Medical Grand Rounds

PCI for stable angina: A missed opportunity for shared decision-making

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Percutaneous coronary intervention (PCI) continues to be frequently performed for patients with stable coronary artery disease, despite clear evidence that it provides minimal benefit over optimal medical therapy and entails small but not inconsequential risks. Many patients and doctors do not fully understand the risks and benefits of PCI, even when presented with the evidence, and this makes informed consent challenging. The best approach is shared decision-making, with doctor and patient together choosing the best treatment option after considering the evidence and the patient’s preferences.


  • For patients with stable angina pectoris, PCI does not prevent myocardial infarction or death.
  • Optimal medical therapy with aspirin and a statin can reduce the risk of myocardial infarction and should be recommended for all patients with stable angina, regardless of whether they undergo PCI.
  • PCI improves symptoms of angina faster than medical therapy alone, but more than half of patients will be free of angina in about 2 years with either option.
  • In the absence of information to the contrary, most patients and some doctors assume that PCI is life-saving and are biased towards choosing it. As a result, patients are rarely able to give true informed consent to undergo PCI.



Multiple randomized controlled trials have compared percutaneous coronary intervention (PCI) vs optimal medical therapy for patients with chronic stable angina. All have consistently shown that PCI does not reduce the risk of death or even myocardial infarction (MI) but that it may relieve angina temporarily. Nevertheless, PCI is still commonly performed for patients with stable coronary disease, often in the absence of angina, and patients mistakenly believe the procedure is life-saving. Cardiologists may not be aware of patients’ misperceptions, or worse, may encourage them. In either case, if patients do not understand the benefits of the procedure, they cannot give informed consent.

See related editorial

This article reviews the pathophysiology of coronary artery disease, evidence from clinical trials of the value of PCI for chronic stable angina, patient and physician perceptions of PCI, and ways to promote patient-centered, shared decision-making.


While climbing 4 flights of stairs, a 55-year-old man noticed tightness in his chest, which lasted for 5 minutes and resolved spontaneously. Several weeks later, when visiting his primary care physician, he mentioned the episode. He had had no symptoms in the interim, but the physician ordered an exercise stress test.

Six minutes into a standard Bruce protocol, the patient experienced the same chest tightness, accompanied by 1-mm ST-segment depressions in leads II, III, and aVF. He was then referred to a cardiologist, who recommended catheterization.

Catheterization demonstrated a 95% stenosis of the right coronary artery with nonsignificant stenoses of the left anterior descending and circumflex arteries. A drug-eluting stent was placed in the right coronary artery, with no residual stenosis.

Did this intervention likely prevent an MI and perhaps save the man’s life?


Understanding the pathogenesis of MI is critical to having realistic expectations of the benefits of stent placement.

Doctors often describe coronary atherosclerosis as a plumbing problem, where deposits of cholesterol and fat build up in arterial walls, clogging the pipes and eventually causing a heart attack. This analogy, which has been around since the 1950s, is easy to for patients to grasp and has been popularized in the press and internalized by the public—as one patient with a 95% stenosis put it, “I was 95% dead.” In that model, angioplasty and stenting can resolve the blockage and “fix” the problem, much as a plumber can clear your pipes with a Roto-Rooter.

Despite the visual appeal of this model, 1 it doesn’t accurately convey what we know about the pathophysiology of coronary artery disease. Instead of a gradual buildup of fatty deposits, low-density lipoprotein cholesterol particles infiltrate arterial walls and trigger an inflammatory reaction as they are engulfed by macrophages, leading to a cascade of cytokines and recruitment of more inflammatory cells. 2 This immune response can eventually cause the rupture of the plaque’s fibrous cap, triggering thrombosis and infarction, often at a site of insignificant stenosis.

In this new model, coronary artery disease is primarily a problem of inflammation distributed throughout the vasculature, rather than a mechanical problem localized to the site of a significant stenosis.


Next Article:

Having the COURAGE to include PCI in shared decision-making for stable angina

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