Incidence and Prognostic Factors of Radial Artery Occlusion in Transradial Coronary Catheterization
Abstract
:1. Introduction
2. Materials and Methods
2.1. Study Design and Setting
2.2. Patient Selection
2.3. Data Collection
2.4. Peri-Procedural Characteristics and Evaluation of Radial Artery Patency
2.5. Statistics
2.6. Study Approval and Ethics
3. Results
4. Discussion
- (A)
- Pre-procedural: (i) the female gender;
- (B)
- Procedural: (ii) access site cross-over from the radial artery to another artery, (iii) an increased total time of the sheath remaining in the radial artery and (iv) radial artery spasms;
- (C)
- Post-procedural: (v) the presence of hematomas, (vi) post-catheterization dabigatran use, (vii) manual hemostasis and (viii) numbness in the fingers of the punctured arm.
- (A)
- Procedural: (i) radial artery spasms, (ii) the use of intra-arterial nitroglycerin as a vasodilator;
- (B)
- Post-procedural: (iii) the presence of symptoms, either pain or numbness.
- (A)
- Pre-procedural (non-modifiable): age, the female gender, a low body mass index (BMI), diabetes mellitus, chronic kidney disease, peripheral arterial disease and smoking;
- (B)
- Procedural (modifiable): previous ipsilateral radial artery punctures, inadequate periprocedural anticoagulation, the administration and type of intra-arterial vasodilators (sheath size, radial artery diameter and sheath-to-radial artery diameter ratio >1), repeated radial punctures, radial artery spasms, the procedural duration, aspirin use, statis use and glycoprotein inhibitor (GPI) use;
- (C)
- Post-procedural (modifiable): occlusive (non-patent) or prolonged hemostasis.
- The female gender: The female gender has been described as predisposing patients to RAO in several studies. It is assumed that their lower BMI and their decreased radial artery diameter, especially when combined with the use of large bore sheaths, predispose these patients to more spasms and radial artery injury and subsequently to RAO. However, this is not a consistent finding among all studies. In our study, being female was a predictor for increased RAO only in the angiography group, while it lost its significance in the PCI subgroup, indicating that procedural and post-procedural factors are probably more important when proceeding to PCIs [11,16,18,19,30,53].
- Access site cross-over from the radial artery to another artery: The need for cross-over from the radial artery to another artery usually implies that either the artery was punctured multiple times with no successful sheath insertion or that after the sheath insertion, a complication occurred, like a radial artery spasm or injury to the radial artery, and the procedure could not be completed through the initial access site. Moreover, loops of the radial artery at the forearm or subclavian artery tortuosity may lead to cross-over either due to spasms or due to the inability to cannulate the coronary arteries. In each case, however, many catheters, wires and manipulation maneuvers are usually applied. In all of the above cases, the common denominator is the increased injury to the radial artery wall and, as stated in the pathophysiology explanation, this induces RAO. Not many studies have evaluated this, probably because they focus on other endpoints, like multiple punctures and spasms (which, as described, can result in access site cross-over) [11,16,18,19,25,28,30,37,38,39,40,41,42,43]. In the present study, patients were included only if they had a successful insertion of at least one radial artery sheath, so sheath-related arterial wall injury (and not only puncture/needle injury) was a case for all our patients. However, we did not systematically record the cause of cross-over (spasms, radial or subclavian tortuosity or other reasons), so we cannot provide more details about that. Access site cross-over was a significant RAO predictor only for the whole group and not for the PCI subgroup [11,16,18,19,30].
- An increased total time of the sheath remaining in the radial artery: The radial sheath, apart from the injuries it causes to the arterial wall during its insertion, also reduces blood flow locally and promotes blood stasis and thrombus formation. However, there are studies with opposing evidence on whether a longer or shorter procedure duration promotes RAO (expressed usually as the procedural time) [11,16,18,19,25,28,30,37,38,39,40,41,42,43]. We recorded the time from sheath insertion until sheath removal and found that this was a borderline significant predisposing factor for RAO in the whole population but not in the PCI subgroup.
