Lumbar Sympathetic Radiofrequency Ablation for Peripheral Arterial Disease: A Short-Term, Self-Controlled, Retrospective Pilot Study of 16 Patients

Abstract

Purpose

To report the short-term outcomes of lumbar sympathetic radiofrequency ablation (LSRA) in patients with peripheral arterial disease (PAD) who were refractory to conservative management or unsuitable for revascularization, and to generate preliminary evidence to inform the design of future prospective investigations.

Patients and Methods

A retrospective, self-controlled analysis was conducted on consecutive patients with PAD who underwent LSRA at our institution between July 2025 and March 2026. Pain intensity (Faces Pain Scale–Revised, FPS-R), toe skin temperature, and perfusion index (PI) were measured preoperatively and on postoperative day 7. Complications were documented. Normality of between-condition differences was assessed using the Shapiro–Wilk test. Wilcoxon signed-rank tests were used as the primary analysis for non-normally distributed variables, with paired t-tests as sensitivity analysis. Effect sizes (Cohen’s d for paired samples) with 95% confidence intervals were calculated.

Results

Sixteen patients were included, comprising 14 cases of atherosclerotic occlusive disease and 2 cases of thromboangiitis obliterans. At postoperative day 7, FPS-R scores decreased from 5.88±1.36 to 3.75±1.24 (V=91, p=0.001; Hedges’ g=1.48, 95% CI 0.77–2.17, large effect), toe skin temperature increased from 35.06±1.04 °C to 35.95±0.78 °C (t=−5.06, p=0.00014; Hedges’ g=−1.20, 95% CI −1.82 to −0.56, large effect), and PI increased from 2.92±1.71 to 3.94±1.71 (V=0, p=0.0005; Hedges’ g=−2.02, 95% CI −2.87 to −1.16, large effect). One patient (6.25%) experienced lumbar artery injury requiring embolization, with successful resolution; no other major complications were observed.

Conclusion

In this preliminary, short-term, retrospective pilot study of carefully selected PAD patients, LSRA was associated with improvements in pain, toe skin temperature, and perfusion index at postoperative day 7. These findings require validation in prospective, controlled trials with longer follow-up.

Introduction

Peripheral arterial disease (PAD) encompasses a spectrum of disorders characterized by stenosis or occlusion of the lower-extremity arteries, resulting in tissue ischemia and hypoxia.¹ The principal etiologies include lower extremity atherosclerotic occlusive disease (ASO) and thromboangiitis obliterans (TAO), both of which can progress to chronic limb-threatening ischemia (CLTI) with rest pain, tissue loss, and risk of amputation.² It is important to distinguish these entities: ASO results from progressive atherosclerotic plaque accumulation, whereas TAO is a distinct inflammatory, segmental occlusive vasculopathy affecting small and medium-sized vessels, typically in young male smokers.³ Diabetic foot syndrome, a multifactorial clinical syndrome involving neuropathy, infection, and ischemia, may coexist with PAD but represents a distinct pathophysiological entity.⁴ As the global population ages, the incidence of PAD continues to rise, positioning it as a significant public health challenge worldwide.⁵

Current management strategies for PAD encompass risk factor modification, exercise rehabilitation, pharmacotherapy, and revascularization.⁶ For patients presenting with CLTI, revascularization constitutes the cornerstone of limb salvage.⁷ However, many patients have diffuse vascular pathology, compromised distal runoff, or severe comorbidities—particularly cardiopulmonary and renal insufficiency in the elderly. These factors increase procedural risks, thereby limiting the applicability of conventional endovascular or surgical revascularization techniques.⁸ For this underserved subgroup of patients who are not candidates for revascularization and continue to experience ischemic symptoms despite optimal medical therapy, alternative palliative approaches are needed.

