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Hochman J.S., et al. "Coronary Intervention for Persistent Occlusion after Myocardial Infarction". The New England Journal of Medicine. 2006. 355(23):2395-2407.
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Clinical Question

Among stable, high risk patients presenting with subacute myocardial infarction (3-28 days prior) with poor or absent flow of the affected artery, does late PCI+optimal medical therapy reduce mortality, MI, or NYHA class IV HF symptoms when compared to optimal medical therapy?

Bottom Line

Among stable, high risk patients presenting with subacute myocardial infarction (3-28 days prior) with poor or absent flow of the affected artery, late PCI+optimal medical does not reduce mortality, MI, or NYHA class IV HF symptoms when compared to optimal medical therapy alone

Major Points

The open artery hypothesis suggests reperfusion of the infarct-related artery salvages myocardium and preserves LV function, thereby increasing survival[1]. Early reperfusion in the setting of acute MI is proven to improve mortality as shown in ISIS-2 (1988), GUSTO (1993), and numerous other trials. However, some patients present outside the acute window of intervention or otherwise fail to meet indications for thrombolysis and have persistently occluded coronary arteries. Prior to this trial, several observational studies suggested a mortality benefit with late reperfusion as a result of reduced infarct expansion and LV remodeling. PCI, the current gold standard for establishing reperfusion, can lead to harmful periprocedural complications including perforations, distal embolization, and MI. Given the paucity of data to guide management, the Occluded Artery Trial (OAT) enrolled patients with recent MI (3-28 days prior) to test the hypothesis that a strategy of late PCI would provide a mortality benefit in patients presenting late after a STEMI.

Published in 2006, OAT randomized 2,166 stable patients with MI and delayed presentation to undergo PCI+optimal medical therapy (OMT) or receive OMT alone. With a mean follow-up of 2.9 years, there was no significant difference in the primary outcome (composite of all-cause mortality, myocardial reinfarction, or NYHA class IV HF) between the PCI+OMT and OMT groups (17.2% vs. 15.6%, P=0.20 [CI 0.92-1.45]). A subgroup analysis suggests that PCI+OMT may benefit those age >65.

It is important to note that drug eluting stents (DES) were not approved until later years of recruitment and consequently, only 8% of patients in the PCI arm received DES. Patients in the PCI arm suffered from significantly lower levels of angina at 1 year but this difference was not significant at 3 years. The results of this particular study suggest that PCI in the context of subacute MI does not improve mortality, similar to the subsequent finding in COURAGE (2007) that compared PCI vs. OMT in stable CAD.


ACCF/AHA STEMI Guidelines (2013, adapted)[2]

  • Delayed PCI >24 hours after STEMI:
    • May be considered as part of an invasive strategy in stable patients if there is a significant stenosis in a patient infarct artery (class IIb, level B)
    • Should not be performed in asymptomatic, hemodynamically and electrically stable patients with 1- or 2-vessel disease without evidence of severe ischemia if there is an occluded infarct artery (class III, level B)


  • Multinational, multicenter, randomized controlled trial
  • N=2,166 patients 3-28 days post MI with total occlusion of the infarct related artery
    • PCI+OMT (n=1,082)
    • OMT (n=1,084)
  • Setting: Numerous centers in 25 countries
  • Enrollment: 1998-2005
  • Mean follow-up: 2.9 years
  • Analysis: Intention-to-treat
  • Primary outcome: All-cause mortality, nonfatal MI, or NYHA class IV HF


Defined in depth elswhere.[3]

Inclusion Criteria

  • Recent MI (3-28 days), defined by at least 2 of A, B, or C or B and D:
    • A. Symptoms of ischemia for ≥30 min
    • B. Elevated cardiac markers (eg, troponin)
    • C. New Q waves in >2 related leads
    • D. ST elevation or depression, new LBBB, loss of R-wave voltage, TWI in ≥2 leads
  • TIMI flow 0 or 1 in infarct-related artery (IRA) or arteries
  • High risk by any of the following:
    • EF <50% or proximal occlusion
    • LAD proximal to the second major diagonal branch
    • Large right coronary artery
    • Circumflex, if supplying large obtuse marginal and part of inferior wall (i.e., large dominant or co-dominant vessel)

Exclusion Criteria

  • Age <18 y or pregnancy
  • Clinical indication for revascularization
  • Serious illness limiting 3-year survival
  • Severe CKD (creatinine >3.0 mg/dL)
  • Severe valvular disease
  • History of anaphylaxis to radiographic contrast
  • Infarct artery too small, lesion beyond extreme tortuosity, or a poor candidate for PCI
  • Chronic occlusion of IRA
  • NYHA classes III-IV HF (patients may be treated for acute heart failure complicating MI and rescreened)
  • Cardiogenic shock or sustained hypotension (SBP <90 mm Hg or CI <2.2 L/min per m2)
  • LV aneurysm in the same location as index MI and present before index MI
  • Contraindication to anticoagulation or antiplatelets
  • Qualifying IRA that has been grafted previously; patients with prior CABG may be enrolled if the IRA was not previously grafted
  • Dilated or hypertrophic cardiomyopathy

Baseline Characteristics

From the PCI Group.