- Radial artery spasm: Spasms of the radial artery are a well-recognized factor that increases RAO rates and are implicated as such in many studies, although they were not proven as a main factor in the meta-analyses by Rashid et al. and Hahalis et al. [11,16,18,19,30]. However, spasm prevention is recommended, and relevant measures should be applied, mainly by the use of vasodilators [19]. Vascular spasms likely indicate a response of the artery to injury or friction with the equipment, subsequently reducing blood flow and promoting RAO. In the present study, a radial artery spasm was recognized as an independent RAO predictor both for the whole population and for the PCI subgroup.
- Radial artery vasodilators: Nitroglycerin is a vasodilating agent and is traditionally used intra-arterially during transradial catheterization to prevent radial artery spasms, usually at a dose of 200–500 μg. However, in the latest randomized study and the latest meta-analysis, intra-arterial nitroglycerin did not show any advantage in preventing radial artery spasms or RAO [54,55]. Only subcutaneous nitroglycerin was found to prevent radial spasms or RAO [55]. Verapamil, a calcium channel blocker, is also used intra-arterially as a vasodilator during transradial catheterization, at a dose of 2.5–5 mg. These two agents can be also combined and administered simultaneously in transradial procedures [56]. Verapamil only or verapamil in combination with nitroglycerin is probably more effective in preventing radial spasms and RAO than nitroglycerin alone [56,57]. In the present study, when nitroglycerin was selected from the operator as a vasodilator, it was administered intra-arterially, just after the sheath placement at a dosage of 200 μg. When verapamil was selected, it was also administered intra-arterially just after the sheath insertion at a dosage of 2.5 mg. The multivariate analysis showed that vasodilators had no effect on RAO for the whole cohort, but for the PCI subgroup, nitroglycerin compared to verapamil increased the odds of RAO, while verapamil seems to have a favorable effect in preventing RAO.
- The presence of hematoma: Hematoma formation in the forearm represents another complication of transradial catheterization. It is usually due to radial or brachial artery perforation and indicates severe radial artery trauma from one side, while the blood that accumulates in the forearm region compresses from outside of the radial artery on the other side. Moreover, in order to manage and minimize the extent of hematomas, additional external direct pressure on the forearm usually with a sphygmomanometer and a pressure bandage has to be applied. All these events promote blood stasis and may predispose patients to RAO [11,21,30,44]. In the present study, the presence of any hematoma in the forearm according to the EASy classification was a predictor for RAO in the whole patient group but not in the PCI subgroup.
- Post-catheterization dabigatran use: Dabigatran is a non-vitamin K antagonist oral anticoagulant (NOAC) and acts as a direct thrombin (factor II) inhibitor in the coagulation cascade. It is indicated for thromboembolism prevention in patients with atrial fibrillation and for the treatment of deep vein thrombosis and pulmonary embolism [58]. It would be better like this: “Although very effective for the prevention and treatment of thrombi in the venous circulation (lower shear stress and velocity) and the left atrial appendage, when it comes to the arterial circulation and when devices are implicated, there are some observations that may need attention. In the RE-DUAL PCI study, in which dabigatran was used (instead of warfarin) as part of a dual antithrombotic regimen in combination with a clopidogrel or ticagrelor in patients with atrial fibrillation undergoing PCIs, the dabigatran groups had numerically (although not statistically significant) more myocardial infarctions [59]. Dabigatran also showed increased thromboembolic events in patients with mechanical heart valves, left ventricular assist devices and when used periprocedurally during radiofrequency ablation for atrial fibrillation [60,61,62]. The above data may indicate that dabigatran is not very effective in preventing arterial thrombi or may increase thrombogenicity when devices and catheters are inserted in the arterial circulation, as is the case in coronary angiography. In contrast, rivaroxaban, another NOAC acting as a direct factor X inhibitor, showed more promising results in preventing arterial or device-related thrombi [63,64,65]. That is the reason we checked dabigatran and found it to be an independent predictor of RAO for the whole group but not for the PCI subgroup. We recognize that this is a finding not described before and may not look reasonable at first sight, but it could be further investigated in larger samples of patients receiving dabigatran peri-procedurally during transradial catheterization.
