# Coronary Physiology and FFR > Coronary physiology for NEET-SS Cardiology: FFR 0.80 cut-off, iFR 0.89, FAME trials, coronary flow reserve, microvascular disease and IMR. - Canonical URL: https://prepelephant.com/topics/neet-ss/cardiology/coronary-physiology-ffr - Exam / course: NEET-SS · Subject: Cardiology - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Coronary Physiology and FFR", PrepElephant, https://prepelephant.com/topics/neet-ss/cardiology/coronary-physiology-ffr ## Direct answer A 60 per cent mid-LAD stenosis on angiography answers nothing by itself — luminography cannot tell you whether a lesion limits flow. Fractional flow reserve (FFR) does: it is the ratio of maximal achievable flow through a stenotic artery to the flow if the artery were normal, derived from the distal-to-aortic pressure ratio during maximal hyperaemia, with a cut-off of 0.80 or below signalling a lesion worth stenting. The wire-free resting analogue, instantaneous wave-free ratio (iFR), uses 0.89 and was non-inferior to FFR in DEFINE-FLAIR and iFR-SWEDEHEART. When both are normal yet the patient has angina, the problem may be the microcirculation — coronary flow reserve (CFR) below 2.0 or an index of microcirculatory resistance (IMR) above 25. ## What you must remember - **FFR formula and cut-off:** distal coronary pressure divided by aortic pressure at maximal hyperaemia (adenosine 140 micrograms/kg/min); FFR at or below 0.80 justifies PCI, above 0.80 favours deferral with excellent outcomes. - **FAME trial (2009):** FFR-guided PCI cut major adverse events from about 29 to 18 per cent at one year versus angiography-guided PCI; FAME 2 showed FFR-guided PCI plus medical therapy reduces urgent revascularisation compared with medicine alone. - **iFR cut-off 0.89:** no adenosine needed; DEFINE-FLAIR and iFR-SWEDEHEART established non-inferiority to FFR with less procedural discomfort. - **Microvascular disease (INOCA):** angina with unobstructed arteries — CFR below 2.0, IMR above 25; diagnose with thermodilution or Doppler wire, and consider acetylcholine testing for vasospasm. - **Where FFR is unreliable:** acute myocardial infarction (microvascular injury distorts hyperaemia), severe aortic stenosis, and severe left ventricular hypertrophy. - **Hyperaemic agents:** intravenous adenosine remains the reference; intracoronary adenosine or regadenoson are practical alternatives. - **Deferred lesions behave:** an intermediate stenosis with FFR above 0.80 carries a low annual event rate when left alone — deferral is a decision, not neglect. ## Approach to an intermediate stenosis, step by step Take the common scenario: a 58-year-old with exertional angina, angiography showing a haziness in the mid-LAD measured at 55 per cent, and an operator reaching for a stent. The disciplined sequence is different. First, ask whether any non-invasive ischaemia data exist — a stress test with a matching anterior defect already answers the question. If not, cross the lesion with a pressure wire and record resting iFR; if the value is 0.90 or higher with concordant FFR, defer. If iFR is borderline, induce hyperaemia and read the FFR, then perform a slow pullback to map exactly where the pressure drops — a focal drop localises the culprit, a diffuse gradual fall suggests vessel-wide disease that stenting cannot fix. When the epicardial arteries are genuinely unobstructed but the patient still has typical angina, move to the microcirculation: CFR and IMR on the same wire, plus acetylcholine provocation for spasm. This is how "normal angiogram, real disease" patients — disproportionately women — get a diagnosis instead of a discharge letter saying "no blockage". ## Where students slip The commonest error is treating FFR as a measure of anatomy; it is a measure of flow reserve, which is why a mildly irregular 40 per cent vessel in a hypertensive diabetic can produce disabling angina with a normal FFR — the microcirculation is the culprit, and a stent will not help. The second slip is quoting FFR in settings where it is unvalidated: never lean on FFR in the infarct-related artery during primary PCI, and be cautious in severe aortic stenosis, where the valve should usually be addressed first. Finally, candidates mix up CFR and FFR under viva pressure — remember the shorthand "FFR for the pipe, CFR for the plumbing": epicardial stenosis versus the whole system including microvessels. ## Frequently asked questions ### What FFR value mandates treatment of a stenosis? FFR of 0.80 or below at maximal hyperaemia identifies a flow-limiting lesion for PCI; values above 0.80 are deferred with favourable outcomes. ### How does iFR differ from FFR? iFR is measured at rest during the diastolic wave-free period without adenosine, uses a 0.89 cut-off, and was non-inferior to FFR in DEFINE-FLAIR and iFR-SWEDEHEART. ### What defines coronary microvascular dysfunction? Angina with unobstructed epicardial arteries plus impaired coronary flow reserve (below 2.0) or raised IMR (above 25), often with positive acetylcholine testing for spasm. ### Why is FFR unreliable after acute myocardial infarction? Microvascular injury in the infarct bed blunts maximal hyperaemia and falsely elevates FFR, so measurements in the culprit vessel soon after STEMI do not reflect true stenosis significance. ### What did the FAME trials change in practice? FAME showed FFR-guided PCI reduces adverse events versus angiography-guided PCI, and FAME 2 showed it reduces urgent revascularisation versus medical therapy alone, cementing physiology-guided decisions.