Improvement of Renal Function in Atrial Fibrillation Patients via Catheter Ablation and Left Atrial Appendage Closure: A Case Report

Introduction

According to the latest 2025 report from the American Heart Association and the National Institutes of Health, atrial fibrillation (AF) affects approximately 2% to 4% of the U.S. population, equating to an estimated 6 to 12 million individuals [1]. The risk of AF is significantly higher in patients with chronic kidney disease (CKD)s – approximately 1.6 times that of the general population – while AF itself exacerbates renal dysfunction [2]. AF is an age-related condition, and the coexistence of multiple comorbidities in elderly patients intensifies the thrombosis-bleeding paradox [3,4]. For high-risk elderly AF patients with CKD, cerebrovascular disease, or other multifactorial conditions, anticoagulation therapy has been proven to significantly reduce composite endpoint events, including acute myocardial infarction, ischemic stroke, intracranial hemorrhage, and all-cause mortality [5]. Cardiorenal syndrome refers to a pathophysiological state in which cardiac and renal dysfunction mutually exacerbate one another [6,7]. Patients with AKI have a higher risk of developing acute kidney disease, CKD, and even end-stage renal disease, and there is a causal relationship between AKI and CKD [8]. A bidirectional relationship exists between AF and CKD, involving mechanisms such as chronic inflammation, renin-angiotensin-aldosterone system activation, abnormal calcium handling, and a prothrombotic state [5]. However, the patient with CKD stage G3a complicated by AKI on CKD and a high HAS-BLED score often faces limited anticoagulation options, due to impaired renal function, which further complicates the management of AF and increases therapeutic challenges [9]. For patients with non-valvular AF with high thromboembolic risk who are unable to receive long-term oral anticoagulant therapy, percutaneous left atrial appendage closure can be used as a preferred alternative strategy for stroke prevention (Class IIa recommendation) [2]. Therefore, for patients with AF who have concurrent heart failure (HF) and CKD, striking a balance between achieving effective rhythm control and protecting renal function has emerged as a critical challenge in clinical practice. This report describes a rare case of AF with concomitant HF and CKD. Notably, in this case, the patient successfully achieved sinus rhythm restoration, experienced improved renal function, and was relieved from the need for long-term anticoagulant therapy following the combination of catheter ablation and left atrial appendage closure. This case provides novel insights into the therapeutic management of this specific subset of patients.

Case Report

INITIAL ASSESSMENT:

Upon admission, the patient’s vital signs were as follows: temperature 36.4°C, respiratory rate 21 breaths per minute, heart rate 144 beats per minute (bpm), blood pressure 144/95 mm Hg, and ambient oxygen saturation of 98%. The patient appeared well-developed, well-nourished, and of normal build, with clear consciousness and full cooperation. Physical examination revealed no abnormalities of the thorax, with coarse breath sounds bilaterally and moderate crackles heard in the lower lobes of both lungs. The heart rhythm was irregular, with variable intensity of the first heart sound. No pathological murmurs were heard in any of the valvular auscultation areas, and no pericardial friction rub was present. The abdomen was flat, with no palpable liver or spleen below the costal margin, and no edema was observed in the lower extremities.

ADMISSION FINDINGS:

On admission, the electrocardiogram (ECG) showed rapid AF with a heart rate of 144 bpm, complete right bundle branch block, and ST-T changes. Continuous 48-h ECG monitoring revealed persistent AF. Chest digital radiography was consistent with X-ray signs of chronic bronchitis. Transthoracic echocardiography demonstrated an enlarged left atrium with a diameter of 40 mm, left ventricular end-diastolic diameter of 45 mm, left ventricular end-systolic diameter of 28 mm, mild mitral and tricuspid regurgitation, mild pulmonary hypertension, and left ventricular ejection fraction of 65%. Renal ultrasonography showed bilateral simple renal cysts (1.3×1.0 cm on the left and 1.0×1.0 cm on the right) and a right renal calculus. Laboratory test results revealed a serum creatinine level of 479 μmol/L, corresponding to an eGFR of 7.47 mL/min/1.73 m2, consistent with CKD complicated by AKI, and an N-terminal pro-B-type natriuretic peptide level of 5204.9 pg/mL. Other laboratory test results showed no significant abnormalities (Table 1). Despite the patient’s symptoms of chest tightness, the multiple tests for myocardial enzymes and troponin were within the reference range, ruling out acute coronary syndrome. The admission diagnosis was persistent AF, with a CHA2DS2-VASc score of 6 and HAS-BLED score of 5. Factors included a history of hypertension, renal dysfunction, age over 65 years, stroke history, and combination antiplatelet therapy.

