Coronary-subclavian steal syndrome causing myocardial infarction after arteriovenous fistula creation: a case report

Abstract

Coronary subclavian steal syndrome (CSSS) caused by left subclavian artery (LSA) stenosis is a rare cause of myocardial infarction in patients having coronary artery bypass grafting (CABG), and it has also been observed after an arteriovenous fistula (AVF) was made. A 79-year-old woman who had undergone CABG years earlier and an AVF creation 1 month before experienced a non-ST-elevation myocardial infarction (NSTEMI). While selective catheterization of the left internal thoracic artery graft was impossible, a computed tomography scanner showed patency of all bypasses and proximal subocclusive LSA stenosis, and the digital blood pressure measurements objectified a haemodialysis-induced distal ischaemia. LSA's angioplasty and covered stent placement were successfully performed, resulting in symptom remission. A CSSS-induced NSTEMI due to a LSA stenosis aggravated by a homolateral AVF several years after CABG has been documented only infrequently. If vascular access is required in the presence of CSSS risk factors, the contralateral upper limb should be preferred.

Keywords: Arteriovenous fistula; Coronary subclavian steal syndrome; Non ST Segment Elevation Myocardial Infarction; Subclavian stenosis; haemodialysis access-induced distal ischaemia.

Figure 1

(A) Pre‐interventional electrocardiogram shows a ST depression >2 mm in the leads DII, aVF, V4, V5 and V6 suggestive of inferior lateral ischaemia (black arrows). (B) Post‐interventional electrocardiogram shows the regression of ST depression (grey arrows).

Figure 2

Evolution of troponin levels which shows a decrease after a peak reached at Day 3. The percutaneous intervention consisting of a left subclavian artery balloon angioplasty and covered stent placement across the left subclavian artery stenosis was performed at Day 5.

Figure 3

(A) Coronary angiography shows the left subclavian artery stenosis (white arrow). (B) Post‐procedural angiographic image shows the covered stent within the left subclavian artery (black arrows).

Figure 4

(A) Sagittal section through the left subclavian artery highlights the high‐grade stenosis at its origin (white arrow). (B) 3D reconstructed images of the aortic arch show the severe stenosis of the left subclavian artery (white arrow).

Figure 5

(A) Pre‐interventional spectral Doppler ultrasound (DUS) of the left subclavian artery shows a widening of the velocity band in the spectral waveform, raised peak systolic velocities (PSV) of 253 cm/s (white arrow), and raised end‐diastolic velocities (EDV) of 94 cm/s (black arrow) in the stenotic jet. The systolic upstroke time (SUT) is measured at 225 ms (blue arrow), thus considered prolonged. (B) At the same location, post‐interventional spectral DUS found lowered PSV and EDV (158 and 58 cm/s, respectively) with shortened SUT (115 ms). The clear (black) window under the waveform's systolic component suggests the absence of turbulence.

Figure 6

(A) Pre‐interventional left‐arm Doppler ultrasound (DUS) estimates the AVF flow volume at 741 mL/min. The AVF flow volume was obtained from the lumen's diameter of the left brachial artery, measured on cross‐sections of a rectilinear arterial segment 6 cm proximal to the arteriovenous anastomosis, and the time‐average velocity in the same arterial segment. Three flow rates were measured, and the final result was the mean of these three measurements. (B) Using the same method of AVF flow volume measurement, the post‐operative DUS of the AVF estimates the flow volume at 903 mL/min.

Figure 7

Formalized report of the systolic pressure measurement at the thumb, the index finger, and the middle finger of each hand (first the right hand, then the left) by LASER Doppler flowmetry. Three measurements were taken on each finger being evaluated (<10 mmHg difference between measurements required otherwise the measurement was discarded). The right‐arm systolic blood pressure was 152 mmHg. The left hand's digital systolic blood pressure was significantly lower than the right, pointing to distal ischaemia brought on by haemodialysis.