Radial Artery Spasm Leading to Occlusion in Patients Undergoing Coronary Angiogram Via Radial Access

Transradial (TR) approach for PCI has gained widespread popularity secondary to decreased
bleeding and reduced vascular access site complications as compared to transfemoral (TF)
access. Other advantages of the TR technique include improved patient satisfaction,
decreased length of stay and an enhanced economic outlook . Radial artery spasm (RAS) is a
well-known obstacle associated with transradial approach and is also the most common cause
of procedural failure . The reported incidence of RAS varies from 5% - 30%. Predictors of
spasm include younger age, female gender, diabetes, smaller wrist circumference and lower
body weight. With the advent of newer techniques such as smaller sheath size, hydrophilic
coating of the sheath and use of vasodilator drugs during the procedure the incidence of RAS
has reduced significantly but it still continues to be a cumbersome problem. The marked
muscle mass in the radial artery wall, which is greater than that of the other arteries, and
its high density in alpha-adrenergic receptors explain its propensity to go in to spasm.
This spasm produces pain and difficulty in catheter manipulation and thereby increasing the
chances of complications such as arterial avulsion. It's hypothesized that there might be
vascular endothelial damage during catheter manipulation when patients have RAS which can
activate the coagulation cascade and can result in radial artery occlusion.

Radial artery occlusion (RAO) is a frequent complication of radial artery cannulation. In
the perioperative period, rates of RAO have been reported to be as high as 30%-40% .
Postoperatively, however rate of RAO drop down to as low as 3%-10%. Spontaneous
recanalization of the radial artery occurs frequently, and consequently, the prevalence of
persistent RAO is much lower post-operatively. Radial artery occlusion can be documented by
an abnormal Barbeau's test , visible obstruction on two-dimensional ultrasound or absence of
Doppler flow signal distal to the puncture site. Radial artery occlusion is usually
clinically quiescent and doesn't require any intervention secondary to dual blood supply of
the arm. The presence of RAO, however, makes repeat ipsilateral radial access difficult.
Predictors of RAO include low body weight, advanced age, female gender, degree of systemic
anticoagulation, the hemostasis process as well as a low radial artery diameter to sheath
size ratio. The mechanism for development of RAO are supposed to be thrombus formation
following vessel injury, intimal hyperplasia and negative remodeling of the vessel after the
stretching that radial artery undergoes during cannulation. Development of RAO has been
related to the severity of the lesion suffered by the artery during the procedure thus,
radial spasm which supposedly occurs secondary to vessel trauma may be associated with
subsequent occlusion of radial artery.

There has been only one study to date by Ruiz-Salmerón et al that looked at the association
of RAS with the development of RAO. They found no significant difference in the radial
artery occlusion rate in patients who experienced radial artery spasm. The major limitation
of that study however was the assessment of radial artery patency by plethysmography and
pulse oximetry which could underestimate the true incidence of RAO. However, in this study
the investigators intend to use the Doppler ultrasound (the gold standard) to detect the
patency of radial artery and will be able estimate the true incidence of RAO in patient who
experience RAS during the procedure.

Inclusion Criteria:

- All patients with an informed consent undergoing successful and atraumatic
transradial cannulation for either diagnostic angiography/percutaneous coronary
intervention ( PCI) over 18 years of age

Exclusion Criteria:

1. Unsuccessful and traumatic radial cannulation

2. Previous failed attempts at transradial access

3. Cardiogenic shock

4. Negative Allen's test

5. Arterio-Venous Fistula or Graft

6. Prior upper extremity vascular manipulation resulting in anatomical changes

7. Upper Extremity vessel stenting