The most award winning
healthcare information source.
TRUSTED FOR FOUR DECADES.
Is Preventative PCI Better Than Optimal Medical Therapy in Patients with Stable CHD?
Abstract & Commentary
By Harold L. Karpman, MD, Clinical Professor of Medicine, UCLA School of Medicine. Dr. Karpman reports no financial relationship to this field of study.
Synopsis: Although the addition of PCI to optimal medical therapy in patients with chronic stable CHD reduced the prevalence of angina, it did not reduce the long-term rates of death, nonfatal myocardial infarctions and hospitalizations for acute coronary syndromes and, therefore, PCI can be safely deferred in these patients, even those with extensive, multivessel involvement and inducible ischemia provided that intensive, multifaceted medical therapy is instituted and maintained.
Source: Antman EM, et al. Circulation. 2005;111:2013.
Percutaneous coronary intervention (PCI) has clearly been demonstrated to reduce the incidence of death and myocardial infarctions (MI) in patients who present with acute coronary syndromes (ACS).1-6 However, the same benefit has not been demonstrated in patients with chronic stable coronary artery heart disease (CHD)7-11 and treatment guidelines have therefore recommended intensive medical therapy as the initial therapeutic approach in the latter group of patients.7,8 Despite these facts and the treatment guideline recommendations, preventative PCI has become a common therapeutic approach as the initial management strategy for patients with chronic CAD.12-13 The numbers are enormous. For example, in 2004 in the US, more than one million coronary stent procedures were performed despite the fact that 85% of these procedures were undertaken electively in patients with stable CHD.14
Previous studies have demonstrated only that PCI decreases the frequency of angina and improves short-term exercise performance7, 8, 11 but the effects of this procedure on cardiovascular events in patients with stable CHD has remained uncertain. Boden and his associates representing the Clinical Outcomes Utilization Revascularization and Aggressive Drug Evaluation (COURAGE) trial research group designed their trial to determine whether PCI coupled with optimal medical therapy (ie, intensive medical therapy, a reduction of risk factors, and lifestyle intervention) effectively reduced the risk of death and nonfatal MIs in patients with stable CHD compared to a group of patients receiving only optimal medical therapy.15 The trial carefully studied 2287 patients from 50 US and Canadian centers who had objective evidence of myocardial ischemia and significant CHD. The primary outcomes was death from any cause and nonfatal MIs during a follow-up of 2.5 to 7.0 years. The final study results revealed that there was no significant differences between the optimal medical therapy group with or without PCI in the composite of death, MI and stroke or for hospitalization for acute coronary syndrome and/or for MI.
The important findings in the COURAGE study15 clearly demonstrate that, as the initial management strategy, PCI added to optimal medical therapy did not reduce the primary composite endpoints of death and nonfatal MI or reduce the incidence of major cardiovascular events, as compared with optimal medical therapy alone in patients with chronic stable CHD despite a high baseline prevalence of coexisting diseases, objective evidence of ischemia and/or extensive CHD as seen on angiography. These findings are almost certainly explained, at least in part, by differences in atherosclerotic plaque morphology and vascular remodeling associated with acute coronary syndromes as compared with the lesions observed in patients with chronic stable CHD. Since vulnerable plaques do not usually cause significant stenosis before rupture and secondary precipitation of an acute coronary syndrome,16 focal management of even severely stenotic coronary lesions with PCI in patients with stable CHD did not significantly reduce the rate of death and MIs presumably because the treated stenotic lesions were not likely to trigger an acute coronary event in patients with chronic stable CAD. These findings reflect the fact that unstable coronary lesions that lead to MIs are not necessarily severely stenotic and, on the other hand, severity stenotic lesions are not necessarily unstable and predictive of an impending MI. It should be noted that the results of this excellent study may have been influenced by the facts that male patients made up 85% of the study population, there was a lack of ethnic diversity, and only bare-metal stents were utilized because drug-eluting stents were not available until late into the enrollment process.
In summary, it would appear safe to conclude that, at least for male patients, optimal medical therapy can be implemented safely and is as effective as PCI with bare-metal stents in patients with stable CHD recognizing the possibility that this conclusion may not be valid when drug-eluting stents are used. Optimal medical therapy in the patients enrolled in the COURAGE trial was quite successful at achieving goals for both lipid and blood pressure levels, but patients were less successful in meeting the more difficult objectives of weight loss, smoking cessation, and increased exercise activities. Although the addition of PCI to optimal medical therapy reduced the prevalence of angina, it did not reduce the long-term rates of death, nonfatal myocardial infarctions, and hospitalizations for acute coronary syndromes.
1. Antman EM, et al. Circulation. 2005;111:2013.
2. Keeley EC, et al. Lancet. 2003; 361:13-20.
3. [No authors listed] Lancet. 1999;354:708-715.
4. Cannon CP, et al. N Engl J Med. 2001;344: 1875-1887.
5. Fox KA, et al. Lancet. 2002;360:741-751.
6. Mehta SR, et al. JAMA. 2005;293:2908-2917.
7. Parisi AF, et al. N Engl J Med. 1992;326:6-10.
8. Coronary angioplasty versus medical therapy for angina: the second randomized intervention and treatment of angina (RITA-2) trial. Lancet. 1997;350:461-468.
9. Pitt B, et al. N Engl J Med. 1999;341:70-76.
10. Hueb W, et al. J Am Coll Cardiol. 2004;43: 17431751.
11. Henderson RA, et al. J Med Coll Cardiol. 2003;42:1161-1170.
12. Gibbons RJ, et al. J Am Coll Cardiol. 2003;41:159-168.
13. Smith SC, et al. Circulation. 2006; 113:156-175.
14. Rosamond W, et al. Circulation. 2007;115(5):e69-e171.
15. Boden et al for the COURAGE trial research group. N Engl J Med. 356;15:1503-1516.
16. Naghavi M, et al. Circulation. 2003;108:1664-1672