The late open-coronary artery hypothesis: dead, or not definitively tested?
Continued controversy surrounds the optimal therapeutic approach to the patient who does not undergo percutaneous coronary intervention (PCI) early during acute myocardial infarction, when ischemic myocardium could still be salvaged, and who presents days to weeks after the acute event with persistent total occlusion of the infarct-related coronary artery. The Occluded Artery Trial (OAT) demonstrated no measurable effect of PCI on outcome. There were trends, however, for more frequent reinfarctions and a higher estimated 4-year cumulative primary event rate. Because patient selection included only patients with 1- or 2-vessel coronary disease, and because interventionalists were permitted to perform PCI on the noninfarct-related arteries, >85% of patients in the intervention group had no coronary arteries with significant obstructions after PCI, a situation that would cause the functional regression of existing collaterals. If subsequent plaque rupture and total occlusion of any of the 3 coronary arteries occurred (expected in 5% to 15% of patients with acute coronary syndromes over the first 1 to 2 years), the impaired collateral flow immediately after new acute occlusion would predispose to greater myocardial injury and therefore greater patient risk, which could explain the negative effects of the OAT study, and which raises the disturbing possibility that complete revascularization in patients with recent acute coronary syndromes could possibly lead to greater risks in the following 1 to 2 years in those patients who experience recurrent acute coronary occlusion. Conversely, late opening of the culprit artery in patients with multivessel coronary disease, without all arteries being patent, may favorably alter late outcomes. In conclusion, the therapeutic implications of the OAT study apply to a specific patient cohort; whether late opening of the culprit artery improves or impairs outcome appears critically to depend on the specific cohort treated.
Epstein
Stephen E
SE
Pichard
Augusto D
AD
Kent
Kenneth M
KM
Satler
Lowell
L
Suddath
William O
WO
Lindsay
Joseph
J
Waksman
Ron
R
D054058:Acute Coronary Syndrome / Q000503:physiopathology; D003097:Collateral Circulation / Q000502:physiology*; D003326:Coronary Circulation / Q000502:physiology*; D006801:Humans; D009203:Myocardial Infarction / Q000503:physiopathology* / Q000628:therapy*; D011379:Prognosis; D012008:Recurrence; D013997:Time Factors; D016896:Treatment Outcome; D020257:Ventricular Remodeling / Q000502:physiology