI on thromboembolic risk in individuals with AF, particularly in those taking anticoagulants.
Several studies have introduced the concept of metabolic status to improve cardiovascular risk stratification. For example, the metabolically healthy obesity phenotype refers to obese individuals who do not exhibit features of metabolic syndrome. In contrast to metabolically healthy obesity, the remaining obese patients are classified as having metabolically unhealthy obesity. However, the concept of metabolically healthy obesity and its association with cardiovascular events remains controversial and has been insufficiently studied in patients with AF, particularly in those receiving anticoagulation therapy.
In a study by Caleyachetty et al. [37], obese patients without metabolic abnormalities had a higher risk of cerebrovascular disease, coronary heart disease, and HF than normal-weight patients with no metabolic abnormalities. Additionally, the risk of cerebrovascular disease, coronary heart disease, and HF increased with the number of metabolic abnormalities, regardless of weight status (normal weight, overweight, or obese). In a retrospective study, Fauchier et al. [38] compared patients with and without obesity. During recruitment, patients with AF constituted a small percentage of the study participants (less than 10%). In age-, sex-, and smoking-adjusted analyses, obesity was associated with a higher risk of new-onset AF and HF in patients without metabolic abnormalities than in non-obese patients without metabolic abnormalities. Moreover, men with obesity but without metabolic abnormalities had a higher risk of clinical events than non-obese men without metabolic abnormalities, whereas women with obesity but without metabolic abnormalities had a lower risk for most events than non-obese women without metabolic abnormalities. Corica et al. [39] conducted a post hoc analysis of the GLORIA-AF registry to evaluate the impact of metabolic status on the risk of clinical events in individuals with established AF, categorised according to BMI (normal weight, overweight, and obese). A higher BMI was associated with a metabolically unhealthy status. Normal-weight metabolically unhealthy patients had a higher risk of the primary composite outcome as well as thromboembolism. Conversely, a lower risk of cardiovascular death and major adverse cardiovascular events was observed in metabolically healthy obese individuals.
Our findings indicate that BMI alone may not be a reliable indicator of adverse events in anticoagulated patients with AF. Despite variations in comorbidities, long-term outcomes were similar across BMI categories. Interestingly, patients with normal weight had a comparable risk of complications as those who were overweight or obese, suggesting that treatment effectiveness and other clinical factors may be more relevant. The small proportion of normal-weight patients in our cohort may reflect broader population trends, underscoring the need for further studies on the complex interaction between BMI, metabolic status, and cardiovascular risk in AF.
This study has several limitations. The sample size was relatively small, and all participants were referred for electrical cardioversion, introducing potential selection bias. BMI was assessed only at baseline, with no follow-up weight data. The use of standard imaging may have led to overdiagnosis of thrombi. Creatinine clearance was estimated using the MDRD formula, which may not fully reflect dabigatran or rivaroxaban adequacy. Adherence to non-vitamin K antagonist anticoagulants was not confirmed by diagnostic testing. We also did not assess LAA function or structure in detail.
Conclusions
In this study, BMI was not a significant predictor of adverse cardiovascular outcomes in patients with AF receiving OACs. Although normal-weight individuals had fewer comorbidities and better echocardiographic profiles, these did not translate into improved long-term outcomes.
Our findings challenge the role of BMI as a standalone risk marker and highlight the importance of additional clinical and echocardiographic factors. Further research should explore the combined impact of BMI, metabolic health, and anticoagulation quality on outcomes in AF.
Funding
No external funding.
Ethical approval
Approval number: 21/2010.
Conflict of interest
The authors declare no conflict of interest.
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