Effect of Distal Embolisation on Myocardial Perfusion Reserve Following Percutaneous Coronary Intervention: A Quant

1. Effect of Distal Embolisation on Myocardial Perfusion Reserve Following Percutaneous Coronary Intervention: A Quantitative MR Perfusion Study Selvanayagam JB MBBS, DPhil; Cheng ASH MBBS; Jerosch-Herold M PhD; Rahimi K MD;Porto I MD; Neubauer S MD; Banning AP MD From the University of Oxford Centre for Clinical Magnetic Resonance Research, University of Oxford, UK & Department of Cardiovascular Medicine, Flinders Medical Centre, Adelaide, Australia and Advanced Imaging Research Center, Oregon Health & Science University, Portland, OR, USA

2. Background • Studies using intra-coronary Doppler have shown that a proportion of patients demonstrate persistent impairment in microcirculatory function after PCI, • even after substantial conduit area enlargement • using high resolution quantitative CMR, we sought to investigate this by evaluating PCI-induced changes in myocardial perfusion reserve index (MPRI) and procedure-related myonecrosis • HYPOTHESES • MPRI is impaired in segments with new ‘distal’ PCI-induced injury • myocardial segments ‘upstream’ to the injury in the territory of the culprit vessel would not demonstrate persistent microvascular dysfunction after PCI

3. 98 patients screened 30 excluded: clinical history of MI, CTO, contraindications to MRI/adenosine 68 patients eligible 10 declined 14 excluded: HE on CMRscan pre PCI 44 patients CMR scan pre PCI 40 patients CMR scan 24 hours post PCI 20 patients CMR scan 6 months post PCI Methods

4. Results

5. Results 3 5 . 2 2 Mean MPRI Score (95% CI) 6 months FU 24h Post PCI Pre PCI Control Distal HE Upstream

6. Results Table 1 MPRI z - No of Pre - PCI 24h post - PCI Change after 24h value p - value segments 1. Affected segments in all 40 patients 2.06 2.52 0.46 No HE 322 (1.99, 2.13) (2.42, 2.62) (0.36, 0.56) - 4.82 <0.001 2.16 2.00 - 0.16 HE (distal) 82 (1.95, 2.37) (1.82, 2.1 9) ( - 0.29, - 0.02) 2. Affected segments in 21 patients with distal new injury 2.18 2.35 0.17 No HE 170 (2.07, 2.30) (2.22, 2.47) (0.04, 0.29) - 6.85 <0.001 2.16 2.00 - 0.16 HE (distal) 82 (1.95, 2.37) (1.82, 2.19) ( - 0.29, - 0.02) 3. All seg ments in 21 patients with distal new injury 2.18 2.31 0.13 Upstream (reference group) 141 (2.05, 2.30) (2.17, 2.44) (0.03, 0.23) - - 2.22 2.05 - 0.17 Distal 70 (1.98, 2.45) (1.84, 2.26) ( - 0.32, - 0.02) - 4.88 <0.001 2.22 2.43 0.20 Remote 90 (2.08, 2.37) (2.2 5, 2.60) (0.02, 0.39) 0.68 0.50 2.24 2.42 0.19 No PCI 146 (2.08, 2.39) (2.31, 2.54) (0.04, 0.33) 0.70 0.48 HE denotes hyperenhancement, MPRI myocardial perfusion reserve index, PCI percutaneous coronary intervention. Upstream=myocardial segments supplied by the culprit vessel proximal to the distal HE; Remote=segments that underwent PCI in a second vessel in the same patients but not displaying new injury; distal HE=segments demonstrating new distal injury; No PCI=Segments that are subtended by arteries that did not undergo PCI

7. Results Table 2 Rest MBF (ml/min/g) Stress MBF (ml/min/g) P value 2.2 (2.0, 2.4) Pre PCI (HE negative) 1.0 (0.9, 1.1) 1.0 (0.9, 1.1) Pre PCI (HE positive) 2.2 (1.9, 2.5) 0.01* 1.0 (0.9, 1.1) 2.8 (2.3, 3.3) Early Post PCI (HE negative) 1.9 (1.7, 2.1) 0.03* Early post PCI (HE positive) 1.0 (0.9, 1.2) 2.7 (2.3, 3.0) 0.8** Late post PCI (HE negative) 1.1 (0.9, 1.3) 0.03** Late Post PCI (HE positive) 1.2 (0.9, 1.4) 2.8 (2.3, 3.3) HE denotes hyperenhancement, MBF myocardial blood flow, PCI percutaneous coronary intervention. *when compared with pre-PCI value, **when compared with 24 hour post-PCI value

8. Results Remote: segments in the same patientssubtended by a vessel that was intervened upon and which had no new HE Upstream: segments supplied by the culprit vessel, proximal to the distal HE Distal HE: segments demonstrating new distal HE

9. Conclusions • MPRI is reduced in segments demonstrating new ‘distal’ irreversible injury at 24 hours after PCI • These reductions are transient and confined to the segments with injury • Microcirculatory impairment early after PCI may be due to both new myonecrosis and transitory macro/microvascular plugging of the vascular bed