41 Insights from positron emission tomography into the mechanism of the coronary sinus reducer

Aims Despite evidence suggesting angina improvement after Coronary Sinus Reducer (CSR) implantation, the underlying mechanism remains to be confirmed. In a pilot study, we sought to assess changes in quantitative myocardial perfusion after CSR implantation in patients with refractory angina secondary to advanced coronary artery disease (CAD) using Rubidium-82 (Rb-82) Positron Emission Tomography (PET). Methods Data was collected prospectively for patients undergoing clinically indicated CSR implantation. Rb-82 PET was performed at rest and stress at baseline and median 6 months follow-up. QPET software was used for automatic segmentation into a 17 segment American Heart Association model and quantification of rest and stress myocardial blood flow (MBF, ml/min/g) and myocardial perfusion reserve (MPR). Results Five patients (3 male; 2 female) with mean age 69±16 years were recruited. Median Canadian Cardiovascular Society class was 3. Median number of anti-anginal medications was 3 and was unchanged during the follow-up period. 85 myocardial segments were analysed. Rest and stress MBF were corrected for rate-pressure product. Wilcoxon signed-rank tests were used to compare paired global and segmental perfusion values. A linear mixed-effects model with random slopes and intercepts was used to assess the relationship between baseline segmental MPR and associated change in MPR (delta MPR) after CSR implantation. Globally, there was no significant change in rest (P>0.99), stress MBF (P=0.63) or MPR (P=0.81) from baseline to follow-up. At a segmental level, there was no significant difference in MPR (P>0.57). However, the magnitude of change in MPR was related to the degree of baseline ischaemia (Figure 1). More ischaemic segments (baseline MPR<1.67) saw a greater increase in MPR after CSR whereas segments with higher baseline MPR values (MPR≥1.67) experienced a decrease (P=0.03, conditional R2 = 0.675). The median change in MPR in segments with a baseline MPR<1.67 (n=59) was 8.9% (delta MPR: +0.08; P=0.001) driven by a greater increase in stress MBF (15.6%, IQR: -2.1-42.2) compared to rest MBF (8.2%, IQR: -8.3-23.5; median of differences: 9.1%, P=0.0006) (Figure 2). In segments with baseline MPR≥1.67 (n=26) a 13.8% decrease in MPR was observed (delta MPR: -0.27; P=0.0003) driven by a greater decrease in stress MBF (-23.8%, IQR: -32.7-76.2) compared to rest MBF (-0.4%, IQR -24.33-72.9; median of differences: -11.5%, P= 0.0008). These changes in MPR remained significant when stratified by segments of the left (MPR<1.67: +0.08 [P=0.01]; MPR≥1.67: -0.20 [P=0.004]) and right (MPR<1.67: +0.11 [P=0.03]; MPR≥1.67: -0.27 [P=0.02]) coronary artery distributions. Conclusions To our knowledge, this is the first study showing changes in quantitative myocardial perfusion by PET after CSR implantation. Our segmental analysis demonstrates a relationship between baseline MPR and change in MPR after CSR implantation. In segments with MPR <1.67, the significant increase in MPR associated with CSR implantation was driven predominantly by greater increases in stress than rest MBF. By contrast, in segments with MPR≥1.67, follow-up MPR fell, driven by a reduction in stress MBF. Global values were unchanged. These quantitative preliminary data suggest redistribution of perfusion during stress as an effect of CSR implantation in patients with refractory angina secondary to advanced CAD. These pilot data require confirmation in adequately powered, double-blinded, randomised, sham-controlled studies. Conflict of Interest Nil

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