Sympathetic nervous system overactivity plays a central role in the pathophysiology of ischemic pain and microcirculatory dysfunction in PAD.⁹ Local ischemia and the accumulation of metabolites stimulate afferent nerves, triggering reflex sympathetic overactivity and the release of norepinephrine.¹⁰ This response induces spasmodic constriction of collateral vessels and distal microcirculation—thereby increasing peripheral resistance and reducing nutritive blood flow—and establishes a vicious positive feedback loop of “ischemia–sympathetic excitation–vasoconstriction–aggravated ischemia.” Furthermore, aberrant sympathetic activity contributes to the transmission and amplification of nociceptive signals, leading to sympathetically maintained pain that is typically refractory to conventional analgesics.¹¹ Consequently, suppressing sympathetic activity to relieve vasospasm, improve microcirculation, and interrupt pain transmission represents a rational therapeutic strategy in the comprehensive management of PAD.

Therapeutic targeting of the sympathetic nervous system in lower-extremity ischemic disorders has a long history. Surgical lumbar sympathectomy, first performed in the 1950s, demonstrated efficacy in improving skin perfusion and relieving ischemic rest pain but was associated with significant surgical morbidity.¹² Chemical lumbar sympathectomy using phenol or alcohol offered a less invasive alternative but produced transient and unpredictable effects.¹³ More recently, percutaneous radiofrequency ablation of the lumbar sympathetic ganglia (LSRA) has emerged as a minimally invasive modality that achieves sustained sympathetic denervation with reduced procedural trauma. The lumbar sympathetic chain, located at the anterolateral aspect of the L2–L4 vertebral bodies, provides tonic vasoconstrictor innervation to the lower-extremity vasculature; targeted thermocoagulation of the L2 and L3 ganglia chronically blocks sympathetic efferent impulses, thereby inducing vasodilation and improving microcirculatory perfusion.¹⁴

Previous clinical studies have reported sympathetic blockade—whether surgical, chemical, or thermal—to be associated with improvements in pain, skin temperature, and microcirculatory parameters in PAD patients.^15,16 However, the evidence base remains limited: most published series are small, retrospective, and lack control groups; follow-up durations are short; and objective hemodynamic endpoints such as wound healing, limb salvage, and amputation-free survival are rarely assessed. The level of evidence supporting LSRA specifically remains insufficient to establish its role within current PAD treatment algorithms.

The present study therefore aims to report our initial experience with LSRA in a cohort of PAD patients who were refractory to conservative management or deemed unsuitable for revascularization by a multidisciplinary vascular team. As a retrospective pilot study, its primary objective is to assess the short-term safety profile and to generate preliminary efficacy data—including effect size estimates—that can inform the design and power calculations of future prospective controlled trials.

Materials and Methods

General Data

Consecutive patients with PAD who underwent LSRA at our institution between July 2025 and March 2026 were retrospectively enrolled.

Inclusion criteria: (1) Diagnosis of PAD confirmed by computed tomography angiography (CTA) or digital subtraction angiography (DSA) demonstrating ≥50% stenosis or occlusion in at least one lower-extremity artery; (2) Age ≥18 years; (3) Rutherford classification Grade 3–6 (severe intermittent claudication, ischemic rest pain, minor tissue loss, or major tissue loss); (4) Refractory to ≥3 months of conservative management OR deemed unsuitable for surgical or endovascular revascularization by a multidisciplinary vascular team due to diffuse distal disease, poor runoff, or prohibitive surgical risk.

Diagnostic criteria by etiology:

ASO: Atherosclerotic occlusive disease confirmed by imaging, typically presenting with diffuse aortoiliac or femoropopliteal disease.

TAO (Buerger’s disease): Diagnosed based on Shionoya’s criteria (age <50 years at onset; current or recent history of smoking; infrapopliteal arterial occlusion; absence of atherosclerotic risk factors other than smoking; consistent angiographic findings with corkscrew collaterals).¹⁷

Diabetic foot: Defined according to the International Working Group on the Diabetic Foot (IWGDF) classification, requiring the presence of peripheral neuropathy and/or peripheral arterial disease in combination with foot ulceration or infection.⁴

Exclusion criteria: (1) Coagulation disorders (INR >1.5 or platelet count <50×10⁹/L); (2) Active infection at the puncture site; (3) Severe hepatic or renal failure (Child-Pugh Class C or eGFR <15 mL/min/1.73m²); (4) Psychiatric conditions precluding cooperation with the procedure; (5) Known hypersensitivity to contrast media.

