FIGURE 10-1 Incidence of RAO according to time (A) and the method of detection (B).

Although not feasible routinely because of costs and logistic constraints, the reference technique for RAO detection remains the visible obstruction in two-dimensional ultrasound and the absence of anterograde Doppler flow signal distal to access puncture site.^15,20 This must be differentiated from using a simple Doppler probe, which might detect a signal even if the RA is completely or partially obstructed due to reverse flow. Consequently, detection of RAO using Doppler probe only can grossly underestimate the true incidence of RAO. This might partially be improved if one compresses the ulnar artery while assessing the radial flow.

More recently, we and others have used the modified oxymetry-plethysmography technique to assess the incidence of RAO postcatheterization. This technique was initially described by Cheng et al.²¹ as a more sensitive technique than the Allen test, and Barbeau et al. used it as a semiquantitative method of assessment prior radial catheterization.²²

Briefly, the pulse oximeter sensor is placed over the index finger and the plethysmographic signal observed. Both radial and ulnar arteries are simultaneously compressed to observe loss of plethysmographic signal. The RA is then released, and the return of plethysmographic signal is observed. Return of signal confirms RA flow and hence patency. The absence of return of signal implies RAO.

It should be emphasized that spontaneous recanalization of RA is relatively frequent, and consequently, the incidence of persistent RAO is lower over medium- to long-term follow-up.^15,17,20 The wide variation of reported incidence of RAO in the literature could therefore be explained not only by population and procedural variables, but also by the diverse methods and time of assessment for RA patency.

Pathophysiology of Radial Artery Occlusion

RAO is likely to be a multifactorial process due to the interplay of several factors, which in principle may relate to three main mechanisms: (a) arterial wall injury, endothelial denudation, and local vascular reactions induced by sheath insertion; (b) interruption of antegrade flow during procedure due to the presence of sheath or postprocedure due to the type and duration of compression; (c) “a” and “b” may facilitate local thrombus formation and occlusion, and/or chronic inflammatory process, leading to intimal hyperplasia and thickening of intima media, which may result in delayed luminal obliteration or reduction.

The RA is a primarily muscular vessel, with a dominant supply of α-1 adrenoceptors to its smooth muscle cells.²³ Shear stress at the time of sheath insertion evokes these receptors, leading to vasospasm due to local release of catecholamines, endothelin-I, and angiotensin-II.²³ In turn, this induces friction of the arterial wall in contact with the sheath, thereby further increasing shear stress, leading to itimal tear and medial dissection. In addition, the RA has a mean internal diameter of 2.69 ± 0.4 mm in men and 2.43 ± 0.38 mm in women (range, 1.15–3.95 mm).²⁴ It is therefore closer to the outer diameter of the catheters being placed in its lumen. As a result of these factors, the constrained intraluminal environment due to limited clearance between the catheter and the arterial wall may result in reduced pericatheter antegrade blood flow, raising the risk of arterial thrombosis.²⁵

RA injury has been well described by Yonetsu et al.²⁶ Through the use of optical coherence tomography (OCT) to assess acute RA injuries immediately following TRA catheterization, this recent study demonstrated acute RA injury in a substantial number of patients, with intimal tear in 67% of patients and medial dissection in 36%.²⁶ More direct evidence comes from Staniloae et al.,²⁷ who studied the early histological changes induced by TRA catheterization. Thirty-four subjects undergoing coronary artery bypass grafting (CABG) had their left RA harvested to serve as conduits. Fifteen of these had undergone TRA catheterization via left RA immediately prior to CABG, while 19 noncatheterized right radial arteries served as controls. Five-millimeter biopsy sections were obtained from distal and proximal ends of the RA, and examined by a single pathologist blinded to the clinical data. The distal end of the left RA group had significantly more intimal hyperplasia (73% vs 21%), periarterial tissue necrosis (26% vs 0%), and adventitial inflammation (33% vs 0%) in close proximity to entry site, when compared to the noncatheterized distal right radial arteries. Of note, no significant difference was noted in the proximal parts of both arteries (albeit numerically more intimal proliferation in left radial arteries). While these findings are relevant and may have implications on the use of RA as a conduit, they also highlight the extent of injury induced by the introducer sheath.²⁷ The extensive damage associated with sheath insertion and denuded endothelium may initiate a cascade of events not only predisposing to thrombosis resulting in RAO, but also triggering intima-media hyperplasia with nonocclusive narrowing of the RA over long term.^26,28

