What are the ACCF/AHA guidelines for use of percutaneous coronary intervention (PCI) in the treatment of STEMI?

Answer

The salient recommendations from the 2013 update of the ACCF/AHA STEMI guidelines, which were written in collaboration with the PCI guideline writing group, are as follows^[2]:

Emergency medical services should transport patients directly to a PCI-capable hospital for primary PCI, with an ideal goal of a first medical contact (FMC)-to-device time of 90 minutes or less
Non–PCI-capable hospitals should immediately transfer patients to a PCI-capable hospital, with an FMC-to-device goal of 120 minutes or less; the concept of door-in-door-out time is discussed, and whereas no specific time frame is set, it is emphasized that a time of ≤30 minutes (associated with lower in-hospital mortality), is achieved in only 11% of patients; factors to improve (shorten) treatment time for PCI-treated patients include use of prehospital electrocardiography (ECG) to diagnose STEMI, emergency physician activation of the PCI team, use of a central paging system to activate the PCI team, and establishing a goal of having the PCI team arrive in the catheterization laboratory within 20 minutes of being paged
Primary PCI is indicated (class I) in patients with ischemic symptoms < 12 hours and contraindications to thrombolytic therapy (irrespective of the time delay from FMC), patients with cardiogenic shock, and patients with acute severe heart failure (irrespective of the time delay from MI onset); primary PCI is reasonable (class IIa) in patients with ongoing ischemia 12-24 hours after symptom onset

When thrombolytic therapy is used as the primary reperfusion strategy in a non–PCI-capable facility, the goal remains administration of such therapy within 30 minutes of hospital arrival. Whereas a great deal of research has been devoted to comparing primary PCI, facilitated PCI, and thrombolytic strategies, the guidelines emphasize that “the appropriate and timely use of some form of reperfusion therapy is likely more important than the choice of therapy.”

The use of thrombolytic therapy followed by referral for intentional PCI (facilitated PCI) has not been shown to be superior to primary PCI and may actually worsen outcomes, with increased risk of stroke and bleeding (ASSENT 4). However, urgent transfer to a PCI-capable hospital for coronary angiography and possible “rescue PCI” is reasonable for STEMI patients with failed reperfusion or reocclusion after thrombolytic therapy.^[2]Indeed, the term facilitated PCI is now considered obsolete.

The recommended strategy for thrombolysis is a full dose of a thrombolytic, aspirin, clopidogrel, and immediate transfer to a PCI-capable facility.

On the basis of the OAT (Occluded Artery Trial) data, delayed PCI of a totally occluded infarct artery more than 24 hours after STEMI should generally not be performed in most asymptomatic patients.^[53]

PCI of a noninfarct artery at the time of PCI in patients without hemodynamic compromise is classified as a “class III – harm” recommendation and should not be performed.

Trials are planned that will assess the risks and benefits of complete revascularization at the time of STEMI. The treatment of non–infarct-related artery in STEMI and cardiogenic shock remains a controversial area, with some evidence of benefit for revascularization.^[54]

Current STEMI guidelines recommend the use of a GPIIb/IIIa inhibitor (class IIa abciximab, tirofiban or eptifibatide) at the time of primary PCI in selected patients who are receiving unfractionated heparin (those who have a large thrombus burden or inadequate P2Y12 receptor antagonist loading). Routine use of GPIIb/IIIa inhibitors with bivalirudin is not recommended and may be considered as an adjunctive or “bailout” strategy in selected cases.

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Media Gallery

Percutaneous transluminal coronary angioplasty (PTCA). Rotational atherectomy catheter (Rotablator) is designed for removal of plaque from coronary arteries. This device has diamond-studded burr at its tip, rotates at about 160,000 rpm, and is particularly well suited for ablation of calcific or fibrotic plaque material.
Percutaneous transluminal coronary angioplasty (PTCA). TRISTAR stent.
Percutaneous transluminal coronary angioplasty (PTCA). NIR stent.
Percutaneous transluminal coronary angioplasty (PTCA). Wallstent.
Example of intravascular ultrasonography (IVUS) image in percutaneous transluminal coronary angioplasty (PTCA).
Mechanism of restenosis following percutaneous transluminal coronary angioplasty (PTCA).
Fractional flow ratio (FFR). Pressure wire is advanced across left anterior descending (LAD) artery stenosis, and intracoronary adenosine is given. FFR ratio is recorded at baseline and then after adenosine push is given. Here, LAD lesion and FFR post adenosine are shown.

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Author

George A Stouffer, III, MD Ernest and Hazel Craige Distinguished Professor of Medicine and Cardiology, Chief of Cardiology, University of North Carolina Medical Center

George A Stouffer, III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Coauthor(s)

Pradeep K Yadav, MD Interventional Cardiology Fellow, Department of Cardiology, University of North Carolina at Chapel Hill School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Karlheinz Peter, MD, PhD Professor of Medicine, Monash University; Head of Centre of Thrombosis and Myocardial Infarction, Head of Division of Atherothrombosis and Vascular Biology, Associate Director, Baker Heart Research Institute; Interventional Cardiologist, The Alfred Hospital, Australia

Karlheinz Peter, MD, PhD is a member of the following medical societies: American Heart Association, German Cardiac Society, Cardiac Society of Australia and New Zealand

Disclosure: Nothing to disclose.

Additional Contributors

Josh W Todd, MD Interventional Cardiologist, Knoxville Heart Group

Josh W Todd, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Mian Atif Yousuf, MD Interventional Cardiology Fellow, Department of Cardiology, University of North Carolina at Chapel Hill School of Medicine

Mian Atif Yousuf, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Acknowledgements

Jeb Burchenal, MD Assistant Professor of Medicine, University of Colorado School of Medicine; Consulting Staff, South Denver Cardiology Associates

Jeb Burchenal, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Jorge Davalos, MD Interventional Cardiology Fellow, University of North Carolina at Chapel Hill

Jorge Davalos, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Medical Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Robert Vincent Kelly, MD Consulting Staff, Division of Interventional Cardiology, University of North Carolina Hospital

Disclosure: Nothing to disclose.

James Maddux, MD Consulting Staff, Department of Cardiology, International Heart Institute

James Maddux, MD is a member of the following medical societies: American Medical Association and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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