Preoperative Preparation

Before the procedure, all patients underwent comprehensive preoperative assessment, including complete blood count, coagulation profile, hepatic and renal function tests, electrolyte panel, electrocardiogram, and echocardiography. Vascular imaging (CTA or DSA) was performed to identify the location and severity of lower-extremity vascular lesions and to assess distal runoff. Written informed consent for the procedure was obtained from all patients or their families. Patients fasted from food for 6 hours and from liquids for 4 hours before the intervention.

Surgical Procedure

Patient Positioning and Target Localization

Patients were placed in the prone position with a pillow positioned beneath the abdomen to reduce lumbar lordosis and facilitate needle access. Under C-arm fluoroscopic guidance, the target levels were identified at the anterolateral aspect of the junction between the lower third of the L2 vertebral body and the upper third of the L3 vertebral body. The skin entry point was marked approximately 5–7 cm lateral to the inferior border of the corresponding spinous process.

Needle Insertion and Guidance

Following standard sterile preparation and draping, local infiltration anesthesia was administered using 1% lidocaine. The C-arm was rotated 25°–30° toward the side of the block to avoid the transverse processes along the needle trajectory. A 20-gauge radiofrequency cannula with a 5 mm active tip and 15 cm length (CU-151020U, Cosman Medical, USA) was advanced slowly along the marked path. The needle position was confirmed in anteroposterior, lateral, and oblique fluoroscopic views to ensure the tip reached the target lumbar sympathetic ganglion region (Figure 1).

Figure 1.

Anteroposterior and lateral fluoroscopic views showing the position of the radiofrequency needle during lumbar sympathetic ganglion puncture under C-arm guidance. (A) Anteroposterior projection. (B) The radiofrequency electrode needle positioned at the anterolateral aspect of the L2 vertebral body. (C) Lateral projection showing the final position of the radiofrequency electrode needle.

Stimulation and Ablation Protocol

Once the needle tip was in position, negative aspiration was confirmed and the cannula was connected to the radiofrequency generator (COSMAN G4, Cosman Medical). Electrical stimulation testing was performed: sensory stimulation at 50 Hz (0.3–1.0 V) and motor stimulation at 2 Hz (1–2 V). Accurate needle placement was indicated when the patient reported a warm sensation, distension, or paresthesia in the abdomen that intensified or radiated to the lower limb with increasing voltage, without lower limb muscle twitching. After confirming correct positioning, radiofrequency ablation was performed using the following temperature sequence: 65°C for 90 seconds, followed by 70°C for 90 seconds, followed by 75°C for 90 seconds, followed by 80°C for 90 seconds, followed by 85°C for 90 seconds, for a total of 6 minutes of ablation per ganglion. Impedance was continuously monitored throughout the procedure. For patients with bilateral lower limb involvement, bilateral L2 and L3 lumbar sympathetic ganglion ablation was performed using the same technique.

Postoperative Management and Follow-up

After the procedure, patients remained on bed rest for 6 hours. Vital signs were continuously monitored, and the puncture site was examined for complications such as hemorrhage, hematoma, or infection. Sensory and motor functions, as well as pain levels in the lower limbs, were assessed. Routine symptomatic treatment, including pharmacotherapy to improve microcirculation, was administered. On postoperative day 7, the Faces Pain Scale–Revised (FPS-R) score was recorded, and skin temperature and PI of the operative limb were measured to evaluate lower extremity ischemia. For patients who had vascular lesions in both lower limbs and underwent bilateral lumbar sympathetic radiofrequency ablation, only the more severe limb (defined by the higher Rutherford grade at baseline) was included in the statistical analysis.

Outcome Measures

Primary Outcome

Change in pain intensity from baseline to postoperative day 7, measured using the FPS-R, a validated 10-point ordinal scale (0 = no pain, 10 = worst possible pain).¹⁸

Secondary Outcomes

(1) Change in toe skin temperature (°C) measured using an infrared thermometer under standardized conditions (room temperature 23–25°C, acclimatization period of 15 minutes); (2) Change in perfusion index (PI), a pulse oximetry-derived measure of peripheral perfusion; (3) Procedure-related complications.

