Indications for performing coronary physiologic measurements include those lesion subsets whose clinical relevance is uncertain following angiography. These include intermediate severity stenosis, assessment of culprit lesions in patients with multivessel coronary artery disease and guiding therapy in patients with tandem lesions or diffuse disease in an epicardial vessel. Coronary physiologic studies are useful in areas poorly studied angiographically eg. ostia and bifurcations, and can also be used to assess prognosis following stent implantation. Coronary physiologic testing is useful in assessing ischemic potential of patients with prior myocardial infarction (MI), in patients with treated unstable coronary syndromes and to assess the collateral circulation. Table 29.1 summarizes the indications for using coronary physiologic measurements.

The contraindications to physiologic measurements are few. According to current guidelines, no physiologic measurement (FFR/CVR) is needed for clinical decisions when the clinical, angiographic and objective ischemia markers are concordant for the diagnosis. Other contraindications include the inability to use anticoagulation for angioplasty sensor wire placement, unstable clinical syndromes (relative contraindication) and unsatisfactory hemodynamic recording equipment [2].

Intracoronary physiologic measurements are made with standard angioplasty equipment and techniques. Doppler flow velocity can be measured using a Doppler-tipped angioplasty guidewire. This guidewire is a 175 cm long, 0.014 in. diameter, flexible, steerable wire with a piezoelectric ultrasound transducer integrated into the tip (FloWire; Volcano Therapeutics, Del Mar, CA)

Several companies make pressure wire/catheter products. Unique handling characteristics arise from special construction of the device. Current pressure wire sensors are either piezo-electric or optical. Pressure wires also differ from regular workhorse wires having to incorporate the thin wires or optical fibers that transmit the pressure signals (Fig. 29.2).

After diagnostic angiography or during angioplasty, the sensor guidewire is passed through an angioplasty Y-connector attached to a diagnostic or guiding catheter. (Note: Side holes in large diameter guiding catheters have been used to alleviate catheter related partial obstruction of the coronary ostium. Side hole guiding catheters required an approximate doubling of the intracoronary (IC) adenosine dose due to loss of drug from the side holes during instillation.) Intravenous (IV) heparin 40–70 units/kg and IC nitroglycerin (100–200 μg) are given several minutes before the guidewire is advanced into the artery.

For flow velocity, the sensor tip is advanced at least 5–10 artery-diameter lengths (>2 cm) beyond the stenosis to measure velocity in a region of re-established laminar flow. Resting flow velocity data are recorded. Induction of coronary hyperemia by IC or IV adenosine is performed, continuously recording through peak hyperemic flow velocity. Coronary flow velocity reserve, CFVR is computed as maximal hyperemic to basal average peak velocity (APV). Poor Doppler signal acquisition may occur in 10–15 % of patients even within normal arteries. Like transthoracic echo Doppler studies, the operator must adjust the guidewire position (sample volume) to optimize the velocity signal [3].

For translesional pressure (FFR) measurements, the wire pressure is first matched to the guide catheter pressure in the central aortic location, and then the wire is advanced into the artery beyond the stenosis. Baseline pressure is recorded, followed by induction of coronary hyperemia with IC or IV adenosine, continuously recording both guide catheter and sensor-wire pressures. FFR is computed Pressure_distal/Pressure_aorta at maximal hyperemia. Pressure_distal is recorded from the pressure wire, Pressure_aorta is recorded from the guide catheter that delivers the pressure wire. Pressure signal artifacts may be reduced by careful attention to technique.

Stenosis severity should always be assessed using measurements obtained during maximal hyperemia. Adenosine is the most common agent for hyperemia. It has a short half-life, with a return to basal flow within 30–60 s after cessation of infusion. IV and IC adenosine are very well tolerated with ~10 % drop in mean arterial pressure but may be accompanied by short lived symptoms of dyspnea or chest burning. Although transient, AV block may rarely occur at higher IC doses in the RCA. IV adenosine uses weight-adjusted dosing (140 mcg/kg/min), and is required for the evaluation of ostial lesions or for the assessment of diffuse disease during pullback recordings. Compared to IC, IV administration has a higher incidence of side effects such as flushing, chest tightness, bronchospasm, nausea, and transient AV block or bradycardia. IC adenosine doses that produced maximal hyperemia equivalent to IV adenosine are 50–100 mcg for the right coronary artery, 100–200 mcg for the left coronary artery produces [4].

Alternative to adenosine includes Regadenson, an α2A adenosine receptor agonist that induces coronary vasodilatation and increased myocardial blood flow in a manner reportedly equivalent to adenosine with fewer adverse effects and IC nitroprusside. Regadenoson has a half-life of 2–3 min in the initial phase, 30 min in the intermediate phase and 2 h in the terminal phase. It is administered as single intravenous bolus (0.4 mg), and thus may be easier to use, but its cost and prolonged effect may complicate the measurement of multiple lesions or arteries [5].

IC nitroprusside can be an alternative to IC adenosine. Serial doses of IC nitroprusside (boluses of 0.3, 0.6, and 0.9 mcg/kg) [6] produced equivalent coronary hyperemia with a longer duration (about 25 %) compared with IC adenosine. IC nitroprusside (0.9 mcg/kg) decreased systolic blood pressure by 20 % with minimal change in heart rate, whereas IC adenosine had no effect on these parameters. IC nitroprusside, in doses commonly used for the treatment of the no-reflow phenomenon, can produce coronary hyperemia suitable to measure FFR without detrimental systemic hemodynamics.

A summary of pharmacologic hyperemic agents for cath lab measurements is provided in Table 29.2.