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).