Comment
CSSS is estimated to complicate between 0.2-6.8% of CABG
operations[1] and is due to subclavian artery stenosis (SAS) or
occlusion which has been reported to be present in up to 5.3% of
patients undergoing CABG, and in 11.8% of those with a history of
peripheral vascular disease (PVD) [2]. It typically presents after
surgery with symptoms ranging from stable angina to acute coronary
syndrome and even sudden cardiac death that may occur many months
postoperatively usually following left arm exertion[3].
Here we report an unusual presentation of CSSS, presenting
intraoperatively with haemodynamic instability after weaning from CPB,
presumably representing myocardial ischaemia due to inadequate LIMA
flow. We hypothesise that this was due to the change in coronary
vascular resistance occurring. With an unloaded heart on CPB, there is a
low resistance vascular bed offering minimal resistance to LIMA flow
throughout the cardiac cycle, but upon weaning from CPB there is
increased coronary vascular resistance[4] and only diastolic
perfusion which was presumably compromised due to the collateral origin
of the LIMA. This would also explain why upon taking down the artery
there was apparently good flow from the LIMA. Given the apparent
unreliability of the LIMA graft, the decision was made to use a vein
graft instead.
In view of the relatively high incidence of SAS in the CABG population,
it is surprising that there are no recommendations on screening for this
problem in guidelines on coronary revascularisation, especially in the
era of increasing use of bilateral internal mammary arteries. There are
two relatively inexpensive options for screening: i) measurement of
bilateral brachial blood pressure – where a difference in systolic
pressure of 15 or 20mmHg has been suggested to be diagnostic of
haemodynamically significant SAS; and ii) ultrasound doppler – which is
often performed to exclude carotid artery disease, where systolic
vertebral artery flow reversal is suggestive of haemodynamically
significant SAS. In patients with suspicion of SAS, diagnostic options
include computed tomography or magnetic resonance angiography, or
digital subtraction angiography, and following confirmation of diagnosis
there is opportunity to intervene and treat the problem, for example
with stenting, to minimise the risk of CSSS postoperatively[5].
In our patient, subsequent measurement of bilateral brachial artery
pressures identified a 30mmHg difference in systolic pressure and would
have alerted to the presence of SAS had this been performed
preoperatively. As such we believe there may be some value in screening
patients pre-operatively and are now introducing bilateral brachial
blood pressure measurement as a routine screening for SAS in patients
undergoing CABG and propose an algorithm (Figure 2).