Thrombotic RAO following percutaneous cannulation for monitoring has long been described, with an incidence as high as 30% to 40%. In 100 consecutive patients requiring arterial monitoring for major elective operations, Bedford et al. demonstrated a 35% incidence of occlusive RA thrombi, by performing contrast arteriography prior to decannulation, and confirming using both Allen test and Doppler examination following decannulation.²⁹ In another series, Bedford et al. also demonstrated a 38% incidence of thrombotic RA occlusion in patients undergoing radial cannulation for perioperative management.⁶ A postmortem specimen from a participant in the study showed an organized RA thrombus corresponding to the exact length of occlusion, which had been precisely determined antemortem by the absence of Doppler flow signal over the area.⁶

Similarly, Pancholy reported the finding of an occlusive “plug” successfully retrieved from 5 out of 12 reaccessed radial arteries, which had been occluded for less than 4 weeks.³⁰ Histopathological examination of aspirated material was consistent with an organizing thrombus, with signs of neovascular microchannel formation.³⁰ Therefore, it is reasonable to assume thrombus formation as the main mechanistic process for early RAO. Kim et al. reported an occlusive RA thrombus in a male patient as visualized with an ultrasound examination the day following transradial cardiac diagnostic procedure.³¹ Their patient had a “normal Allen” test prior to the procedure, and RAO was asymptomatic. A month later, and while on antiplatelet therapy, the RA recanalized with a normal appearance on ultrasound.³¹ Similarly, Zankl et al.³² assessed RA patency the day after the procedure by using duplex ultrasonography over in 488 patients who underwent either diagnostic procedures (with 4F) or PCI (5–6F). The study demonstrated partial or complete thrombotic RAO in 11% of patients.³²

Therefore, existing evidence from histopathological as well as clinical studies with echo-duplex examinations indicates that RAO in the acute to subacute phase is often due to thrombus formation, with various degrees of spontaneous recanalization on medium to long term.

A separate potential mechanism of “gradual” RAO relates to progressive intimal hyperplasia following unique or repeat RA cannulation. The resultant endothelial damage following radial cannulation and sheath insertion may trigger a cascade of events leading to intimal hyperplasia and vascular remodeling. Using intravascular ultrasound imaging of the RA following cardiac catheterization in 100 subjects, Wakeyam et al.²⁸ demonstrated significantly smaller mean distal radial arterial diameter in those who had repeat TRA compared to first TRA procedure. Similarly, and using OCT, Yonetsu et al.²⁶ demonstrated significant intimal tear as well as chronic intimal thickening of RA following repeat TRA.

Factors Associated with Increased Risk of Radial Artery Occlusion/Predictors of Radial Artery Occlusion

Multiple patient- and procedural-related factors have been shown to influence or predict the occurrence of RAO (Table 10-1). These come from observational studies, registries, as well as randomized studies.

TABLE 10-1  Predictors of RAO

Patient-Related Factors: Gender, Age, Body Mass Index, Peripheral Arterial Occlusive Disease, and Diabetes

In a large series of >7,215 patients who underwent TRA coronary intervention, Zhou et al.³³ described an incidence of 0.94% of RAO. The study analyzed risk factors associated with RAO by using a logistic regression model, and as compared with those who did not develop RAO, there were more female and diabetic patients in the RAO group.³³ In the same study, the size of introducer sheath, heparin dose, and duration of compression were independent risk factors of RAO.³³ More recently, in a prospective vascular ultrasound registry of 455 patients undergoing TRA angiography and interventions, Uhlemann et al.¹⁵ demonstrated by a multivariate analysis that, besides the use of 6F sheaths, female gender (OR: 2.36, 95% CI: 1.50–3.73, P < 0.001), younger age (OR: per year 0.96, 95% CI: 0.94–0.98, P = 0.001), and the presence of peripheral arterial occlusive disease (OR: 2.04, 95% CI: 1.02–4.22, P = 0.04) independently predicted RAO in all patients.¹⁵ It should be noted that in both studies, RA was compressed, hence probably maintained occluded during hemostasis.

