The headline in the New York Times summarized the initial reaction of the cardiology community – “unbelievable” – but still seemed to understate the ground-shaking implications of a recent study of coronary stenting.
The report of The Objective Randomised Blinded Investigation with Optimal Medical Therapy of Angioplasty in Stable Angina (ORBITA)Trial was published last week in the Lancet. In brief, investigators in the UK (hence “randomised”) enrolled about 200 patients with angina, objective evidence of inducible myocardial ischemia and angiographic and hemodynamic evidence of significant single vessel coronary artery disease. Half the group received a drug eluting stent, with excellent technical results. The other half got a sham angioplasty. Both groups were treated medically. The key finding: “real” stenting produced no measurable benefit in exercise time increment (the primary endpoint) compared with a “placebo procedure.” The study was well done, with true blinding of patients and evaluating physicians, careful selection of endpoints, and sufficient power to support the conclusion. Whoa.
As a cardiologist, I had no trouble believing the findings of previous well-done, placebo-controlled studies that had revealed the lack of efficacy of kyphoplasty or meniscal surgery, but this was harder to wrap my head around. It has been a core tenet of cardiology for, well, forever, that angina is a reflection of myocardial ischemia, that ischemia reflects an imbalance of myocardial oxygen supply and demand, and that a severe epicardial coronary stenosis is the archetypical substrate. If you fix the stenosis, you fix the ischemia and fix the angina. That is why PCI for symptom relief in chronic stable angina has been a Class 1 recommendation in national practice guidelines. Now, it all seems a lot more complicated, and it is far from clear what is going on here physiologically.
What is clear is that this is another huge blow to the “oculostenotic reflex” (see it, stent it) that has driven interventional cardiology for decades. Thoughtful clinicians have recognized for years that PCI in stable angina does not prevent heart attacks or forestall death, but we all thought that it at least made people feel better. Now that seems to be an illusion.
If we follow the evidence, then, as the accompanying editorial suggests, this might be “the last nail in the coffin for PCI in stable angina.” I doubt it. I bet that PCI in stable patients is far from dead. It is too much of a sacred cow (and generates too much income for hospitals and doctors) to go quietly into the night. Instead, I think this study is going to be the “opening salvo” in an intense fight over the utility of a procedure done 500,000 times a year in the US and Europe for an indication that is now very much in question.
What do you think?