Original Research

Comparison of Minimum Pressure and Patent Hemostasis on Radial Artery Occlusion After Transradial Catheterization

Roberto L. da Silva, MD1,2,3; Pedro B. de Andrade, MD, PhD4; Alexandre A.C. Abizaid, MD, PhD1; Paulo F.R. Britto, MD2; Filippe B. Filippini, MD2; Renata M.M. Viana, MD1; Amanda G.M. Sousa, MD, PhD1; Fausto Feres, MD, PhD1; José R. Costa Jr, MD, PhD1

Roberto L. da Silva, MD1,2,3; Pedro B. de Andrade, MD, PhD4; Alexandre A.C. Abizaid, MD, PhD1; Paulo F.R. Britto, MD2; Filippe B. Filippini, MD2; Renata M.M. Viana, MD1; Amanda G.M. Sousa, MD, PhD1; Fausto Feres, MD, PhD1; José R. Costa Jr, MD, PhD1

Abstract: Objectives. The aim of this study was to compare two hemostatic techniques, minimum pressure technique and patent hemostasis, on radial artery occlusion (RAO) after transradial catheterization. Background. RAO is an infrequent complication of transradial procedures. One of the strategies used to reduce this complication is the patent hemostasis technique. Use of minimum pressure in hemostatic wristband, without monitoring patency, might have the same efficacy for preventing RAO. Methods. This is a multicenter study encompassing patients submitted to transradial catheterization. After pneumatic wristband application, the band was deflated to the lowest allowable volume while preserving hemostasis. Radial artery patency was subsequently evaluated. The group with no return of plethysmographic curve was labeled “minimum pressure,” and the group in which the signal returned was labeled “patent hemostasis.” RAO was verified by Doppler evaluation within the first 24 hours of the procedure. Results. A total of 1082 patients were enrolled, with mean age of 61.4 ± 10.4 years. The majority (61.0%) were male and 34.5% had diabetes. Patent hemostasis was achieved in only 213 cases (20%). Early RAO occurred in 16 patients (1.8%) in the minimum pressure group and in 4 patients (1.9%) in the patent hemostasis group (P=.97). No major bleeding was observed among the entire cohort. EASY scale for hematoma grade was similar between the cohorts (EASY grades 1-3: 7.0% in the minimum pressure group vs 7.5% in the patent hemostasis group; P=.96). Conclusion. Checking radial patency during hemostatic compression may not be necessary after the procedure when adopting a mild and short hemostatic compression. 

J INVASIVE CARDIOL 2020;32(4):147-152. Epub 2020 March 11.

Key words: hemostasis, radial artery occlusion, transradial catheterization

The use of transradial access (TRA) for coronary catheterization has increased over the years, worldwide.1 The radial artery is nowadays utilized by default for percutaneous coronary procedures at many centers, due to the reduced rates of vascular and bleeding complications and easier postprocedural management.2,3 The use of TRA also improves patient comfort, saves costs, and has an equivalent procedural success rate when compared with the femoral approach.4,5

Although TRA is widely accepted by cardiologists and patients, some problems still exist. One of the major limitations is the development of postprocedural radial artery occlusion (RAO), ranging from 1%-12%.6,7 The benign nature of such an event has been constantly emphasized because of the dual blood supply to the hand from the palmar arch. Mostly, the occurrence of RAO is asymptomatic, and symptomatic RAO requiring medical attention is very rare, but hand ischemia caused by RAO has been described.8,9 The most important aspect is that once the artery is occluded, it cannot be used as the access site for future catheterization, as a conduit for bypass surgery, or for fistula formation in hemodialysis patients. 

The use of smaller-caliber catheters, adequate dose of heparin administration, immediate sheath removal after procedure, patent hemostasis technique, and short duration of compressive bandage are the key elements to reduce the risk of RAO.10-13 Notably, the presence of radial pulse does not exclude RAO due to presence of collateral circulation; it can be more accurately defined by absence of antegrade flow in vascular Doppler ultrasound.14

Indeed patent hemostatic compression, bleeding control while maintaining radial arterial flow, appears to be the single most important factor in reducing RAO. Maintaining patent hemostasis has been shown to be feasible, with minimal conversion to manual compression immediately after diagnostic catheterization. But ideally, control of patency is required each 15 minutes.15

We therefore sought to evaluate whether using a “minimum pressure” technique in hemostatic wristband, that is, applying the same principle of “patent hemostasis” but without controlling patency, has the same efficacy in preventing RAO. 