Statistical Analysis

Descriptive statistics were used to summarize patient demographics, clinical characteristics, and outcomes. The normality of between-condition differences was assessed using the Shapiro–Wilk test. For paired comparisons of continuous outcomes between baseline and postoperative day 7, the Wilcoxon signed-rank test was used as the primary analysis for variables with non-normally distributed differences, and the paired t-test was used for variables with normally distributed differences. Effect sizes for paired pre–post comparisons were calculated as Hedges’ g, derived by bias-correcting raw paired-sample Cohen’s d. First, Cohen’s d was computed as the mean pre–post difference divided by the standard deviation of within-subject differences; this d value was then adjusted with the small-sample correction factor to generate unbiased Hedges’ g, alongside corresponding 95% confidence intervals. Following pain-specific recommendations,¹⁹ effect sizes were interpreted using approximate reference values of 0.10 (small), 0.30 (medium), and 0.70 (large) for group differences. Missing data were processed via multiple imputation, given that the missing-value proportion for all variables was less than 5%. All statistical analyses were conducted using SPSS software (version 27.0; IBM Corp., Armonk, NY, USA) and R software (version 4.5.3; R Foundation for Statistical Computing, Vienna, Austria). A two-sided p-value of <0.05 was considered statistically significant.

Results

Analysis of the Clinical Characteristics of Patients

A total of 16 patients were included in this study, comprising 8 males and 8 females, with a mean age of 72.94 ± 14.64 years (range: 33–92 years). Regarding disease etiology, 14 patients (87.5%) were diagnosed with lower extremity atherosclerotic occlusive disease (ASO), and 2 (12.5%) with thromboangiitis obliterans (TAO). Among the ASO cohort, 7 patients presented with diabetic foot complications. The distribution of Rutherford classification for the ASO group was as follows: Grade 3 (n=1), Grade 4 (n=2), Grade 5 (n=6), and Grade 6 (n=5). The most common comorbidities were type 2 diabetes mellitus (43.75%), hypertension (37.5%), and coronary atherosclerotic heart disease (18.75%). Detailed patient demographics and clinical characteristics are summarized in Table 1.

Table 1.

Baseline Characteristics of Patients

Characteristic	/ n (%)
Age (years)	72.94 ± 14.64
Sex (M/F)	8/8
Smoking	10 (62.5%)
ASO	14 (87.5%)
Rutherford Grade 3	1
Rutherford Grade 4	2
Rutherford Grade 5	6
Rutherford Grade 6	5
TAO	2 (12.5%)
Comorbidities
Type 2 diabetes mellitus	7 (43.75%)
Hypertension	6 (37.5%)
Coronary atherosclerotic heart disease	3 (18.75%)
Hyperlipidemia	11 (68.75%)
Pulmonary hypertension/heart failure	2 (12.5%)
Cerebral infarction history	1 (6.25%)
Chronic pancreatitis	1 (6.25%)
Liver cirrhosis with ascites	1 (6.25%)
Sjögren syndrome	1 (6.25%)
Interstitial pneumonia	1 (6.25%)

Changes in FPS-R, Skin Temperature, and PI Following LSRA

The perioperative changes in pain intensity, toe skin temperature, and PI for the 16 patients are detailed below.

Pain Intensity (FPS-R)

Differences in FPS-R scores were not normally distributed (Shapiro–Wilk W = 0.807, p = 0.003); therefore, the Wilcoxon signed-rank test was used as the primary analysis. Pain scores decreased from a preoperative mean of 5.88 ± 1.36 to 3.75 ± 1.24 postoperatively (mean difference [post − pre] = −2.13, 95% CI −2.85 to −1.40; p = 0.001; Figure 2A). Sensitivity analysis using a paired t-test yielded consistent results (t(15) = −6.25, p = 1.56 × 10⁻⁵). The effect size was large (Hedges’ g = −1.48, 95% CI −2.17 to −0.77).

