Long-Term Outcome Comparison of Coronary Angioplasty vs Standard Medical Therapy

Abstract & Commentary

Synopsis: It appears safe to conclude that patients with mild-to-moderate angina can be safely managed with continued medical therapy, but percutaneous coronary intervention is certainly indicated and appropriate if anginal symptoms are not controlled by maximum, aggressive medical management.

Source: Henderson RA, et al. J Amer Coll Cardiol. 2003;42:1161-1170.

The options for treating patients with angina pectoris include carefully regulated anti-anginal medications, percutaneous coronary intervention (PCI), or coronary artery bypass surgery (CABG). Randomized clinical trials1-3 suggest that PCI is slightly less effective at relieving angina than CABG, but neither revascularization strategy provides a prognostic advantage in the majority of patients. Several smaller trials have compared the PCI approach with the results obtained by a variety of medical treatment strategies, but most have reported only limited follow-up data.4-8

Henderson and colleagues designed the second Randomized Intervention Treatment of Angina (RITA-2) trial to compare the long-term results of percutaneous transluminal angioplasty (PTCA) vs medical therapy in 1018 patients considered suitable for either treatment. The primary trial end point was the 5-year rate of death or nonfatal myocardial infarction (MI). The initial strategy of PTCA was found not to influence the risk of death or MI but it did improve angina and exercise tolerance. Henderson et al concluded that patients with angina pectoris who were considered suitable for PTCA or medical therapy can be safely managed with continued medical therapy alone however, PTCA is appropriate if symptoms are not controlled medically.

Comment BY Harold L. Karpman, MD, FACC, FACP

The RITA-2 trial results provide the only currently available randomized evidence comparing the long-term consequences of PCI vs medical treatment in patients with angina pectoris. The extensive follow-up for a median 7-year period reported in this article clearly demonstrated that the initial policies of PTCA and medical therapy in patients considered suitable for either treatment are comparable with respect to death and nonfatal MI but that an initial policy of PTCA was associated with a lower prevalence of subsequent angina and with improved exercise tolerance. It should be clearly recognized that medical management initially consisted only of appropriate antianginal (ie, usually a beta-adrenoceptor blocker with a calcium antagonist and/or with long-acting nitrates) therapy for symptom relief. Also, it should be noted that there was a substantial initial reduction in anginal symptoms in patients randomized to PTCA compared with patients assigned medical therapy but that this treatment difference attenuated with the passage of time. The most powerful predictors of symptomatic status at 5 years were the presence of restlessness, the exercise time, and the angina grade at baseline.

The RITA-2 trial enrolled patients from 1992 through 1996, and, of course, there have been significant advances in both medical (ie, use of clopidogrel, glycoprotein IIb/IIIa receptor antagonists, etc) and interventional treatment (ie, increased use of coronary stents, availability of drug-coated stents, etc). It is therefore important to recognize the relatively limited value of the RITA-2 trial results, which deserve to be updated with new long-term studies comparing current PCI interventional therapy with modern medical treatment. However, it appears safe to conclude that patients with mild-to-moderate angina can be safely managed with continued medical therapy, but the PCI approach is certainly indicated and appropriate if anginal symptoms are not controlled by maximal, aggressive medical management. 

Dr. Karpman, Clinical Professor of Medicine, UCLA School of Medicine, is Associate Editor of Internal Medicine Alert.

References

1. Henderson RA, et al. Lancet. 1998;352:1419-1425.

2. BARI Investigators. J Am Coll Cardiol. 2000;35: 1122-1129.

3. King SB, et al. J Am Coll Cardiol. 2000;35:1116-1121.

4. Folland ED, et al. J Amer Coll Cardiol. 1997;29: 1505-1511.

5. Hartigan PM, et al. Am J Cardiol. 1998;82:1445-1450.

6. Hueb WA, et al. Circulation. 1999;100(Suppl 2): 107-113.

7. Pitt B, et al. N Engl J Med. 1999;341:70-76.

8. Dakik HA, et al. Circulation. 1998;98:2017-2023.