- Manual hemostasis: Instead of placing a device, hemostasis can be achieved by direct pressure on the puncture site after sheath removal by the operator or nurse. Despite a shorter hemostasis time (which could be beneficial for RAO prevention), manual compression depends on the person applying the pressure, making it very variable and not reproducible [66]. Probably, especially during the first minutes after sheath removal, a very high level of pressure is applied in order to avoid bleeding, and this deteriorates blood flow in the already traumatized radial artery. When compared to device hemostasis in a randomized study, manual hemostasis had a similar RAO incidence [17]. In the present study, manual hemostasis was applied only after diagnostic coronary angiography and was found to be an independent predictor of RAO.
- Presence of symptoms (pain in the forearm or numbness in the fingers of the punctured arm): RAO may be symptomatic in up to 58.8% of patients, presenting as pain in the forearm, numbness/paresthesia, paresis or acute ischemia [20,22,23,24,25,26]. Forearm nerve injury may happen either directly, during puncture or during device hemostasis, or indirectly due to radial artery injury, spasms or hematomas and subsequent nerve ischemia. The presence of symptoms probably indicates a higher degree of radial artery injury, further predisposing patients to RAO. In this study, RAO was symptomatic in one third of patients, expressed mainly as pain in the forearm. Pain was an independent predictor of RAO in the PCI subgroup, while numbness was an RAO predictor both for the whole group and the PCI subgroup.
5. Limitations
6. Conclusions
Supplementary Materials
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Variable | Radial Artery Occlusion (n = 129) | Radial Artery Patency (n = 1222) | p-Value |
---|---|---|---|
Age (years) # | 66 (21) | 65 (16) | p = 0.03 |
Female gender | 40 (31%) | 297 (24.3%) | p = 0.09 |
BMI (kg/m2) # | 29 (7.3) | 29 (5.5) | p = 0.28 |
BSA (m2) # | 1.9 (0.2) | 2 (0.3) | p = 0.77 |
GFR (mL/min/1.73 m2) # | 89 (37) | 85 (47) | p = 0.11 |
Platelets (109/L) # | 241 (98) | 222 (79) | p = 0.33 |
LVEF (%) # | 55 (27.5) | 55 (15) | p = 0.53 |
CHA2DS2-VASc # | 2 (3) | 3 (3) | p = 0.28 |
Hemoglobin (g/dL) # | 13.8 (2.5) | 13.9 (2) | p = 0.59 |
INR # | 0.97 (0.1) | 0.99 (0.1) | p = 0.57 |
Smoking | 63 (49.6%) | 482 (41.1%) | p = 0.07 |
ACS presentation | 50 (44.2%) | 451 (41.9%) | p = 0.63 |
STEMI presentation | 12 (10.6%) | 118 (11%) | p = 0.91 |
Stable CAD presentation | 34 (30.1%) | 317 (29.5%) | p = 0.89 |