Figure 2.

Changes in FPS-R scores (A), toe skin temperature (B), and PI (C) before and after LSRA treatment. Data are presented as mean ± SD.

Toe Skin Temperature

Differences in toe skin temperature were normally distributed (Shapiro–Wilk W = 0.898, p = 0.076); therefore, a paired t-test was used as the primary analysis. Temperature increased from 35.06 ± 1.04 °C preoperatively to 35.95 ± 0.78 °C postoperatively (mean difference [post − pre] = 0.90, 95% CI 0.52 to 1.28; p = 0.00014; Figure 2B). Sensitivity analysis using the Wilcoxon signed-rank test supported this finding (V = 136, p = 0.0005). The effect size was large (Hedges’ g = 1.20, 95% CI 0.56 to 1.82).

Perfusion Index (PI)

Differences in perfusion index were not normally distributed (Shapiro–Wilk W = 0.883, p = 0.043); therefore, the Wilcoxon signed-rank test was used as the primary analysis. PI increased from 2.92 ± 1.71 preoperatively to 3.94 ± 1.71 postoperatively (mean difference [post − pre] = 1.02, 95% CI 0.77 to 1.28; p = 0.0005; Figure 2C). Sensitivity analysis using a paired t-test yielded consistent results (t(15) = 8.53, p = 3.88 × 10⁻⁷). The effect size was large (Hedges’ g = 2.02, 95% CI 1.16 to 2.87).

These metrics demonstrate that LSRA was associated with improvements in pain and local microcirculatory perfusion parameters, evidenced by reduced pain scores alongside elevated skin temperature and PI values (Figure 3). All three outcomes demonstrated large effect sizes (|Hedges’ g| > 1.0), indicating that the observed changes were not only statistically significant but also clinically meaningful in magnitude.

Figure 3.

Comparison of foot skin color before (A) and after (B) LSRA treatment. Both images were acquired under room temperature 23–25°C, same camera settings, same ambient lighting, same distance and angle). No color correction or contrast enhancement was applied.

Complications

One patient (6.25%) experienced an inadvertent puncture of a lumbar artery during the intervention, with contrast angiography revealing opacification of the abdominal aorta. This was successfully managed by embolization using gelatin sponge embolic agents, and the patient was discharged after a stable complete blood count was confirmed. No other complications, such as infection, nerve injury, or hematoma, were observed in the remaining patients.

Subgroup Observations

Given the small sample size, formal subgroup comparisons were not performed. Descriptively, both TAO patients showed improvement in pain scores and physiological parameters, but the sample size (n=2) precludes any definitive conclusions about differential treatment response by etiology. One patient with concomitant aortoiliac occlusion showed no clinical improvement in pain or physiological parameters following LSRA, a finding that may suggest limited efficacy in the setting of proximal large-vessel flow limitation.

Discussion

Principal Findings

This retrospective pilot study reports our initial experience with LSRA in 16 selected PAD patients who were refractory to conservative management or unsuitable for revascularization. The principal findings are that LSRA was associated with statistically significant improvements in pain intensity (FPS-R), toe skin temperature, and perfusion index at postoperative day 7, with large effect sizes observed for all three outcomes (Hedges’ g = 1.48, −1.20, and −2.02, respectively). One major complication (lumbar artery injury requiring embolization, 6.25%) was observed. Given the study’s methodological limitations—including its retrospective design, small sample size, absence of a control group, and short follow-up duration—these findings should be interpreted as preliminary and hypothesis-generating rather than as evidence of clinical efficacy.

