NEW YORK (Reuters Health) – Among stable patients with persistent total occlusion of the infarct-related artery after myocardial infarction, those who undergo late percutaneous coronary intervention (PCI) fare no better over 5 years than those treated medically, according to a report in Circulation online October 24.
The findings come from an extension of the Occluded Artery Trial (OAT), which demonstrated that late PCI after MI did not reduce a composite of death, reinfarction or heart failure over 2.9 years of follow-up. Dr. Judith S. Hochman, at New York University School of Medicine, New York, and colleagues extended the follow-up phase for an additional 3 years to see if late trends might favor either treatment arm.
In the trial, 2201 patients with persistent infarct-related artery total occlusion were randomized 3-28 days after MI to undergo PCI or to receive optimal medical therapy. The trial excluded patients with severe inducible ischemia, rest angina, class III-IV heart failure, and 3-vessel/left main disease.
During a median follow-up of 5.8 years, death from any cause, nonfatal MI, or class IV heart failure — the composite primary outcome — occurred in 230 patients in the PCI group and 219 in the medical arm. The difference was not statistically significant with a hazard ratio of 1.04 (p=0.68), the team found.
There was less angina in the PCI group during the first year of follow-up, but thereafter there was no statistical difference between groups, the investigators report.
In the PCI group, the type of stent used made no difference, the report indicates: the 6-year event rate was 20.4% for drug-eluting stent use and 18.9% with bare metal stents (hazard ratio 1.20; p=0.53).
Based on these results, Dr. Hochman and colleagues conclude, “Robust long-term data confirm that there is no benefit on cardiovascular events associated with a routine strategy of PCI in stable patients with persistent total occlusion of the IRA (infarct-related artery), 1- or 2-vessel coronary artery disease, and the absence of severe inducible ischemia in the subacute phase after MI.”
Reference:
Circulation 2011;124.
