Radial artery occlusion (RAO) can result from transradial catheterization. We compared the incidence of RAO with 2 heparin dosage regimens after transradial coronary angiography, and we evaluated the efficacy and safety of transient homolateral ulnar artery compression to achieve acute radial artery recanalization. Patients referred for coronary angiography were randomized to very-low-dose heparin (2,000 IU) or low-dose heparin (5,000 IU). On sheath removal, hemostasis was obtained using the TR band with a plethysmography-guided patent hemostasis technique. In the case of RAO as assessed by duplex ultrasonography 3 to 4 hours after hemostasis, immediate 1-hour ulnar artery compression was applied. Hematomas >15 cm 2 were also assessed. We randomized 465 patients, 222 in the 2,000-IU group and 243 in the 5,000-IU group. The baseline and procedural characteristics were comparable in both groups. The incidence of initial RAO was 5.9% in the 2,000-IU group and 2.9% in the 5,000-IU group (p = 0.17), with a compression time of 2.10 ± 0.78 hours and 2.25 ± 0.82 hours, respectively (p = 0.051). After ulnar artery compression, the final incidence of RAO was 4.1% in the 2,000-IU group and 0.8% in the 5,000-IU group (p = 0.03). The incidence of local hematoma was 2.3% and 3.7% in the 2,000- and 5,000-IU groups, respectively (p = 0.42). In conclusion, acute RAO after transradial catheterization can be recanalized by early 1-hour homolateral ulnar artery compression. This simple nonpharmacologic method was effective and safe in patients with very-low- and low-dose heparin. Nevertheless, the incidence of final RAO remained significantly lower after a higher anticoagulation level.
Radial artery occlusion (RAO) after transradial artery catheterization is usually an asymptomatic complication. However, it can prevent additional radial access for staged or repeat procedures. Its incidence at hospital discharge has been reported with a wide range (5% to 12%), and it usually decreases over time. The incidence of RAO is affected by many factors, such as patient weight, the ratio between the radial artery diameter and sheath size, repeated procedures, prolonged cannulation time, compression method, and heparin dose. Since its inception, an inverse relation has existed between the anticoagulation level obtained after heparin administration and the incidence of RAO. The combination of low doses and conventional occlusive radial artery compression have been associated with a greater incidence of RAO. However, most of these reports included larger sheaths and the use of compression methods of the radial artery to obtain hemostasis. Recently, it has been demonstrated that artery occlusion during compression is associated with a greater risk of RAO. Thus, the concept of radial artery patent hemostasis has been validated and is now recognized as an important measure to reduce the incidence of RAO. It remains unknown whether lower heparin doses could be used when using patent hemostasis after transradial catheterization. In the present study, we evaluated the incidence of RAO with 2 doses of heparin, a very low dose (2,000 IU) and a low dose (5,000 IU) in patients undergoing transradial coronary angiography. We also assessed the efficacy and safety of transient homolateral ulnar artery compression as a nonpharmacologic method to recanalize acute RAO.
Methods
A total of 700 patients from our same-day discharge program were randomized in a 1:1 ratio before cardiac diagnostic catheterization from the radial artery to a very low (2,000 IU) or low (5,000 IU) dose of unfractionated heparin. All these patients had a good pulsating radial artery and a type A or B response during oximetry-plethysmography testing. Right-handed patients (89%) were preferentially catheterized from the left radial artery. Patients taking warfarin or admitted for elective percutaneous coronary intervention were not enrolled in the present study. A total of 235 patients were excluded after diagnostic angiography when a different final dose of heparin had been administered owing to ad hoc angioplasty or in the case of conversion to another artery approach (n = 9). A total of 465 patients were included in the present study, 222 in the 2,000-IU group and 243 in the 5,000-IU group. The institutional review board approved the study, and all patients provided written informed consent.
After palmar arch permeability assessment and randomization, sterile preparation and local anesthesia with 1 to 2 ml of 1% trimecaine were performed. The radial artery was cannulated using a through and through puncture technique, and only 5Fr hydrophilic 10-cm-long sheaths (Radiofocus Introducer II, Terumo, Tokyo, Japan) were used. After sheath insertion, a radial cocktail containing 2.5 mg of verapamil and heparin 2,000 or 5,000 IU diluted in a 10-ml syringe was injected gradually through the sheath side arm into the radial artery. Coronary angiography was preferentially performed using a single diagnostic universal 5Fr Tiger catheter (Terumo), although standard 5Fr diagnostic coronary catheters could also be used.
