Outcomes With Distal Transradial Access in Patients With Advanced Chronic Kidney Disease

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J INVASIVE CARDIOL 2024. doi:10.25270/jic/24.00200. Epub August 14, 2024.

Radial artery occlusion (RAO), a complication of transradial access, has an incidence of 4.0% to 9.1% in patients with advanced chronic kidney disease (CKD) and may preclude its use creation of arteriovenous fistula. Distal transradial access (dTRA) has lower rates of RAO compared with TRA, but prior studies excluded patients with advanced CKD. This was a single center study of patients with advanced CKD who underwent coronary procedures with dTRA from January 1, 2019 to May 12, 2022 who were retrospectively evaluated for radial artery patency in follow-up with reverse Barbeau testing or repeat access of the artery. Of 71 patients, 66% were on hemodialysis and the remainder had CKD 3 to 5. Access was ultrasound-guided, and all received adequate spasmolytic therapy and patent hemostasis. Proximal radial arteries were patent in 100% of the patients at follow-up. Our data suggest that dTRA is safe for patients with advanced CKD and preserves radial artery patency.

Transradial access (TRA) reduces bleeding and vascular complications compared with transfemoral access, and is a class 1 recommendation for coronary procedures.¹ TRA carries a 1% to 10% risk of radial artery occlusion (RAO), typically asymptomatic, but with implications for patients with chronic kidney disease (CKD) and hemodialysis (HD), in whom preservation of radial arteries for future/repeat arteriovenous fistula (AVF) creation is necessary.^2,3 Patients with advanced CKD undergoing TRA are at high risk of RAO (4.0%-9.1%) and AVF failure (20%-50% within first year).^3-7 Previous trials comparing distal TRA (dTRA) with proximal TRA indicate lower rates of RAO with dTRA, however, these studies largely excluded patients with advanced CKD (≥ 3b and hemodialysis (HD)).^8,9 In this study, we characterize radial artery patency after dTRA in patients with advanced CKD in a retrospective, single-center, real-world study and compare outcomes with that of the largest published historical comparator of proximal TRA in patients with advanced CKD.⁷

Patients with advanced CKD who were referred to NYU Langone (NYU Langone Health System) for elective coronary procedures from January 1, 2019 to May 12, 2022 were retrospectively reviewed.  Radial artery patency was assessed with reverse Barbeau testing or repeat access for staged percutaneous coronary intervention (PCI) or for an arterial line. Reverse Barbeau testing was selected in place of ultrasonographic assessments for RAO, as follow-up occurred in clinical settings with limited access to, and limited technical expertise of providers in ultrasonography. Furthermore, data suggests that reverse Barbeau is a high reliability screening method for RAO.¹⁰ A total of 110 patients were screened, with 4 excluded due to the absence of advanced CKD and 35 excluded due to lack of follow-up. The study was approved by the NYU Langone Institutional Review Board, and informed consent was waived due to the retrospective and anonymized nature of the study.

Access was ultrasound-guided, anterior wall puncture performed in the anatomic snuffbox and contralateral to existing AVF if present.. As is consistent with accepted radial artery preservation strategies, short (7 cm) hydrophilic sheaths were used to minimize injury and spasmolytic therapy (verapamil 2.5 mg) was administered.¹¹ Initial cases were performed with 5-French (Fr) short sheaths for diagnostic cases (upsizing to 6 Fr for PCI), and later cases were done using 6-Fr short thin-walled sheaths. Weight-based dosing of heparin with boluses or bivalirudin for PCI were administered. The SafeGuard device (Merit Medical) was used for patent hemostasis, with deflation 30 minutes after diagnostic and 2 hours after PCI.

Non-inferiority (NI) was tested by comparison with the largest published cohort of TRA in patients with advanced CKD, which also assessed RAO with reverse Barbeau.⁷ The synthesis method was used to evaluate an NI margin using the point estimate of the historical study as M1. The inferiority margin (M2) was a 50% retention of M1. Risk difference with 95% confidence interval (CI) was obtained for RAO, radial artery spasm, radial artery hematoma, or access crossover comparing proximal TRA vs dTRA. NI was demonstrated if the 95% CI did not cross the prespecified margin (P < .025 was considered significant as determined by the Wald method). Superiority was tested if non-inferiority was met and demonstrated if the upper bound of 97.5% CI of risk difference did not cross zero. A Yates’ continuity correction was applied for 0 events. SAS version 9.4 (SAS Institute) was used for analyses.

Baseline/procedure characteristics and outcomes are reported in the Table. Of 71 patients, 66% (n = 47) were on HD and 13% (n = 9) underwent PCI.  Sheath sizes were 5 Fr in 59% (n = 42) and 6 Fr in 41% (n = 29). The median follow-up was 35 days (25^th, 75^th percentiles; 25, 77). One patient crossed over from left dTRA to femoral access (crossover rate 1.4%) due to proximal radial artery calcification. All patients undergoing PCI were on dual antiplatelet therapy, while 29 patients undergoing diagnostic were on single antiplatelet therapy. There was no radial artery spasm or hematoma. Patency was assessed with reverse Barbeau testing in 51 patients, and by repeat access in 20 patients.  Proximal radial arteries were patent in 71 patients (100%) at follow-up. The rate of RAO observed in our study was non-inferior and superior to the historical rate of RAO for proximal TRA in patients with advanced CKD (Figure 1).  Our study is hypothesis-generating, and a prospective head-to-head trial of dTRA vs proximal TRA in patients with advanced CKD is warranted to further assess safety and efficacy.

The limitations of this study include size, low event rate, and the single-center and single-arm design. Nonetheless, these findings demonstrate that the incorporation of dTRA into a RAO avoidance strategy is safe and feasible for patients advanced CKD.

Ramya C. Mosarla, MD¹; Hamza Ahmed, BS²; Shaline D. Rao, MD^1,3; Bernard S. Kadosh, MD¹; Jennifer A. Cruz, DO¹; Randal I. Goldberg, MD¹; Tajinderpal Saraon, MD¹; Bruce E. Gelb, MD⁴; Aprajita Mattoo, MD⁵; Sunil V. Rao, MD¹; Sripal Bangalore, MD, MHA¹ 

From the ¹NYU Grossman School of Medicine, Division of Cardiology, New York, New York, USA; ²NYU Grossman School of Medicine, New York, New York, USA; ³NYU Long land School of Medicine, Division of Cardiology, New York, New York, USA; ⁴NYU Grossman School of Medicine, Department of Surgery, New York, New York, USA; ⁵NYU Grossman School of Medicine, Division of Nephrology, New York, New York, USA.

Data availability statement: The data that support the findings of this study are available on request from the corresponding author.

Disclosures: Dr Bangalore serves on the advisory boards of Abbott Vascular, Biotronik, Boston Scientific, Amgen, Pfizer, Merck, Reata, Inari, Truvic, and Viatris. The remaining authors report no financial relationships or conflicts of interest regarding the content herein.

Address for correspondence: Sripal Bangalore, MD, MHA, New York University School of Medicine, New York, NY 10016, USA. Email: sripalbangalore@gmail.com; X: @sripalbangalore