This is a prospective, multicenter, non-randomized, observational study encompassing patients submitted to diagnostic and/or therapeutic percutaneous coronary procedure by radial access. All adult patients undergoing transradial catheterization at three centers between August 2017 and December 2018 were considered for inclusion. With an all-comers design, eligible patients were ≥18 years old with a clinical indication for coronary angiography (ad hoc angioplasty was allowed) or percutaneous coronary intervention (PCI) if the following prerequisites are met: (1) choice of the operator to use the transradial access route; and (2) use of 5 or 6 Fr sheath size. Baseline patency of the palmar arch, by Allen test or Barbeau test, was not obligatory. Exclusion criteria were: (1) primary angioplasty due to acute myocardial infarction; (2) intubation; (3) complications during procedure (cardiac arrest, pulmonary edema, cardiogenic shock, and stroke); (4) prior inclusion in this trial; (5) known allergy or intolerance to nitrates; (6) medication with continuous intravenous nitrates or any nitrates within the last hour; and (7) use within 24 hours prior to randomization of phosphodiesterase inhibitors. The study protocol was presented to the institutional medical ethics committees of all participating hospitals to comply with local standards. All patients provided written informed consent.

Outcome definitions. The primary outcome was the incidence of early RAO, confirmed by the absence of antegrade flow in vascular duplex ultrasound, up to 24 hours after catheterization. The secondary outcomes were: (1) late RAO, wherein all patients with early occlusion were scanned for recanalization, by the presence of antegrade flow in vascular duplex ultrasound, 30 days after catheterization; and (2) presence of local hematoma or major bleeding.

Study definitions. A radial puncture attempt was defined as any skin puncture with positive blood draw through the needle. A local hematoma was classified according to the EASY scale: grade 1, ≤5 cm diameter; grade 2, ≤10 cm diameter; grade 3, >10 cm but not above the elbow; grade 4, extending above the elbow; and grade 5, anywhere with ischemic threat of the hand.16 Major bleeding was graded according to the Bleeding Academic Research Consortium definitions:  type 3a, bleeding with hemoglobin drop  ≥ 3 g/dL and  < 5 g/dL, or packed red blood cell transfusion; type 3b, bleeding with hemoglobin drop  ≥5 g/dL, cardiac tamponade, bleeding requiring surgical intervention, or bleeding requiring intravenous inotropic drugs; type 3c, intracranial hemorrhage, with subcategories confirmed by autopsy, imaging examinations or lumbar puncture; intraocular bleeding with vision impairment); or type 5 bleeding (type 5a, possibly fatal bleeding and type 5b,  definitive fatal bleeding).17

Transradial procedure. Local anesthesia was administered with a subcutaneous injection of 1% lidocaine after skin preparation. Radial artery access was obtained using either anterior or counterpuncture technique based on the operator’s preference, using a 21 gauge bare needle or 20/22 gauge sheath-covered needle, after which a 5 Fr or 6 Fr hydrophilic sheath was inserted over a guidewire. Then, the patient received heparin (5000 U) through the radial sheath as an intra-arterial bolus. Additional heparin was given in cases of PCI (total 100 IU/kg). No routine intravenous sedation was given. The use of additional medication, either vasodilators or analgesics, was left to the operator’s discretion. Transradial coronary angiography and/or PCI were performed according to standard techniques, at the operator’s discretion. Radial spasm was detected by patient report of pain in the forearm, and measured using a numeric scale applied at the end of the procedure. The scale varied from 0 to 10 (0 corresponding to “no pain” and 10 to “worst possible pain”). Operators reported the presence of spasm according to the difficulty perceived during manipulation or withdrawal of the introducer sheath or catheter.