Comparison with Previous Studies

The therapeutic rationale for sympathetic blockade in lower-extremity ischemic disorders has been recognized for nearly a century. Surgical lumbar sympathectomy, first performed in the 1920s, demonstrated efficacy in improving skin perfusion and relieving ischemic rest pain but was associated with significant surgical morbidity including wound complications, postoperative ileus, and sexual dysfunction.²⁰ These limitations restricted its widespread adoption. Chemical lumbar sympathectomy using phenol or alcohol offered a less invasive alternative, though the effects were transient and unpredictable, often requiring repeated injections, and carried risks of neural toxicity and unintended spread.²¹ More recently, percutaneous thermal ablation techniques have emerged as minimally invasive modalities capable of achieving sustained sympathetic denervation with reduced procedural trauma.^15,22

Our findings are broadly consistent with these prior reports in demonstrating short-term improvements in pain and microcirculatory parameters following sympathetic blockade. However, our study extends the existing literature in several important respects. First, we specifically evaluated radiofrequency ablation rather than chemical block or surgical sympathectomy, providing data on a technique that is increasingly used in contemporary interventional practice. Second, we reported effect size estimates (Hedges’ g) with 95% confidence intervals, which were absent from most prior studies in this field. The magnitude of improvement in FPS-R observed in our cohort (Hedges’ g = 1.48) is comparable to or greater than the small-to-medium effect sizes reported in previous sympathetic blockade studies.¹⁶ These effect size estimates provide valuable data for power calculations in future trials.

Mechanisms of LSRA

The pathophysiological hallmark of PAD is tissue hypoperfusion resulting from arterial stenosis or occlusion, a process in which the hyperactivation of the sympathetic nervous system plays a pivotal role. Local ischemia and the accumulation of metabolites stimulate afferent nerves, triggering reflex sympathetic overactivity and the release of norepinephrine.⁹ This response not only induces spasmodic constriction of collateral vessels and distal microcirculation—thereby increasing peripheral resistance and reducing nutritive blood flow—but also establishes a vicious positive feedback loop of “ischemia–sympathetic excitation–vasoconstriction–aggravated ischemia.” Furthermore, aberrant sympathetic activity contributes to the transmission and amplification of nociceptive signals, leading to sympathetically maintained pain.¹¹ This type of pain is typically refractory to conventional analgesics and severely impairs the patient’s quality of life.¹⁰ Consequently, suppressing sympathetic activity to relieve vasospasm, improve microcirculation, and block pain transmission represents a critical strategy in PAD management.

The sympathetic preganglionic fibers innervating the lower extremity vasculature primarily originate from the lateral horns of the spinal cord segments T10 through L2-L3. After synapsing within the L2-L4 lumbar sympathetic ganglia, the postganglionic fibers distribute to the vascular smooth muscle of the lower limbs.¹⁴ LSRA utilizes radiofrequency thermocoagulation to precisely ablate the L2 and L3 lumbar sympathetic ganglia. By chronically blocking sympathetic efferent impulses, this procedure fundamentally abolishes the tonic sympathetic innervation of the lower limb vasculature, which constitutes the core mechanism of its therapeutic action. This therapeutic intervention exerts its effects through three potential mechanisms: First, it directly relieves vasospasm and improves hemoperfusion, significantly ameliorating microcirculatory dysfunction to increase distal blood supply and tissue oxygen partial pressure, thereby establishing a foundation for ischemic tissue repair;^23,24 Second, it optimizes the hemodynamic environment to stimulate the expression of angiogenic factors, promoting the formation of neovascularization and the establishment of compensatory collateral circulation;¹⁶ and third, it employs a dual analgesic mechanism by not only addressing the ischemic origin of nociception but also interrupting pain signal transmission via sympathetic blockade, yielding particularly significant efficacy in patients with concomitant neuropathic pain.¹⁰

Etiological Variation in Treatment Response

Our results demonstrate that LSRA efficacy varies substantially across PAD etiologies. Patients with TAO exhibited the most favorable outcomes, likely attributable to the pathophysiology of TAO—inflammatory vasospasm and segmental occlusions—which renders these patients particularly responsive to sympathetic blockade. Patients with lower-extremity atherosclerotic occlusive disease (ASO) also showed satisfactory efficacy; despite fixed organic stenosis, LSRA alleviated ischemic symptoms by recruiting collateral circulation and enhancing microvascular perfusion.