Procedural Factors

Radial Artery Diameter: Ratio of Internal Radial Artery Diameter to Outer Sheath Diameter

The relationship between sheath size and RAO has long been established. Occlusion is directly related to the size of the introducer sheath and is influenced by the ratio of the inner radial arterial diameter to the outer sheath diameter, as demonstrated by Saito et al.¹¹ In a series of 250 patients who underwent ultrasound examinations before and after TRA catheterization, they reported an incidence of RAO of 4% in patients with an RA internal diameter greater than the outer diameter of the sheath (ratio < 1) versus 13% in those with a ratio <1.¹¹ These findings have been confirmed in a study by Dahm et al.¹² on 171 subjects undergoing TRA PCI randomized to 5F versus 6F sheath. The study revealed that the radial diameter to catheter ratio was <1.0 for all 6F patients in whom profound radial spasm occurred. In addition, RAO occurred in 1.1% of the 5F group versus 5.9% of the 6F group at 1 month (P = 0.05).¹² More recently, Uhlemann et al.¹⁵ showed in their observational analysis of 455 patients that the risk of RAO was significantly higher with 6F (30.5%) than with 5F sheaths (P < 0.001). Using both Allen test and Doppler, Bedford demonstrated a negative linear relationship between the size of the cannulated radial arteries and the incidence of thrombotic occlusions.⁶ Hence, in accordance with the relationship between vessel trauma and risks of RAO, it can be concluded that the smaller the sheaths/catheters are, the lesser the risks of RAO.

Anticoagulation: Type, Dose, and Route of Administration

For the purpose of cardiac catheterization, once the radial puncture has been successfully performed, and after sheath insertion, unfractionated heparin is administered intravenously at a dose of 5,000 units for diagnostic procedures, for it has been shown to greatly reduce the incidence of thrombotic RAO associated with RA cannulation.

Dosing of Heparin. Anticoagulation during TRA procedures is paramount, as it has been shown to significantly reduce the incidence of RAO.³⁴ As described by Lefevre et al. in the original report of the role of heparin in TRA, the effect of heparin in the prevention of RAO appears to be dose dependent, with a substantial reduction in the incidence of RAO by increasing the dose of heparin from 2,000 to 3,000 and further to 5,000 IU.³⁴ This has been substantiated further in a recent study of the incidence and predictors of RAO in a large cohort of < 7,000 patients who underwent TRA coronary intervention.³³ In a more recent study, Bernat et al.³⁵ compared the echo-duplex incidence of RAO with a single intravenous heparin bolus of 2,000 IU versus 5,000 IU. Using patent hemostasis (see below), he and his colleagues demonstrated that immediate posthemostasis RAO rate was higher in the 2,000 IU group compared to the 5,000 IU group (5.9% vs 2.9%, P = 0.17).³⁵ The authors also described a nonpharmacological technique of 1-hour ulnar compression to treat RAO, with again higher efficacy with higher heparin dose (final incidence of RAO was 4.1% in the 2000 IU group vs 0.8% in the 5000 IU group, P = 0.03). Thus, it seems prudent to recommend a minimal fixed dose of 5,000 IU or 70 IU/kg heparin after radial sheath insertion, even for simple diagnostic angiography.

The role of new anticoagulants, such as bivalirudin, a direct thrombin inhibitor, in conjunction with radial access remains to be discussed. Plante et al. performed a study comparing a single 70 IU/kg heparin bolus administered at the completion of the diagnostic angiography to bivalirudin administration in the case of ad hoc PCI.³⁶ Overall, the incidence of RAO at 30 days in the heparin-only group was 7% compared with 3.5% in the bivalirudin-only group. Although numerically lower in the bivalirudin group, the difference did not reach statistical significance (P =

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