The Open (Radial) Artery Hypothesis: How We Can Preserve a Better Arterial Access Site.

Radial artery occlusion (RAO) is one of the most common procedural complications of transradial cardiac catheterization, and is thought to be due to a combination of traumatic and nontraumatic factors, including arterial spasm, endothelial injury, microthrombus formation, and/or neointimal hyperplasia [1]. Although often asymptomatic, there are sporadic reports of digital ischemia in the presence of RAO; whether the RAO is directly causing the ischemia or if it is due to embolization of thrombotic material from the occlusive “plug” is unclear. At a minimum, the development and persistence of RAO precludes subsequent transradial access in the affected arm. Over the past twenty years, operators have developed a number of strategies to minimize the incidence of arterial occlusion, including using smaller sheaths (if any), appropriate anticoagulation, and “patent hemostasis” techniques to allow antegrade blood flow through the radial artery during the hemostatic process [2]. Despite the established role of these strategies, survey data indicate that there is wide variation in post-procedure practices [3]. This is especially true regarding the type and dose of anticoagulation used during transradial diagnostic and interventional cases.In this issue of Cardiology, Degirmencioglu and colleagues present the results of a single-center randomized trial comparing two heparin dosing strategies [4]. After screening 520 patients, they excluded 30 (5.7%) patients for prior transradial access or factors associated increased risk of bleeding; an additional 86 (16.5%) patients underwent ad hoc angioplasty and therefore were not included in the analysis. The remaining 404 patients were randomized equally to either a low-dose heparin strategy (2,500 Units) or a high-dose heparin strategy (5,000 Units). By seven days post-procedure, there was no statistically significant difference in the rates of radial artery occlusion (5.9% vs. 5.4%, p=0.83) or Grade III or larger hematoma (4.0% vs. 7.4%), though the low dose strategy was associated with a lower degree of bleeding during deflation of the radial hemostasis device (TR Band, Terumo Interventional Systems, Somerset, NJ, USA) (6.4% vs. 18.3%, pu003c0.001). There were no episodes of major bleeding in either arm of the study.This study adds to the long-standing body of literature evaluating the appropriate dose of heparin during transradial cardiac catheterization. At least some dose of heparin during a transradial cardiac catheterization is used by 95% of practicing interventionalists [3] worldwide. The role of heparin to reduce the rate of radial artery occlusion was initially described 20 years ago in a prospective, nonrandomized study of 415 patients; the rate of RAO at 2 months, assessed using Doppler ultrasound, was 71% among the first 49 patients that received no heparin, 24% among the next 119 patients receiving 2,000–3,000 units of heparin, and 4.3% in the subsequent 210 patients that received 5,000 units of heparin (pu003c0.05) [5]. More recent studies have attempted to determine the most appropriate dose of UFH to balance efficacy and bleeding. A weight-based regimen of 50U/kg was trialed against a fixed dose of 5,000 Units among 162 consecutive patients in the Adjusted Weight Anticoagulation for Radial approach in Elective (AWARE) study [6], but no RAO was observed in either arm, though the patients randomized to the weight-based regimen had lower radial compression times and a trend toward decreased rates of local hematoma foundation. The current study is consistent with findings from a prior study by Bernat et. al. in which 465 patients undergoing transradial cardiac catheterization were randomized to 2,000 units versus 5,000 units of heparin [7]. Immediately post-procedure, there was no difference in RAO incidence between the two groups (5.9% of the low-dose group versus 2.9% of the higher-dose group, p=0.17), though ulnar artery compression to force blood flow through the radial artery resulted in significantly reduced the rate of RAO in the higher-dose arm (4.1% versus 0.8%, p=0.03). The study by Degirmencioglu, however, did not test maneuvers to reduce RAO rates post-procedure.The other critical aspect of preventing RAO is the use of “patent hemostasis” techniques to allow for antegrade flow through the radial artery. Traditionally, operators had used full occlusive compression for hemostasis following transradial procedures. As with selecting the appropriate anticoagulation dosing, compressive technique following transradial catheterization must balance appropriate hemostasis and bleeding; too little pressure may result in longer compression times and increased rates of local hematoma formation, whereas full occlusion for an extended period of time may lead to increased rates of RAO. The first trial to assess the efficacy of patent hemostasis was the Prevention of Radial Artery Occlusion-Patent Hemostasis Evaluation (PROPHET) Trial [8], in which investigators randomized 436 patients to fully occlusive or patent hemostasis techniques using the HemoBand; rates of RAO were lower in the patent hemostasis group than the occlusive hemostasis group at both 24 hours (5% vs. 12%) and at 30 days (1.8% vs. 7.0%), pu003c0.05 for both. A similar study was performed using the TR Band [9], which was the hemostasis device used in the present study, and demonstrated similar reductions in RAO with patent hemostasis techniques (1.2% vs. 12.0%, pu003c0.001).It should be noted that the investigators in the present study used a nontraditional method to achieve hemostasis when using the TR Band. They report that they maximally inflated the TR Band to 18ml and then deflated it until a radial pulse could be palpated, after which they deflated an additional 2 ml every 15 minutes. This is problematic because the presence of a pulse does not necessarily mean that antegrade flow is present in the radial artery – retrograde flow from the ulnar artery through the palmar arch can result in a palpable radial pulse distal to the hemostasis device. Therefore, it is not clear that the investigators practiced true patent hemostasis. In addition, the authors state that their reported rates of RAO that are similar to the reported literature. While this is true, the reported rate of grade III hematomas is much higher than previously reported [10] and suggest that inappropriate distal placement of the hemostasis device led to extravasation of blood proximally from the arteriotomy. Reassuringly, there were no reported episodes of major bleeding or other significant complications. While the study by Degirmencioglu addresses an important issue, it cannot be taken as the final word on appropriate heparin dosing for transradial procedures.More importantly, this analysis highlights the delicate balance between thrombosis and bleeding at the level of the arterial access site. Adequate anticoagulation is a fundamental part of a broader, multifaceted strategy to achieve radial hemostasis and reduce the incidence of RAO that includes minimizing arterial trauma by using small caliber sheaths, preventing and treating spasm, and using patent, non-occlusive hemostasis to achieve antegrade flow through the radial artery. In addition, all patients should be evaluated for radial patency prior to discharge, with the potential use of ulnar artery compression to facilitate radial artery recanalization. As the popularity of radial access increases worldwide and it becomes the de facto standard of care for cardiac catheterization, the prevention and mitigation of the most common complications of the procedure is essential, and an appropriate anticoagulation dosing strategy is an integral component.