TREATMENT MEASURES:

The patient was treated with volume control, intravenous torasemide (10 mg) for diuresis, oral febuxostat (40 mg once daily) for uric acid reduction, heart rate control using oral bisoprolol (2.5 mg once daily) and intravenous digoxin (0.25 mg), intravenous piperacillin-sulbactam (1.5 g 3 times daily) for infection, and subcutaneous enoxaparin (4000 units once daily) for anticoagulation. After treatment, the heart rate was controlled at 98 to 102 bpm, with occasional sinus rhythm observed. The patient reported significant improvement in chest tightness and palpitations. In the presence of AF with concomitant HF and occasional restoration of sinus rhythm after treatment, the 2024 CARE (Comorbidity and risk factor management, Avoid stroke, Rate and rhythm control, and Evaluation and dynamic reassessment) guidelines classify catheter ablation for symptomatic persistent AF as a Class IIa recommendation. However, the patient could not tolerate transesophageal echocardiography. After thorough discussion with the patient and family regarding the risks and success rates of the pharmacological and catheter-based therapies, they expressed understanding and opted for surgical intervention. They also stated that they would not pursue repeat catheter ablation if AF recurred after the procedure. Preoperatively, intracardiac echocardiography was used to assess thrombotic risk. The patient agreed that the procedure would be canceled if thrombi were detected and declined long-term blood monitoring for coagulation parameters. Considering these factors, a personalized treatment plan was implemented. On hospital day 5, the patient underwent combined radiofrequency catheter ablation and left atrial appendage occlusion, which successfully restored sinus rhythm. On the same day, the patient’s serum creatinine level was 192 μmol/L, corresponding to an eGFR of 22.57 mL/min/1.73 m².

POST-DISCHARGE FOLLOW-UP:

During hospitalization, the patient received anticoagulation therapy with enoxaparin. Given the potential risk of contrast-induced AKI due to intraoperative contrast medium administration, enoxaparin was administered as a short-term, perioperative bridging anticoagulant, which is in line with its recommended role as a temporary alternative for urgent use rather than long-term anticoagulation in AF management. Postoperatively, sinus rhythm returned, and anticoagulant therapy was discontinued once left atrial appendage endothelialization was achieved. For short-term anticoagulation before endothelialization, oral warfarin is administered for 45 to 90 days, with the international normalized ratio maintained within 2.0 to 3.0 (and therapeutic time in range preferably >70%). The patient was also prescribed a combination of spironolactone (20 mg once daily), sacubitril/valsartan (50 mg twice daily), dapagliflozin (10 mg once daily), and bisoprolol (2.5 mg once daily). At follow-up 6 days after surgery, laboratory test results revealed a serum creatinine level of 128 μmol/L (eGFR: 36.84 mL/min/1.73 m2). The patient exhibited significant improvement in HF symptoms and a marked enhancement in quality of life (Figure 1). From discharge to the time of manuscript submission, the patient was attending outpatient follow-up visits, serum creatinine levels remained stable at 110 μmol/L, and functional status corresponded to New York Heart Association class I. At 45 days after surgery, contrast-enhanced computed tomography confirmed complete endothelialization of the left atrial appendage, after which the patient discontinued anticoagulation therapy and was switched to monotherapy with aspirin for antiplatelet treatment. We will continue long-term surveillance to monitor renal function evolution and cardiovascular outcomes.

PROCEDURE DETAILS:

The patient underwent cardiac electrophysiology study under local anesthesia, followed by transcatheter radiofrequency ablation, percutaneous left atrial appendage (LAA) closure, transseptal puncture, and intracardiac echocardiography. An intracardiac echocardiography catheter was used to rule out thrombus in the left atrium and left atrial appendage (Figure 2). A DECANAV 10-pole electrode was advanced into the coronary sinus. After transseptal puncture, a long sheath was positioned in the left atrium (Figure 3A). A Pentaray catheter was then used to construct a CARTO3 three-dimensional map of the left atrium. Based on fluoroscopic imaging, electrocardiographic findings, and intracardiac electrophysiology signals, ablation lines were delineated around the left and right pulmonary vein antra (Figure 3B, 3C). Sequential point-by-point ablation was performed until electrical isolation of the pulmonary veins was achieved, using a power setting of 50 W with ablation index-guided ablation (target AI: 380–480) (Figure 3D). Subsequently, LAA closure was performed. A pigtail catheter was advanced into the left atrium for LAA angiography (Figure 3E, 3F). A 24-mm fixed disc/30-mm outer disc Lacbes LAA occluder was deployed (Figure 3G). After deployment, intracardiac echocardiography imaging confirmed no significant residual shunt (Figure 3H). During the procedure, the patient’s rhythm reverted to sinus rhythm. Anticoagulation was maintained with intravenous heparin (8000 U), adjusted to achieve an activated clotting time greater than 300 s. Contrast medium (iodixanol, 40 mL, low dose) was administered with hydration therapy to mitigate nephrotoxicity.