Arterial hemostasis. A pneumatic compression device designed to assist hemostasis of the radial artery was applied immediately after the procedure according to the following protocol. The sheath was initially pulled by approximately 2-4 cm. Three to 5 mL of blood were aspirated through the sheath to remove any residual thrombus. The device was applied to the patient, with the green marker (located in the center of the larger balloon) positioned exactly at the puncture hole to aid in the location, visualization, and control of possible bleeding. The balloon was inflated with a proper syringe, injecting 15 mL of air, and then the sheath was removed, noticing the absence of active bleeding. In the presence of bleeding, up to 3 mL of additional air was injected to obtain complete hemostasis. Formerly, the device was deflated to the lowest allowable volume (minimum, 7 mL) while preserving hemostasis. If bleeding occurred, sufficient air amount was reintroduced from the bleeding point (up to 1 mL in most cases) to achieve hemostasis. Unlike traditional compression, no fixed amount of air was reinserted from the bleeding point during wristband application, characterizing the least necessary pressure to hemostasis, which is one of the basics principles of patent hemostasis. Radial artery patency was subsequently evaluated by plethysmography and pulse oximetry evaluation, with the sensor placed over the thumb or index finger, and transient occlusion (manual pressure) of the ulnar artery. The group with no return of plethysmographic curve (lack of signal) observed was labeled the “minimum pressure” technique, and the one in which the signal returned was labeled the “patent hemostasis” technique, according to the other basic principle to verify the patency. No subsequent confirmation of patency was done during hemostasis. One hour post diagnostic procedure or 2 hours post intervention, three mL of air was removed every 15 minutes, until complete deflation. If bleeding occurred during any stage of device removal, the volume of air needed for complete hemostasis was injected, restarting the deflation process 60 minutes later. When all the air was removed, the device was removed and the access site was covered with a simple light dressing, which did not encircle the entire wrist.

Evaluation of radial patency. Radial artery patency was evaluated by vascular duplex Doppler ultrasound, using a 6-13 MHz vascular transducer with M-turbo ultrasound scanner (Fujifilm SonoSite) or a 7.5 MHz vascular transducer with Power Vision 6000 ultrasound scanner (Toshiba), performed in all patients within 24 hours of the removal of the compression band. RAO was defined by absence of anterograde flow. The physician who performed the ultrasound scan was blinded to the technique of hemostasis applied. In order to evaluate recanalization, every patient with confirmed RAO was further evaluated 30 days later to reassess patency with a new duplex scan examination.

Statistical analysis. The primary analysis of the study was a comparison between minimum pressure technique and patent hemostasis technique to decrease early RAO. Continuous variables were described as mean ± standard deviation and compared using Student’s t -test for normally distributed variables or assessed using Mann-Whitney test when not normally distributed. Normality was tested using Shapiro-Wilk test. Categorical variables were expressed as frequency (percentage of the group) and were compared with the Chi-square or Fisher’s exact tests. A multivariate logistic regression model, including variables with P<.10 in the univariate analysis, was used to identify the independent predictors of RAO. In the analysis of the primary and secondary endpoints, a two-tailed P-value of <.05 was considered statistically significant. All analyses were performed using SPSS, version 22 (SPSS, Inc).


A total of 1082 patients underwent transradial catheterization and were enrolled between August 2017 and December 2018. Mean patient age was 61.4 ± 10.4 years. The majority (61.0%) were male and 34.5% had diabetes. In 213 cases (20%), the evaluation of anterograde flow by plethysmography indicated patency of the radial artery after applying the hemostatic wristband; these patients constituted the patent hemostasis group. The other 869 cases (80%) constituted the minimum pressure group, and had no demonstration of flow during hemostatic compression. 