On completion of the diagnostic procedure, the radial sheaths were removed, and the inflatable hemostatic device, TR Band (Terumo), was applied at the access site and inflated initially with 15 ml of air and promptly partially deflated for minimum hemostatic pressure. Immediately after transfer to the recovery room, the initial compression was further reduced to maintain radial artery patency, as previously described. In brief, radial artery patent hemostasis was verified, first by placing a pulse oximeter on the thumb, and then observing the continuous plethysmographic signal on the monitor during manual compression of the ulnar artery just proximal to the pisiform bone. Great care was taken to obtain radial artery hemostasis while maintaining minimal pressure with the TR band. The TR band was left in place until hemostasis was completed, usually within ≥2 hours. Within 3 to 4 hours after TR band removal, radial artery patency was verified by duplex ultrasonography (Philips HD11 XE Ultrasound System, Philips Ultrasound, Bothell, Washington). In the case of RAO, immediate 1-hour ulnar artery compression by the same TR band was used for radial artery reopening by increasing peak velocity blood flow into the radial artery with repeat follow-up ultrasound assessment, as suggested by Dr. Tian Jun (China Interventional Therapeutics [CIT], April 2006). All patients were discharged the same day. Hematomas >15 cm 2 before discharge were considered significant. All coronary angiograms were performed by 4 interventional cardiologists with large experience in radial access. Duplex ultrasonography assessment of the radial artery was performed by 3 experienced physicians who remained unaware of the heparin dosing.
Categorical variables are expressed as numbers and percentages and continuous variables as the mean ± SD. The baseline and procedural characteristics were compared using Fischer’s exact test or the chi-square test for categorical variables and Student’s t test for continuous variables. A p value <0.05 was considered significant. All tests were performed using JMP, version 7.0, software (SAS Institute, Cary, North Carolina).
Results
The baseline clinical and procedural characteristics are listed in Table 1 . The distribution of clinical characteristics and risk factors was similar in both groups. Although the technical details associated with the TR band use were similar in both groups, a trend was seen for a reduced radial artery compression time in the 2,000-IU group compared to the 5,000-IU group (2.10 ± 0.78 vs 2.25 ± 0.82 hours, p = 0.051). After hemostasis, the incidence of initial RAO was 5.9% and 2.9% in the 2,000- and 5,000-IU group (p = 0.17), respectively. After ulnar artery compression, the final RAO incidence was 4.1% in the 2,000-IU group and 0.8% in the 5,000-IU group (p = 0.03; Figure 1 ). A trend was seen for greater recanalization success after ulnar artery compression with more potent anticoagulation (31% in the 2,000-IU group and 71% in the 5,000-IU group; p = 0.16). The only significant difference between patients presenting with final RAO or not was the heparin dose (p = 0.03). The incidence of local hematoma in the whole population was 2.3% and 3.7% in the 2,000- and 5,000-IU groups, respectively (p = 0.42). Importantly, ulnar artery compression for 1 hour was well tolerated in all patients and was not associated with any complications ( Figure 2 ). No major access site complications or rebleeding occurred in any patient. RAO was asymptomatic at discharge in all patients.
| Variable | All Patients (n = 465) | Unfractionated Heparin Dose | p Value | |
|---|---|---|---|---|
| 2,000 IU (n = 222) | 5,000 IU (n = 243) | |||
| Age (years) | 62 ± 10 | 62 ± 10 | 62 ± 10 | 0.85 |
| Men | 308 (66%) | 143 (64%) | 165 (68%) | 0.43 |
| Weight (kg) | 87 ± 16 | 86 ± 17 | 87 ± 15 | 0.83 |
| Unfractionated heparin (IU/kg) | NA | 24 ± 5 | 59 ± 11 | <0.0001 |
| Diabetes mellitus | 87 (19%) | 35 (16%) | 52 (21%) | 0.12 |
| Treated hypertension | 335 (72%) | 154 (69%) | 181 (74%) | 0.26 |
| Treated dyslipidemia | 305 (66) | 145 (65%) | 160 (66%) | 0.92 |
| Smokers | 189 (41%) | 84 (38%) | 105 (43%) | 0.26 |
| Acetylsalicylic acid | 323 (69%) | 151 (68%) | 172 (71%) | 0.55 |
| Air volume in TR band (ml) | 12.0 ± 0.6 | 12.0 ± 0.7 | 12.0 ± 0.5 | 0.92 |
| Compression duration (hours) | 2.18 ± 0.81 | 2.10 ± 0.78 | 2.25 ± 0.82 | 0.051 |
| Radial artery diameter (mm) | 2.9 ± 0.5 | 2.9 ± 0.5 | 2.9 ± 0.4 | 0.72 |
| Radial artery flow (cm/s) | 57 ± 25 | 57 ± 28 | 57 ± 22 | 0.71 |
| Initial radial artery occlusion | 20 (4.3%) | 13 (5.9%) | 7 (2.9%) | 0.17 |
| Successful recanalization | 9 (45%) | 4 (31%) | 5 (71%) | 0.16 |
| Radial artery occlusion after ulnar artery compression | 11 (2.4%) | 9 (4.1%) | 2 (0.8%) | 0.03 |
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