Medical Grand Rounds

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

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ABSTRACT

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.

KEY POINTS

  • 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.


 

References

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.

CLINICAL CASE: EXERTIONAL ANGINA

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?

HOW MYOCARDIAL INFARCTION HAPPENS

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.

Significant stenosis does not equal unstable plaque

Not all plaques are equally likely to rupture. Stable plaques tend to be long-standing and calcified, with a thick fibrous cap. A stable plaque causing a 95% stenosis may cause symptoms with exertion, but it is unlikely to cause infarction.3 Conversely, rupture-prone plaques may cause little stenosis, but a large and dangerous plaque may be lurking beneath the thin fibrous cap.

Relying on angiography can be misleading. Treating all significant stenoses improves blood flow, but does not reduce the risk of infarction, because infarction most often occurs in areas where the lumen is not obstructed. A plaque causing only 30% stenosis can suddenly rupture, causing thrombosis and complete occlusion.

The current model explains why PCI is no better than optimal medical therapy (ie, risk factor modification, antiplatelet therapy with aspirin, and a statin). Diet, exercise, smoking cessation, and statins target inflammatory processes and lower low-density lipoprotein cholesterol levels, while aspirin prevents platelet aggregation, among other likely actions.

The model also explains why coronary artery bypass grafting reduces the risk of MI and death in patients with left main or 3-vessel disease. A patient with generalized coronary artery disease has multiple lesions, many of which do not cause significant stenoses. PCI corrects only a single stenosis, whereas coronary artery bypass grafting circumvents all the vulnerable plaques in a vessel.

THE LANDMARK COURAGE TRIAL

Published in 2007, the Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial4 randomized more than 2,000 patients to receive either optimal medical therapy plus PCI or optimal medical therapy alone. The primary outcome was a composite of death from any cause and nonfatal MI. Patients were followed for at least 3 years, and some for as long as 7 years.

There was an initial small upward spike in the primary outcome in the PCI arm due to periprocedural events. By 5 years, the outcomes of the 2 arms converged and then stayed the same for up to 15 years.5 The authors concluded that PCI conferred no benefit over optimal medical therapy in the risk of death or MI.

Some doctors dismiss the study because of its stringent entry criteria—of 35,539 patients assessed, only 3,071 met the eligibility criteria. However, the entry criteria were meant to identify patients most likely to benefit from PCI. Many patients who undergo PCI today would not have qualified for the study because they lack objective evidence of ischemia.6 To enroll, patients needed a proximal stenosis of at least 70% and objective evidence of ischemia or a coronary stenosis of more than 80% and classic angina. Exclusion criteria disqualified few patients: Canadian Cardiovascular Society class IV angina (ie, angina evoked from minimal activity or at rest); a markedly positive stress test (substantial ST-segment depression or hypotension during stage I of the Bruce protocol); refractory heart failure or cardiogenic shock; an ejection fraction of less than 30%; revascularization within the past 6 months; and coronary anatomy unsuitable for PCI.

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

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