Prior CAD | 32 (25.2%) | 339 (33.7%) | p = 0.20 |
Prior PCI | 14 (20.6%) | 155 (27%) | p = 0.26 |
PAD | 2 (3%) | 33 (5%) | p = 0.47 |
Stroke | 3 (4.5%) | 23 (3.5%) | p = 0.67 |
Hypertension | 79 (62.2%) | 713 (60.8%) | p = 0.76 |
Diabetes mellitus | 43 (33.9%) | 362 (30.9%) | p = 0.49 |
Dyslipidemia | 56 (44.1%) | 520 (44.3%) | p = 0.96 |
Family CAD | 20 (15.7%) | 166 (14%) | p = 0.59 |
Atrial fibrilation | 10 (14.9%) | 87 (13.1%) | p = 0.67 |
Heart failure | 15 (22.1%) | 140 (21%) | p = 0.84 |
CKD | 3 (4.4%) | 32 (5%) | p = 0.83 |
Antiplatelets pre | 81 (70.4%) | 751 (67.8%) | p = 0.56 |
Aspirin pre | 71 (61.7%) | 660 (59.6%) | p = 0.65 |
Clopidogrel pre | 45 (39.1%) | 411 (37.1%) | p = 0.67 |
Ticagrelor pre | 11 (9.6%) | 81 (7.3%) | p = 0.38 |
OACs pre | 16 (23.2%) | 175 (25.5%) | p = 0.67 |
LMWH pre | 8 (11.6%) | 103 (15%) | p = 0.44 |
NOACs pre | 7 (10.4%) | 65 (9.5%) | p = 0.80 |
Thrombolysis | 2 (2.9%) | 15 (2.2%) | p = 0.70 |
Preloading asp+clop | 6 (8.7%) | 48 (7%) | p = 0.60 |
Preloading asp+tic | 8 (11.6%) | 63 (9.2%) | p = 0.52 |
Variable | Radial Artery Occlusion (n = 129) | Radial Artery Patency (n = 1222) | p-Value |
---|---|---|---|
Left arm | 5 (3.9%) | 57 (4.8%) | p = 0.81 |
IV UFH > 50 IU/kg | 46 (35.7%) | 554 (45.3%) | p = 0.04 |
IV UFH (IU) # | 4000 (1400) | 4500 (1075) | p = 0.07 |
Radial artery spasm | 16 (15.7%) | 62 (7.2%) | p < 0.01 |
Access site cross-over | 7 (10.6%) | 18 (2.9%) | p < 0.01 |
Radial artery diameter at puncture site (mm) # | 2.7 (0.6) | 3 (0.7) | p = 0.25 |
Final sheath diameter 5 Fr | 86 (67.2%) | 671 (57.1%) | p = 0.03 |
Final sheath diameter 6 Fr | 40 (31.3%) | 491 (41.8%) | p = 0.02 |
Final sheath diameter 7 Fr | 2 (1.6%) | 13 (1.1%) | p = 0.65 |
Sheath/artery ratio # | 0.6 (0.2) | 0.6 (0.1) | p = 0.05 |
Intra-arterial nitroglycerin as vasodilator | 81 (70.4%) | 623 (56.3%) | p < 0.01 |
Intra-arterial verapamil vasodilator | 31 (27%) | 412 (37.3%) | p = 0.03 |
Obstructive CAD identified | 43 (62.3%) | 476 (70%) | p = 0.19 |
Multivessel CAD identified | 33 (25.6%) | 320 (26.2%) | p = 0.88 |
PCI performed | 21 (16.3%) | 314 (25.8%) | p = 0.02 |
>one puncture attempt | 30 (26.3%) | 168 (18.2%) | p = 0.04 |
Total time of sheath in artery (min) # | 30 (30) | 25 (22) | p = 0.46 |
Radiation time (min) # | 4 (4) | 7 (8) | p = 0.45 |
Contrast volume (ml) # | 100 (25) | 100 (70) | p = 0.30 |
Radiation (mGy) # | 147 (418) | 496 (652) | p = 0.61 |
Variable | Radial Artery Occlusion (n = 129) | Radial Artery Patency (n = 1222) | p-Value |
---|---|---|---|
Hemostasis duration (min) # | 75 (167) | 60 (94) | p = 0.50 |