  • Demographics: Age 59 years, male 78%, White race 81%
  • PMH: CVA 4%, PVD 4%, diabetes 18% (on insulin 6%), smoker 39%, angina 22%, MI 12%, HF 2%, PCI 5%, CABG 0.5%, HTN 48%
  • NYHA at randomization: I 83%, II 17%
  • EKG characteristics: New Q waves 67%, ST-segment elevation 68%, ST-segment elevation or Q-wave or R wave loss 87%
  • GFR: 80.8
  • Thrombolytic therapy during first 24hrs after onset of index MI 21%
  • Interval between MI and randomization: 8 days
  • Stress test performed: 27%
  • Ischemia in infarct related artery territory: Severe 0%, Moderate 9%, Mild 34%, None 57%
  • Angiographic details
    • Location: LAD 25%, Left circumflex 16%, RCA 49%
    • TIMI flow grade in infarct-related artery: 0 83%, 1 17%, 3 0.5%, 3 0.2%
    • Collateral vessels present: 87%
    • Multivessel disease: 18%
    • Ejection fraction: Mean 47%


  • Randomization to a group:
    • PCI+OMT: PCI in <24 hours
    • OMT
  • All patients received aspirin, beta blockers, ACE/ARBs, lipid lowering agents as part of OMT
    • After prolonged thienopyridines were reported to be beneficial post-MI, all patients were recommended to be on one of these medications (e.g., clopidogrel) for 1 year


Comparisons are PCI+OMT vs. OMT alone. Except where specified, the centrally-adjudicated (not site-determined) outcomes are presented. Percentages are the estimated 4-year cumulative event rate.

Primary Outcomes

All-cause mortality, nonfatal MI, or NYHA class IV HF
17.2% vs. 15.6% (HR 1.16; 95% CI 0.92-1.45; P=0.20)

Secondary Outcomes

All-cause mortality
9.1% vs. 9.4% (HR 1.03; 95% CI 0.77-1.40, P=0.83)
Fatal and nonfatal reinfarction
7.0% vs. 5.3% (HR 1.36; 95% CI 0.92-2.00, P=0.13)
Of note, PCI+OMT had a significantly higher event rate in the site-determined analysis, which is detailed in table 3 on page 2402.
Nonfatal reinfarction
6.9% vs. 5.0% (HR 1.44; 95% CI 0.96-2.16, P=0.08)
NYHA class IV heart failure
4.4% vs. 4.5% (HR 0.98; 95% CI 0.64-1.49, P=0.92)
CV mortality
6.3% vs. 5.0% (HR 1.12; 95% CI 0.77-1.63, P=0.56)
All-cause mortality or nonfatal reinfarction
14.9% vs. 13.2% (HR 1.21; 95% CI 0.95-1.55, P=0.13)
NYHA class III or IV heart failure
5.9% vs. 6.2% (HR 0.94; 95% CI 0.65-1.34, P=0.72)
All-cause mortality, reinfarction, or NYHA class III or IV HF
18.2% vs. 16.9% (HR 1.14; 95% CI 0.92-1.42, P=0.24)
1.7% vs. 2.0% (HR 0.84; 95% CI 0.43-1.64, P=0.62)

Additional Outcomes

Site-determined PCI or CABG revascularization, excluding protocol-assigned PCI
18.4% vs. 22.0% (HR 0.81; 95% CI 0.66-0.99, P=0.03)
CABG: 4.3% vs. 4.8% (HR 0.95; 95% CI 0.61-1.48, P=0.81)
Repeated elevation of cardiac marker <48 hours after randomization
10.0% vs. 3.3% (P<0.001)
Attempted PCI in PCI+OMT group
Successful PCI: 87%
Crossover to PCI, OMT group
Before 30 days: 3%
After 30 days: 6% (not including those in the before 30 days group)
4 months: 18.7% vs. 25.0% (P<0.001)
12 months: 16.4% vs. 22.0% (P=0.002)
24 months: 13.7% vs. 17.6% (P=0.04)
36 months: 9.1% vs. 10.3% (P=0.53)

Subgroup Analysis

For the primary outcome.

≤65 years: 17.0% vs. 13.2%
>65 years: 17.8% vs. 21.3%
P-value for interaction: 0.05

There were no interactions by sex, race/ethnicity, duration since MI, infarct artery, LVEF, DM, or Killip class.

Adverse Events

PCI related complications
Death: 0.2%
MI: 0.6%
NYHA class IV HF: 0.2%
Cardiac tamponade: 0.2%
Stroke: 0.1%


  • Results are limited by the highly selected patient population which limits generalizability
  • Lower than expected HF endpoints resulted in underpowering[4] (the authors note that they were powered to 80%, though the power calculation was dedigned to have 90% power)
  • The participants had a high level of collaterals at baseline, such patients may be less likely to benefit from an intervention[5]
  • The participants may not have been high-risk enough to benefit[6]


  • Largely funded by grants from the National Heart, Lung, and Blood Institute (NHLBI)
  • Corporate funding (multiple entities) accounted for 6% of total funding

Further Reading

  1. Sadanandan S et al. The late open artery hypothesis--a decade later. Am. Heart J. 2001. 142:411-21.
  2. O'Gara PT et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013. 127:e362-425.
  3. Hochman JS et al. Design and methodology of the Occluded Artery Trial (OAT). Am. Heart J. 2005. 150:627-42.
  4. Anderson JR & Persistent coronary occlusion after myocardial infarction. N. Engl. J. Med. 2007. 356:1681; author reply 1683-4.
  5. Wong B & Persistent coronary occlusion after myocardial infarction. N. Engl. J. Med. 2007. 356:1681-2; author reply 1683-4.
  6. De Luca L & Tomai F Persistent coronary occlusion after myocardial infarction. N. Engl. J. Med. 2007. 356:1682; author reply 1683-4.