Pressurewire

The FFR, coronary flow reserve (CFR), and IMR were measured as described previously.[13] (link) After a 6F guide catheter engaged the coronary artery, a pressure-temperature sensor-tipped guidewire (Pressure Wire; Abbott Vascular, St. Paul, MN, USA) was introduced. Equilibration was fulfilled when the sensor was at the tip of the catheter. The pressure sensor was consistently positioned at the distal segment of a target vessel, intracoronary nitrate (100 or 200 mg) was administered before each measurement., and 4 mL of room temperature saline was briskly injected into the vessel three times to derive the resting mean transit time (Tmn) using a thermodilution curve. Hyperemia was induced by intravenous infusion of adenosine (140 mg/kg per minute) via a peripheral vein. Hyperemic proximal aortic pressure (Pa), distal arterial pressure (Pd), and hyperemic Tmn were measured during sustained hyperemia. FFR was calculated as the lowest average of three consecutive beats during stable hyperemia. CFR was calculated as the ratio of resting Tmn/hyperemic Tmn. The IMR was calculated using the equation Pd × Tmn during hyperemia.

After coronary angiography, FFR measurement was performed when the operator considered the lesion met the inclusion criteria. FFR was measured using a pressure wire (St. Jude Medical, Saint Paul, MN) initially distal to the most distal lesion in the distal part of the culprit lesion. FFR was calculated as the ratio between the average distal pressure and the average aortic pressure recorded during maximal hyperemia induced by injection of ATP via the antecubital vein at 160 μg/L per minute. Pressure data were recorded for at least 3 seconds of stable value before ATP administration and at least 10 seconds of stable value during hyperemia. The pressure wire was returned to the initial part of the guiding catheter to exclude pressure drift during hyperemia. Drift range <0.03 was accepted, otherwise FFR measurement needed to be performed again. Functional significance was defined with the threshold of FFR value ≤0.80; in vessels with an FFR value ≤0.80, the lesion that caused the larger pressure step‐up (ΔFFR) was stented firstly. After stenting to the primary lesion, FFR was measured again and the second lesion was stented with the FFR value ≤0.80. FFR was measured finally after all of the stents were implanted. All PCI procedures were performed using drug‐eluting stents (DES). All pressure tracings were recorded on the RadiAnalyzer Xpress (St. Jude Medical) for offline analysis.

Coronary angiography and FFR measurement were performed in both reference centers according to standard clinical practice techniques, as described earlier.² Briefly, coronary angiogram was acquired via either a radial (preferred) or femoral approach. FFR measurements were performed by using a 0.014‐in. pressure sensor‐tipped wire (PrimeWire Prestige, Volcano Corporation or PressureWire, St. Jude Medical) positioned distal to a lesion during adenosine‐induced hyperemia. A lesion assessed with a hyperemic FFR value >0.80 was considered functionally nonsignificant for causing ischemia. FFR measurements in all clinical settings were included to identify all cases with negative FFR deferred lesions, and this included both planned FFR measurements and ad hoc decisions. In the event of multiple lesions being present in the same epicardial artery branch, the most severe stenosis was used for further follow‐up and analysis.

Images of CCTA were acquired with a 256-row, 16 cm detector CT system (Revolution CT, GE Healthcare). Beta-blockers were administered if necessary. ECG gating was implemented to acquire images at diastolic phase when contrast agent was fully perfused in the coronary arteries. FFR was performed following the clinical practice guideline.[15] FFR was measured in all cases using the VOLCANO instrument and a coronary pressure wire (PrimeWire PRESTIGE Plus pressure Guide Wire). After calibration and equalization, the pressure wire was advanced distally to the stenosis until the pressure sensor landed in a smooth coronary segment. Hyperemia was induced by using an intravenous infusion of adenosine (140 µg/kg per min). The pullback FFR data were recorded from the immediate downstream of the distal stenosis to the ostium of the coronary (PressureWire, St. Jude Medical). FFR was then calculated as the ratio between mean distal pressure (mPd) and mean aortic pressure (mPa). (Eq.1).

This post-hoc analysis included patients from the data sets of previous studies from our institution performed from January 2011 to June 2017.12 (link) All screened patients had suspected or known stable coronary artery disease and underwent invasive CAG with physiological lesion assessment using a pressure–temperature sensor-tipped guide wire (PressureWire; St. Jude Medical, St. Paul, MN, USA). Lesions showing an angiographically visible stenosis of 30%–80% by visual estimation were included. In multivessel coronary artery disease, a single vessel with the lowest FFR value was included for the current analysis. The exclusion criteria were presented in an online supplementary file methods 1. This study was performed in compliance with the Declaration of Helsinki for investigation in human beings. The study protocol was approved by the institutional review board, and all patients provided written informed consent for enrolment in the institutional database for potential future investigations. All patient data and procedural details were obtained from the patients’ medical records.