Is "if it's blocked, open it" correct?

A coronary artery is narrowed. There's evidence of ischaemia. So you open it — this reasoning is intuitive, and it's the everyday logic of the cath lab. But over the past 20 years, this reasoning has been tested repeatedly, and each time its scope has been narrowed.

What was refuted was not that "revascularisation is meaningless." Rather, trial after trial has dissected exactly which scenarios it works in, and for what purpose. For prognosis, or for symptoms? Stable coronary artery disease, or acute coronary syndrome? Left main, or single-vessel? For low ejection fraction, PCI or CABG?

We trace four stages from COURAGE to ISCHEMIA-CKD. At the end, we lay out the scenarios where revascularisation is still needed.

Act I: COURAGE — prognosis didn't change

The 2007 COURAGE trial randomised patients with stable coronary artery disease and objective evidence of ischaemia to PCI plus optimal medical therapy (OMT) versus OMT alone. The primary endpoint (death from any cause plus non-fatal myocardial infarction) was 19.0% vs 18.5%, HR 1.05 (P=0.62). No difference.

Angina symptoms improved with PCI in the first 1–2 years, but by 3 years the difference had narrowed. From here begins the trend of "medical therapy first in stable CAD."

Around the same time, DEFER showed the same thing from a different angle. Even with moderate stenosis on angiography, if FFR≥0.75 (not functionally significant), stenting could be deferred. At 5 years, cardiac death/MI was 3.3% in the Defer group vs 7.9% in the Perform group, versus 15.7% in the reference group (FFR<0.75). Cardiac death/MI related to deferred lesions occurred at under 1% per year, and stenting did not reduce it further. At 15-year follow-up, MI was actually lower in the Defer group (2.2% vs 10.0%).

In other words, from an early stage it was already known that "narrow on angiography" and "should be treated" are separate questions.

Act II: the FFR rescue — "if the lesion causes ischaemia, it works"

The rebuttal to COURAGE was straightforward. Wasn't the lesion selection at fault? Because every angiographically narrow-looking lesion was treated, no difference emerged — treat only the lesions that truly cause ischaemia, and surely it would work.

FAME (2009) tested this. In 1,005 patients with multivessel disease, FFR-guided PCI (stenting only lesions with FFR≤0.80) was compared with angiography-guided PCI (stenting all lesions ≥50%). The 1-year primary composite was 13.2% vs 18.3% (P=0.02), favouring FFR, and death/MI also fell, 7.3% vs 11.1%. Stent number, contrast use, and cost all decreased.

FAME 2 (2012) pushed further. In stable CAD patients with lesions of FFR≤0.80, FFR-guided PCI plus medical therapy was compared with medical therapy alone. The primary composite was 4.3% vs 12.7% (HR 0.32), favouring PCI, and the trial was stopped early at approximately 7 months on the DSMB's recommendation.

But looking at the breakdown, the difference was driven mainly by a reduction in urgent revascularisation. There was no difference in mortality. Misread this point, and FAME 2 becomes the story that "PCI for ischaemic lesions saves lives."

Act III: ORBITA — even symptoms were called into question

If there's no difference in prognosis, surely it at least helps symptoms — that's what everyone in the cath lab believed.

The 2017 ORBITA trial compared PCI against a sham procedure in a double-blind design for stable angina. All patients underwent cardiac catheterisation, but only one group received a stent. The increase in exercise time, the primary endpoint, showed no significant difference between PCI and placebo (between-group difference 16.6 seconds, P=0.2).

This result sparked fierce controversy. Criticisms included the small sample size and the short 6-week follow-up. But the premise that "symptomatic improvement cannot be explained by placebo effect" was, for the first time, experimentally shaken.

The 2023 ORBITA-2 trial complements this. In 301 patients with stable angina, objective ischaemia, and near-zero use of antianginal medication, PCI was compared against a placebo procedure in a double-blind design. The primary endpoint, angina symptom score, was 2.9 for PCI vs 5.6 for placebo (OR 2.21, 95%CI 1.41–3.47, P<0.001). Exercise time also increased (700.9 vs 641.4 seconds).

Put the two together and a picture emerges. Adding PCI on top of optimised medical therapy makes any incremental symptomatic benefit hard to detect. But PCI performed without background medication genuinely improves symptoms. It's neither "PCI doesn't work" nor "it works" — the answer changes depending on what it's compared against.