Successful hemostasis | 108 (84.4%) | 1080 (92.2%) | p < 0.01 |
Manual hemostasis | 41 (31.8%) | 285 (23.6%) | p = 0.04 |
Patent hemostasis | 49 (62%) | 572 (87.5%) | p < 0.01 |
Hematoma | 37 (28.9%) | 160 (13.5%) | p < 0.01 |
Hemorrhage | 7 (5.5%) | 51 (4.3%) | p = 0.52 |
Palpable pulse | 22 (17.1%) | 1177 (96.3%) | p < 0.01 |
Symptoms at radial ultrasound | 22 (31.9%) | 74 (10.8%) | p < 0.01 |
Pain | 19 (27.5%) | 64 (9.3%) | p < 0.01 |
Numbness | 6 (8.7%) | 14 (2%) | p < 0.01 |
Antithrombotics post-cath | 60 (87%) | 579 (90%) | p = 0.42 |
Post-aspirin | 53 (76.8%) | 500 (77.6%) | p = 0.88 |
Post-clopidogrel | 23 (33.3%) | 250 (38.8%) | p = 0.37 |
Post-ticagrelol | 17 (24.6%) | 188 (29.2%) | p = 0.43 |
Post-prasugrel | 0 (0%) | 5 (0.8%) | p = 0.46 |
Post-acenocoumarol | 2 (2.9%) | 6 (0.9%) | p = 0.14 |
Post-NOACs | 9 (13%) | 61 (9.5%) | p = 0.34 |
Univariate | Multivariate Whole Group | Multivariate Only for PCI Subgroup | |
---|---|---|---|
Predictor | OR (95% CI), p-Value | aOR * (95% CI), p-Value | aOR ** (95% CI), p-Value |
Pre-procedural | |||
Female gender | OR = 1.40 (0.94–2.08), p = 0.10 | aOR = 1.72 (1.05–2.83), p = 0.03 | aOR = 1.16 (0.37–3.70), p = 0.80 |
Age | OR = 0.98 (0.97–1.00), p = 0.01 | aOR = 0.99 (0.97–1.01), p = 0.14 | aOR = 0.98 (0.94–1.02), p = 0.39 |
Smoking | OR = 1.41 (0.98–2.04), p = 0.07 | aOR = 1.32 (0.81–2.15), p = 0.26 | aOR = 1.74 (0.66–4.59), p = 0.26 |
Procedural | |||
>one puncture attempt | OR = 1.60, 1.02–2.51, p = 0.04 | aOR = 1.53 (0.91–2.57), p = 0.11 | aOR = 0.39 (0.05–3.15), p = 0.38 |
Sheath diameter (Fr) | OR = 0.67 (0.45–0.99), p = 0.05 | aOR = 0.73 (0.36–1.49), p = 0.39 | aOR = 0.69 (0.19–2.52), p = 0.57 |
Total time of sheath in artery | OR = 1.00 (0.99–1.01), p = 0.82 | aOR = 1.01 (1.00–1.02), p = 0.05 | aOR = 1.01 (0.99–1.02), p = 0.35 |
Radial spasm | OR = 2.73 (1.72–4.34), p < 0.01 | aOR = 2.47 (1.40–4.36), p < 0.01 | aOR = 4.48 (1.42–14.16), p = 0.01 |
Cross-over | OR = 4.01 (1.61–9.99), p < 0.01 | aOR = 4.33 (1.02–18.39), p = 0.05 | aOR = 2.16 (0.25–19.03), p = 0.49 |
Intra-arterial nitroglycerin as vasodilator | OR = 1.85 (1.22–2.81), p < 0.01 | aOR = 1.06 (0.61–1.86), p = 0.83 | aOR = 7.40 (1.67–32.79), p < 0.01 |
Intra-arterial verapamil vasodilator | OR = 0.62 (0.41–0.96), p = 0.03 | aOR = 0.98 (0.56–1.72), p = 0.94 | aOR = 0.17 (0.04–0.76), p = 0.02 |
PCI performed | OR = 0.56 (0.34–0.91), p = 0.02 | aOR = 0.19 (0.06–0.63), p < 0.01 | n.a. |
IV UFH (IU per kg) | OR = 0.99 (0.99–1.00), p = 0.04 | aOR = 0.98 (0.96–0.99), p < 0.01 | aOR = 1.00 (0.99–1.01), p = 0.94 |