There were few differences in baseline clinical characteristics between the groups. Age was lower (61.08 years vs 62.68 years; P=.04), radial artery diameter was bigger (2.8 mm vs 2.4 mm; P<.001), and acute coronary syndromes were more frequent (60.9% vs 28.6%; P<.001) in the minimum pressure group vs the patent hemostasis group, respectively. Procedural characteristics were similar between groups, but the minimum pressure group had longer procedures (21.6 vs 18.2 minutes; P<.001), anterior technique to radial artery puncture was used more frequently (71.9% vs 45.5%; P<.001), and more catheters were used to complete the procedures (2.0 vs 1.6; P<.001) compared with the patent hemostasis group. Diagnostic coronary angiography was the predominant procedure (74.9%), although PCI was more commonly performed in the patent hemostasis group (34.8% vs 22.8% in the minimum pressure group; P=.01) (Tables 1 and 2).

The incidence of the primary outcome of early RAO occurred in 16 patients (1.8%) in the minimum pressure group and 4 patients (1.9%) in the patent hemostasis group (P=.97; odds ratio [OR], 1.02; 95% confidence interval [CI], 0.33-3.08). No major bleeding was observed among the entire cohort. EASY scale hematoma grades 1-3 were similar between the cohorts (7.0% for the minimum pressure group vs 7.5% for the patent hemostasis group; P=.96) (Table 3). None of the patients with RAO experienced any signs and/or symptoms of hand ischemia requiring specific treatment. Three patients in the minimum pressure group and no patients in the patent hemostasis group showed re-establishment of flow at 30-day Doppler assessment.

In the univariate model, several variables were predictors of RAO (with P<.10), including a single clinical characteristic (younger age) and multiple procedure variables (number of puncture attempts, longer procedure time, higher radiation used, spasm classified by operator and by patient use of the pain score). After multivariable adjustment with backward deletion, only age <60 years (OR, 2.87; 95% CI, 1.07-7.64; P=.03) and pain score >4 (OR, 5.16; 95% CI, 1.82-14.62; P<.01) remained as independent predictors of RAO.


Among patients undergoing transradial catheterization, patent hemostasis, as characterized by demonstration of radial artery flow by an oximetric test or other similar test, was found to be present in the minority of patients using standard hemostatic protocols, even with pneumatic wristband application.18 To improve the patent hemostasis rates, some protocols require repeated assessment of radial artery patency or a specified deflation of the band 15 minutes post placement.15,18,19 However, those adjustments increase labor to the nursing staff and require more frequent workflow interruptions for the frequent plethysmographic evaluation of 15 minutes after radial artery flow and, if necessary, adaptation of the hemostatic device, reflecting a possible important limitation in its routine use. Without evaluation after the outset of compression, we obtained demonstration of flow in only one-fifth of the study population, demonstrating that re-evaluation of flow would be mandatory to apply the patent hemostasis technique in all patients.

We found that the balloon of the compression band could be safely deflated to the minimum pressure possible in all patients, without compromising safety or increasing bleeding complications. This specific adjustment in the wristband application, coupled with a short compression time, seems to be equally efficient in obtaining very low rates of RAO, as compared with standard patent hemostasis, which required more attention to patency during the entire hemostasis process. The minimum pressure technique diverges from the patent hemostasis technique regarding the attention to patency during wristband application and throughout the process. This technique may help patient comfort and simplify the nursing team’s work.

This study did not measure the pneumatic band compression pressure, as used in another study,20 and instead used a substitute that was easier to apply: minimum air volume that allowed hemostasis. The lowest quantity of air to maintain hemostasis is the equivalent of the minimum pressure needed for safe compression. Unlike traditional (occlusive) hemostasis, the amount of air was the least necessary to stop bleeding, rather than a fixed amount of air. As expected, the rate of local hematoma around the puncture site and arm was low. No other vascular complications were detected.

It was presumed that a thrombotic process causes RAO after TRA. Sheath insertion and catheter manipulation causes local trauma and endothelial injury, allowing subsequent thrombus formation. Studies with optical coherence tomography and intravascular ultrasound confirmed that hypothesis and have demonstrated postprocedural thrombus generation and considerable vessel trauma, including dissections, ruptures, and thickening of the intima. In small radial arteries, these lesions lead to formation of thrombus, producing occlusion.21,22 Therefore, RAO after TRA appears to be an intricate interaction of trauma, anticoagulation, and flow. 