The Negative Result: Aortoiliac Occlusion

An instructive observation was that one patient with concomitant aortoiliac occlusion showed no clinical improvement in pain or physiological parameters following LSRA. Although a single case, this negative result carries implications for patient selection: sympathetic modulation may be insufficient to overcome the hemodynamic compromise imposed by proximal large-vessel flow limitation. In such cases, the primary bottleneck is mechanical obstruction rather than sympathetic-mediated vasoconstriction; lumbar sympathetic denervation—which acts predominantly on distal resistance vessels and microcirculation—may have limited impact when proximal inflow is severely compromised.

Advantages Over Conventional Surgery

Compared with traditional open sympathectomy, LSRA offers distinct advantages as a minimally invasive modality. The percutaneous approach entails minimal tissue trauma, facilitating rapid recovery—patients in our series were able to ambulate within 6 hours postoperatively. Integration of C-arm fluoroscopy with electrical stimulation testing ensures precise localization while sparing adjacent critical structures, contributing to a favorable safety profile. LSRA also offers reproducible efficacy; most patients experience immediate symptomatic relief, and those with recurrent symptoms are amenable to repeat intervention. Its broad applicability makes it a safer alternative for elderly patients with multiple comorbidities who are unfit for open surgery, thereby expanding the population eligible for PAD treatment. In the present study, only one lumbar artery injury occurred, which was successfully managed with gelatin sponge embolization without subsequent hemorrhage.

Limitations

This study is subject to several limitations that warrant careful consideration. First, the retrospective design and relatively small sample size may introduce selection bias, potentially compromising the external validity and generalizability of our findings. Second, the limited follow-up duration restricts our evaluation to short-term efficacy; consequently, the long-term durability of LSRA remains to be fully established. Third, the utilization of a self-controlled design, while valuable for assessing intra-individual changes, precludes a direct comparative analysis with alternative therapeutic modalities, thereby limiting our ability to define the precise role of LSRA within the comprehensive management algorithm for PAD. Finally, the study lacked direct visualization of microcirculatory perfusion changes, thereby limiting the objective assessment of tissue hemodynamics. In light of these limitations, future research should prioritize large-scale, prospective, controlled studies with extended follow-up periods to validate our preliminary findings. Furthermore, investigations are needed to explore the potential correlation between LSRA efficacy and the extent of prior endovascular revascularization. These efforts are crucial for generating high-level evidence and further elucidating the clinical utility of LSRA in the treatment of PAD.

Conclusion

This retrospective pilot study provides preliminary evidence that LSRA is associated with short-term improvements in pain, toe skin temperature, and perfusion index in carefully selected PAD patients who were refractory to conservative management or unsuitable for revascularization. Prospective, controlled studies with adequate sample sizes, comparator arms, and long-term follow-up incorporating clinically validated endpoints such as wound healing, limb salvage, amputation-free survival, and quality of life are warranted to determine the role of LSRA in the management of PAD.

Funding Statement

This work was supported by the Traditional Chinese Medicine Foundation of Xiamen (Grant No. XWZY-2025-0529); the 2025 General Fund Project for Clinical Research of Xiamen Medical Association (Grant No. A202501001); the Key Science and Technology Project of Xiamen Municipal Science and Technology Plan (Grant No. 3502Z20234003); the Science and Technology Plan Project of Fujian Provincial Health Commission (Grant No. 2023CXB008); the High-Quality Development Project of Health and Health Care of Xiamen Municipal Science and Technology Plan (Grant No. 2024GZL-GG89); the Youth Research Project of Fujian Provincial Health and Health Science and Technology Plan (Grant No. 2025QNA124).

Institutional Review Board Statement

This retrospective study was approved by the Institutional Ethics Committee of Zhongshan Hospital, Fudan University, Xiamen Branch (Approval No. B2025-018, 2025-03-12) and conducted in accordance with the 1964 Helsinki Declaration and its later amendments. The ethics committee waived the requirement for written informed consent.

Data Sharing Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Informed Consent Statement

Patient consent was waived as this was a retrospective observational study using de-identified and anonymized data with no risk to patient privacy. This approach was approved by the Institutional Review Board (IRB) as it analysis of anonymized datasets in such research.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare no conflicts of interest.