IV UFH > 50 IU/per kg | OR = 0.67 (0.46–0.98), p = 0.04 | aOR = 0.56 (0.31–1.00), p = 0.05 | aOR = 4.15 (0.55–31.61), p = 0.17 |
Post-procedural | |||
Successful hemostasis | OR = 0.46 (0.27–0.77), p < 0.01 | aOR = 0.81 (0.31–2.14), p = 0.68 | aOR = 0.66 (0.24–1.82), p = 0.42 |
Manual hemostasis | OR = 1.51 (1.02–2.24), p = 0.04 | aOR = 1.94 (1.01–3.72), p = 0.05 | n.a. |
Hematoma | OR = 2.62 (1.72–3.97), p < 0.01 | aOR = 2.28 (1.28–4.06), p < 0.01 | aOR = 1.82 (0.65–5.06), p = 0.25 |
Post-cath dabigatran | OR = 3.52 (1.23–10.08), p = 0.02 | aOR = 5.15 (1.29–20.55), p = 0.02 | aOR = 3.61 (0.37–34.84), p = 0.27 |
Symptoms at radial artery ultrasound | OR = 3.89 (2.22–6.81), p < 0.01 | aOR = 2.10 (0.79–5.55), p = 0.14 | aOR = 3.80 (1.46–9.87), p < 0.01 |
Pain at radial artery ultrasound | OR = 3.71 (2.06–6.67), p < 0.01 | aOR = 1.64 (0.58–4.66), p = 0.35 | aOR = 2.93 (1.05–8.15), p = 0.04 |
Numbness at radial artery ultrasound | OR = 4.59 (1.70–12.35), p < 0.01 | aOR = 8.25 (1.70–40), p < 0.01 | aOR = 4.66 (1.17–18.57), p = 0.03 |
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Didagelos, M.; Pagiantza, A.; Papazoglou, A.S.; Moysidis, D.V.; Petroglou, D.; Daios, S.; Anastasiou, V.; Theodoropoulos, K.C.; Kouparanis, A.; Zegkos, T.; et al. Incidence and Prognostic Factors of Radial Artery Occlusion in Transradial Coronary Catheterization. J. Clin. Med. 2024, 13, 3276. https://doi.org/10.3390/jcm13113276
Didagelos M, Pagiantza A, Papazoglou AS, Moysidis DV, Petroglou D, Daios S, Anastasiou V, Theodoropoulos KC, Kouparanis A, Zegkos T, et al. Incidence and Prognostic Factors of Radial Artery Occlusion in Transradial Coronary Catheterization. Journal of Clinical Medicine. 2024; 13(11):3276. https://doi.org/10.3390/jcm13113276
Chicago/Turabian StyleDidagelos, Matthaios, Areti Pagiantza, Andreas S. Papazoglou, Dimitrios V. Moysidis, Dimitrios Petroglou, Stylianos Daios, Vasileios Anastasiou, Konstantinos C. Theodoropoulos, Antonios Kouparanis, Thomas Zegkos, and et al. 2024. "Incidence and Prognostic Factors of Radial Artery Occlusion in Transradial Coronary Catheterization" Journal of Clinical Medicine 13, no. 11: 3276. https://doi.org/10.3390/jcm13113276
APA StyleDidagelos, M., Pagiantza, A., Papazoglou, A. S., Moysidis, D. V., Petroglou, D., Daios, S., Anastasiou, V., Theodoropoulos, K. C., Kouparanis, A., Zegkos, T., Kamperidis, V., Kassimis, G., & Ziakas, A. (2024). Incidence and Prognostic Factors of Radial Artery Occlusion in Transradial Coronary Catheterization. Journal of Clinical Medicine, 13(11), 3276. https://doi.org/10.3390/jcm13113276