Discussion

The prevalence of AF in individuals aged 65 years and older can reach up to 10% [3]. The typical drivers of AF onset and progression include a range of comorbidities and associated risk factors, such as hypertension, obesity, diabetes, HF, and CKD, among others [10]. To achieve optimal treatment for patients with AF, these comorbidities and risk factors must be managed early and dynamically [11].

A large-sample study conducted by Diaz et al aimed to evaluate the interaction between HF and AF in terms of renal function using real-world data, with a 5-year follow-up. The study showed a greater than 20% decline in eGFR in 18 513 patients, with an incidence rate of 66.2 per 1000 patient-years. AF significantly increased this risk (hazard ratio 1.13, 95% CI 1.09–1.18, P<0.001), indicating that AF substantially contributes to renal function decline and clinical deterioration in patients with HF [12]. Given the patient’s history of hypertension in the present case, the onset of renal dysfunction was predictable, and renal insufficiency could subsequently serve as precipitating factor for cardiac dysfunction. Fibrosis is a common pathological outcome in both the heart and kidneys. In the heart, myocardial injury triggers remodeling, where myofibroblasts secrete extracellular matrix proteins, promoting cardiac fibrosis and ultimately contributing to HF. In the kidneys, renal tubular epithelial cells undergo epithelial-mesenchymal transition, differentiating into myofibroblasts and leading to tubulointerstitial fibrosis and dysfunction [13]. The renin-angiotensin-aldosterone system plays a pivotal role in this process, activating a cascade of mechanisms that induce fibrosis in the heart, blood vessels, and kidneys, thereby progressing to cardiorenal syndrome [14]. CKD has a high global prevalence, estimated at 9% to 15% [15], and renal dysfunction is one of the most critical risk factors for predicting mortality and adverse outcomes in patients with HF [16]. A Polish prospective study involving 272 non-valvular AF patients with CKD demonstrated significant clinical benefits following left atrial appendage occlusion. During follow-up, the treated cohort exhibited a markedly lower ischemic stroke incidence of 0.25 per 100 patient-years, compared with an expected incidence of 7.00 per 100 patient-years in untreated patients [17]. AF accelerates the progression of CKD through multiple mechanisms, including micro-thromboembolism leading to renal micro-infarction, amplification of systemic inflammation, deterioration of cardiac function with subsequent activation of the renin–angiotensin system, and the nephrotoxic potential of certain therapeutic agents [10]. In the present case, the mechanisms underlying the observed improvement in kidney function encompass: (1) better heart rate control leading to increased cardiac output and improved renal perfusion; (2) reduction of AF-associated inflammation and oxidative stress, thereby mitigating damage to the heart and kidneys; and (3) left atrial appendage occlusion reducing thromboembolism, alleviating microcirculatory dysfunction, interrupting the progression of cardiorenal syndrome, and ultimately improving renal dysfunction for better long-term outcomes.

Based on the patient’s individualized treatment plan, catheter ablation demonstrated effectiveness as first-line therapy for rhythm control in both paroxysmal and persistent AF, showing significant superiority over pharmacological therapy [18]. A post hoc analysis of the randomized trial by Vanassche et al indicated that persistent and permanent AF carry a higher risk of stroke than does paroxysmal AF, suggesting that the type or burden of AF influences stroke risk [19]. Of course, in addition to AF having a tendency to induce HF, factors such as hypertension and nephrotoxic medications [20] can also contribute to adverse outcomes. Traditional imaging methods often require the use of iodine-based contrast agents, which may exacerbate renal burden in patients with impaired kidney function and even lead to contrast-induced nephropathy [21]. By comparison, intracardiac echocardiography does not rely on iodine-based contrast agents, avoiding the risk of renal impairment associated with contrast use. While effectively excluding thrombi, intracardiac echocardiography better preserves renal function, highlighting its advantage [22]. A multicenter cohort study on left atrial appendage closure by Domenico et al showed that AF and CKD often coexist. The study classified patients based on baseline renal function and demonstrated that left atrial appendage closure success rates were high regardless of the severity of renal dysfunction at the time of the procedure. Moreover, left atrial appendage occlusion was associated with a relative reduction in the risk of thrombosis and major bleeding [23]. For our patient, who presented with AF complicated by HF and renal insufficiency, the condition is multifactorial. Appropriate anti-heart failure therapy and renal protective measures are essential. On this basis, assessing surgical risks, preventing complications, and selecting the optimal timing for intervention are critical [24].

Conclusions

This case illustrates a common clinical scenario involving the coexistence of AF, HF, and CKD. It highlights the critical importance of early assessment and intervention in such complex patients. The combination of catheter ablation and left atrial appendage closure demonstrated significant benefits in improving renal function by halting the progression of HF and restoring sinus rhythm. However, single-case reports have inherent limitations, and long-term follow-up is required to validate these findings. Future prospective studies focusing on the optimal timing of catheter-based interventions are warranted to explore the best therapeutic and strategies for patients with varying levels of renal function, thereby providing robust evidence for clinical practice.