Patterns of Regional Myocardial Perfusion Following Coronary Sinus Reducer Implantation.

September 2019 1 Francesco Giannini, MD Anna Palmisano, MD Luca Baldetti, MD Giulia Benedetti, MD Francesco Ponticelli, MD Paola M.V. Rancoita, PhD Neil Ruparelia, MD Guglielmo Gallone, MD Marco Ancona, MD Antonio Mangieri, MD Georgios Tzanis, MD Francesco De Cobelli, MD Alessandro Del Maschio, MD Antonio Colombo, MD Antonio Esposito, MD The coronary sinus (CS) Reducer (Neovasc, Inc, Richmond, BC, Canada) is a percutaneous device aiming at symptoms control in patients suffering from refractory angina. Its clinical effect1 may be exerted through flow redistribution toward ischemic territories as a consequence of increased coronary drainage pressure resulting from CS narrowing.2 Current imaging evidences are limited.1,2 We evaluated the impact of the Reducer upon regional myocardial ischemia in patients with refractory angina using stress Cardiac Magnetic Resonance (stressCMR). Consecutive patients with RA1 and evidence of inducible ischemia involving at least 1 myocardial segment at stress-CMR were included. The study was approved by the institutional review committee, and all patients gave informed consent. Study database is available from the corresponding author on request. Stress-CMR was performed at baseline and 4 months after reducer implantation at 1.5T (Philips Ingenia, Best, The Netherlands). First-pass perfusion was performed using a saturation-recovery prepared balanced steady-state free precession for 3 short-axis slices within each cardiac cycle (45-dynamics). Stress was induced with dipyridamole (0.56–0.84 mg/kg in 4–6 minutes). Ischemic burden was defined as the percentage of LV wall involved by inducible perfusion defect (IPD). Visual inducible perfusion defect was scored according to AHA 16-segment model and transmurality (1=1%–25%; 2=25%–50%; 3=51%–75%; 4=>75%). Segmental myocardial perfusion reserve index (MPRI) was calculated (CVI42, Circle Cardiovascular Imaging, Inc, Canada) according to myocardial layers (subendocardial, mesocardial, subepicardial, and transmural). MPRI<1.3 defined severe ischemia. Patient-level comparisons were carried by paired Wilcoxon signed-rank test. Segment-level ΔMPRI data were analyzed using linear mixed-effects models with random intercept per patient. Two models were defined: to compare ΔMPRI between ischemic and nonischemic segments and among the 3 myocardial layers. Two patients were excluded for poor image quality at baseline CMR. Final population included 15 patients (93.3% males; age 66 [IQR, 58.5–74] years; ejection fraction 57% [55.0–62.5]; 3-vessel disease 86.7%; previous percutaneous (66.6%); and surgical (93.3%) coronary revascularization; Canadian Cardiovascular Society class 3 [3-3]; number of anti-ischemic drugs 3 [3-3]). Four months following reducer implantation, 13 (86.7%) patients improved by at least 1 Canadian Cardiovascular Society class (from 3 [3-3] to 1 [1–2]; P=0.001). At CMR, median per-patient ischemic burden reduced from 13.00% to 10.88% (P=0.0092) and the number of segments with inducible perfusion defect from 6 (2–9) to 5 (2–6; P=0.0138). The overall number of segments with inducible perfusion defect reduced from 92/240 (38%) to 69/240 (29%; P<0.001, by logistic mixed-effects model). Reducer implantation led to a significant increase in transmu© 2019 American Heart Association, Inc. RESEARCH LETTER