Preventing Spasm During Transradial Angiography: Sometimes Less is More

Transradial coronary angiography (TRA) was introduced over 2 decades ago and has been adopted by many clinicians worldwide.¹ It is becoming increasingly popular in elective and emergency situations because of lower vascular access site complication rates and earlier patient mobilization.² However, despite demonstrated benefits, TRA is employed in a minority of patients undergoing PCI.

A recent analysis of the National Cardiovascular Data Registry with more than 600 PCI centers across the U.S., reported use of transradial percutaneous coronary intervention (TR-PCI) in 1.5% of all PCI procedures.³ Technical difficulties and challenges encountered during TR-PCI are believed to be a major reason for underuse of this technique. Dehghani et al identified age >75 years (OR: 3.86; 95% CI: 2.33 to 6.40, P=0.0006), prior CABG (OR: 7.47; 95% CI: 3.45 to 16.19, P=0.0002), and short stature (OR: 0.97; 95% CI: 0.95 to 0.99, P= 0.02) as independent predictors of TR-PCI failure on multi-variate analysis.⁴ In addition to the patient-related factors listed above, there is a procedure-related issue that poses a unique challenge to adopting this technique.

Radial artery spasm (RAS) is one of the most common complications encountered by operators while performing transradial cardiac catheterization and PCI.⁵ It causes patient discomfort and increases the chance for procedural failure. The incidence of RAS varies from 3.8% to 20%, depending on the definition utilized.^6-8 Such a wide range in the rate of RAS can be explained partly by the types of vasodilatory regimens used in different cardiac catheterization laboratories as well as operator experience.

The radial artery is a thick-walled vessel composed mainly of smooth muscle cells with a high concentration of alpha-1 adrenoreceptors. The muscular component and predominance of alpha-1 adrenoreceptors make it susceptible to spasm by circulating catecholamines, vessel cannulation, and manipulation of a guide catheter or wire.⁹ There are a number of mechanisms that can modulate vasoconstriction and vasodilation. Therefore, it is unlikely that a single pharmacological agent can completely eliminate radial artery spasm. Nevertheless, a number of agents have been used in clinical practice with the aim of reducing this problem. Unfortunately there is no clear agreement as to what is (are) the optimal agent(s). (Table)

In this issue of the Journal, the authors present a randomized controlled study evaluating two common intra-arterial (IA) vasodilator regimens used during transradial coronary angiography. They observed no significant difference in the incidence of clinical RAS between Group A (200 μg nitroglycerin plus 2.5 mg diltiazem) versus Group B (200 μg nitroglycerin plus placebo) (5% vs. 7%; P=0.5). In both groups the cocktail was given at the beginning of the procedure. The authors found a higher incidence of local burning pain in the forearm in patients receiving diltiazem plus nitroglycerin compared to nitroglycerin alone (21% vs. 9%; P=0.034). The authors concluded diltiazem plus nitroglycerin showed no advantage compared to nitroglycerin alone in prevention of RAS in transradial approach.  It should be noted that the operators in this study are expert transradial operators with several years of experience. This almost certainly had an impact on keeping the rate of RAS low.¹⁰ 

The relatively low rate of radial artery spasm in this study is comparable to the rate reported in recent publications. In a head-to-head comparison study between two vasodilatory cocktails, all patients received unfractionated heparin plus nitroglycerin (100 μg); they either received verapamil (1.25mg) or placebo. There was no statistically significant difference in the incidence of radial artery spasm.⁶  One possible explanation of the neutral effect of calcium-channel blockers on arterial vasodilation could be the pain-triggered vasoconstriction on intra-arterial injection.

The development of RAS during the procedure can cause the vessel to constrict around the catheter, resulting in severe pain to the patient as well as significant difficulty in manipulation of the catheter by the operator, thereby limiting the successful completion of the case. The identification of the causes of RAS and steps to curtail them would therefore be of great benefit to both the patient and the operator.

