46 Chapter 3 artery were enrolled in the registry. Patients with hemodynamic instability, significant valvular pathology and prior coronary artery bypass graft surgery, as well as patients with a clinical presentation of acute coronary syndromes upon the index procedure, were excluded. Individual vessellevel data for pooled analysis were collected using standardized spreadsheets and a fully compliant cloud-based clinical data platform (Castor EDC, Amsterdam, The Netherlands). Standardized definitions were used for all variables. ILIAS Registry was registered at Clinical trials.gov (ClinicalTrials.gov Identifier: NCT04485234). Coronary angiography and physiological assessment Coronary angiography and intracoronary physiological assessments were performed in all institutions using standard techniques. After diagnostic coronary angiography, invasive physiological indices were measured using either separate pressure- (PressureWire, RADI medical – now Abbott Vascular, St Paul, MN) and Doppler velocity sensorequipped coronary guidewires (FloWire, Endosonics – now Philips Volcano, San Diego, CA), dual pressure- and Doppler flow velocity equipped guide wire (ComboWire, Volcano Corp. – now PhilipsVolcano, San Diego, CA), or a temperature-sensitive pressure sensor equipped guide wire (PressureWire, St Jude Medical- now Abbott Vascular, St. Paul, MN) using routine techniques. Intracoronary nitrate (100 or 200 μg) was administered before physiologic measurements. Using the Doppler velocity technique, baseline (bAPV) and hyperemic average peak flow velocities (hAPV) were labelled baseline and hyperemic flow, respectively. Using the bolus coronary thermodilution technique, resting and hyperemic thermodilution curves were obtained in triplicate using three injections (4 mL each) of room-temperature saline, and the inverse of the average basal (bTmn) and hyperemic mean transit times (hTmn) was labelled baseline and hyperemic flow, respectively. Hyperemia was induced by intravenous infusion of adenosine (140 μg/ kg per min) or adenosine triphosphate (ATP) (150 μg/kg per min) through a peripheral or central vein, intracoronary bolus injection of adenosine (20-200μg), or intracoronary bolus injection of nicorandil (3 mg), according to local standards.6 Derivation of MRR MRR was derived based on the theoretical framework by De Bruyne et al.3 The formula used in this study is a product of CFR and FFR with correction for the impact of changes in hemodynamics from non-hyperemic to hyperemic conditions, as follows: =( ) × ( ℎ ) ⁄ ⁄ Where CFR indicates coronary flow reserve, the ratio of coronary flow (velocity) at maximal hyperemia to coronary flow (velocity) at non-hyperemic conditions, FFR indicates fractional flow reserve (calculated as the ratio of distal coronary pressure to aortic pressure at maximal hyperemia) and Pa, rest and Pa, hyper indicate aortic pressure during non-hyperemic conditions and maximal hyperemia, respectively. Herewith, MRR corrects the vasodilator reserve capacity of the coronary circulation (expressed by CFR)
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