The wristband’s compressive pressure and duration of application have a direct effect on hemostasis; indeed, duration of hemostasis was one of the strongest predictors of RAO.23 This is probably related with flow impairment during compression. In our study, we opted for a short compression time (60 minutes), knowing that ultra-short radial compression time was not associated with beneficial reduction in RAO rates.24 The short compression time could help to explain our low RAO incidence.

RAO was assessed up to 24 hours using Doppler ultrasonography in all patients. At this stage, this approach must be considered the gold-standard technique to characterize both the thrombotic obstruction and the lack of anterograde flow. It is also known that the detection of RAO by the absence of radial pulse underestimates the true incidence, as compared with ultrasound assessment.25 Furthermore, in contrast to Barbeau’s test, duplex scan allows a full appraisal of other vascular complications. One study has used both Doppler ultrasonography and pulse oximetry to measure RAO, with some difference in results.26

The best moment to evaluate RAO is not yet established. Studies have shown that incidence of RAO decreases over time as compared with the first day, when the RAO incidence is highest.7,19 Besides, many of our patients were discharged on the same day. Even in this worst scenario for RAO evaluation, both techniques used in our study population provided very low RAO rates.

Prior trials have shown that a significant proportion of patients (roughly 50%) will have spontaneous recanalization of radial artery posterior evaluations.15,27,28 Despite this fact, we found a late recanalization rate of only 15%.

Multiple prior studies have shown that a dosage of 5000 IU is superior to any lower doses of unfractionated heparin in preventing RAO, without increasing the risk of bleeding.29-31 Rather than calculated doses of heparin based on the patients’ weights, we opted for a fixed dose of 5000 IU in most cases, and used higher and weight-based doses in cases of angioplasty. Anticoagulation of all patients could help to reduce RAO rates in cases in which patent hemostasis was not obtained.

Study limitations. The present study has several important limitations. Primarily, there was no possibility of randomization, since groups were separated after the application of the wristband, when patency was checked and no further evaluation of patency during compression was planned. Although this was a non-randomized trial, clinical and procedural characteristics were well balanced in the two cohorts; however, a few differences between the groups could have produced some bias in the results. In order to reduce bias, the physician who assessed the Doppler scans was blinded to the study allocation. Additionally, this protocol cannot be interpreted as a true “patent hemostasis” protocol because maintenance of radial artery flow during hemostasis, as verified by digital plethysmography, was not verified further during the compression time, and fluctuation in the patient’s arterial pressure could promote a change in the patency status, although most protocols do not re-evaluate the patency after a positive test, just as we did. Changes in hemodynamic status may lead to loss of patency or establishment of patency at a later time during compression. Finally, our study only included patients accessed with 5 or 6 Fr sheaths, so our findings should not be extrapolated to procedures with larger sheaths.


In the present study, the use of minimum pressure and patent hemostasis techniques resulted in very low RAO rates and comparable efficacy in preventing RAO. Both techniques are safe, with low incidence of hematoma formation. Most important, our results indicate that checking radial patency during hemostatic compression may not be necessary after the procedure when adopting a mild and short hemostatic compression.

From the 1Department of Interventional Cardiology, Instituto Dante Pazzanese de Cardiolgia, São Paulo, SP, Brazil; 2Department of Interventional Cardiology, Instituto de Cardiologia de Santa Catarina, São José, SC, Brazil; 3Department of Interventional Cardiology, Hospital Universitário Prof. Polydoro Ernani de São Thiago, Florianópolis, SC, Brazil; and 4the Department of Interventional Cardiology, Santa Casa de Marília, Marília, SP, Brazil.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted September 15, 2019, provisional acceptance given September 24, 2019, final version accepted October 2, 2019.

Address for correspondence: Roberto Léo da Silva, MD, Instituto de Cardiologia de Santa Catarina, Rua Adolfo Donato da Silva, s/n. Praia Comprida, São José, Santa Catarina. CEP 88103-901. Email: roberto.leo@ufsc.br

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