There have been many techniques suggested to decrease the risk of RAS. Adequate analgesia and sedation to result in a painless cannulation of the artery in a relaxed patient are the important initial steps. Spasm is more likely to occur in the setting of multiple unsuccessful attempts at vessel cannulation, making successful radial artery cannulation more difficult.

Despite its marked safety advantage, patient preference, and potential mortality benefit in high-risk patients,¹¹ compared with the femoral approach, the radial approach is not without limitations. RAS should be recognized as a barrier and prevention of RAS incorporated as an integral part of a catheterization laboratory’s quality improvement program. Extreme caution should be adopted when encountering it. The use of a vasodilating cocktail has been advocated for prevention and treatment. While there is no “magic” formula that can eliminate spasm in all cases, the current work contributes to the larger body of evidence in support of nitroglycerin as a particularly efficacious agent for the prevention of RAS.

References

1. Campeau L. Percutaneous radial artery approach for coronary angiography. Cathet Cardiovasc Diagn. Jan 1989;16(1):3-7.
2. Kiemeneij F, Laarman GJ, Odekerken D, Slagboom T, van der Wieken R. A randomized comparison of percutaneous transluminal coronary angioplasty by the radial, brachial and femoral approaches: the access study. J Am Coll Cardiol. May 1997;29(6):1269-1275.
3. Rao S, Ou F, Wang T, et al. Trends in the Prevalence and Outcomes of Radial and Femoral Approaches to Percutaneous Coronary Intervention. A Report From the National Cardiovascular Data Registry. JACC: Cardiovascular Interventions. 2008;1(4):379-386.
4. Dehghani P, Mohammad A, Bajaj R, et al. Mechanism and Predictors of Failed Transradial Approach for Percutaneous Coronary Interventions. JACC: Cardiovascular Interventions. 2009;2(11):1057-1064.
5. Hildick-Smith DJ, Walsh JT, Lowe MD, Shapiro LM, Petch MC. Transradial coronary angiography in patients with contraindications to the femoral approach: an analysis of 500 cases. Catheter Cardiovasc Interv. Jan 2004;61(1):60-66.
6. Chen CW, Lin CL, Lin TK, Lin CD. A simple and effective regimen for prevention of radial artery spasm during coronary catheterization. Cardiology. 2006;105(1):43-47.
7. Coppola J, Patel T, Kwan T, et al. Nitroglycerin, nitroprusside, or both, in preventing radial artery spasm during transradial artery catheterization. J Invasive Cardiol. Apr 2006;18(4):155-158.
8. Varenne O, Jegou A, Cohen R, et al. Prevention of arterial spasm during percutaneous coronary interventions through radial artery: the SPASM study. Catheter Cardiovasc Interv. Aug 2006;68(2):231-235.
9. He GW, Yang CQ. Characteristics of adrenoceptors in the human radial artery: clinical implications. J Thorac Cardiovasc Surg. May 1998;115(5):1136-1141.
10. Dharma S, Shah S, Radadiya R, Vyas C, Pancholy SB, Patel T. Nitroglycerin plus diltiazem versus nitroglycerin alone for spasm prophylaxis with transradial approach.  J Invasive Cardiol. 2012;24(3):122-125.
11. Vorobcsuk A, Konyi A, Aradi D, et al. Transradial versus transfemoral percutaneous coronary intervention in acute myocardial infarction systematic overview and meta-analysis. Am Heart J. Nov 2009;158(5):814-821.
12. Dandekar VK, Vidovich MI, Shroff AR. Complications of transradial catheterization. Cardiovasc Revasc Med. Jan 2012;13(1):39-50.

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From the University of Illinois – Chicago and Jesse Brown VA Medical Center, Chicago, Illinois.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr. Shroff reports consulting for Terumo Medical, Teleflex, Abiomed and the Medicines Company. Dr. Asghar reports no disclosures.
Address for correspondence: Adhir Shroff, MD, MPH, FACC, FSCAI, Associate Professor of Medicine, University of Illinois – Chicago and Jesse Brown VA Medical Center, 840 S Wood St, MC 715, Chicago, IL 60607. Email: arshroff@uic.edu