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(Circulation. 2008;117:261-295.)
© 2008 American Heart Association, Inc.

PCI Focused Update

2007 Focused Update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention

A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: 2007 Writing Group to Review New Evidence and Update the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention, Writing on Behalf of the 2005 Writing Committee

Spencer B. King, III, MD, MACC, FAHA, FSCAI, Co-Chair^*,; Sidney C. Smith, Jr, MD, FACC, FAHA, Co-Chair^*,; John W. Hirshfeld, Jr, MD, FACC, FAHA, FSCAI; Alice K. Jacobs, MD, FACC, FAHA, FSCAI; Douglass A. Morrison, MD, PhD, FACC, FSCAI; David O. Williams, MD, FACC, FAHA, FSCAI; 2005 WRITING COMMITTEE MEMBERS; Sidney C. Smith, Jr, MD, FACC, FAHA, Chair; Ted E. Feldman, MD, FACC, FSCAI; John W. Hirshfeld, Jr, MD, FACC, FAHA, FSCAI; Alice K. Jacobs, MD, FACC, FAHA, FSCAI; Morton J. Kern, MD, FACC, FAHA, FSCAI; Spencer B. King, III, MD, MACC, FSCAI; Douglass A. Morrison, MD, PhD, FACC, FSCAI; William W. O’Neill, MD, FACC, FSCAI; Hartzell V. Schaff, MD, FACC, FAHA; Patrick L. Whitlow, MD, FACC, FAHA; David O. Williams, MD, FACC, FAHA, FSCAI; TASK FORCE MEMBERS: Sidney C. Smith, Jr, MD, FACC, FAHA, Chair; Alice K. Jacobs, MD, FACC, FAHA, Vice-Chair; Cynthia D. Adams, MSN, PhD, FAHA^||; Jeffrey L. Anderson, MD, FACC, FAHA^||; Christopher E. Buller, MD, FACC; Mark A. Creager, MD, FACC, FAHA; Steven M. Ettinger, MD, FACC; Jonathan L. Halperin, MD, FACC, FAHA^||; Sharon A. Hunt, MD, FACC, FAHA^||; Harlan M. Krumholz, MD, FACC, FAHA; Frederick G. Kushner, MD, FACC, FAHA; Bruce W. Lytle, MD, FACC, FAHA; Rick Nishimura, MD, FACC, FAHA; Richard L. Page, MD, FACC, FAHA; Barbara Riegel, DNSc, RN, FAHA^||; Lynn G. Tarkington, RN; Clyde W. Yancy, MD, FACC

	Introduction

Top Introduction Preamble 1. Introduction 2. Patients With Unstable... 3. Facilitated PCI 4. Rescue PCI 5. PCI After Fibrinolysis... 6. Ancillary Therapy for... 7. Antiplatelet Therapy 8. Bare-Metal and Drug-Eluting... 9. Secondary Prevention Staff References

 

Preamble...262

1. Introduction...264

   1.1. Evidence Review...264

   1.2. Organization of Committee and Relationships With Industry...264

   1.3. Review and Approval...264

2. Patients With Unstable Angina/ Non–ST-Elevation Myocardial Infarction...264

   2.1. Electrocardiogram...268

      2.1.1. Comparison of Early Invasive and Initial Conservative Strategies for UA/NSTEMI...269

      2.1.2. Selection for Coronary Angiography...271

      2.1.3. Chronic Kidney Disease...272

3. Facilitated PCI...273

4. Rescue PCI...275

5. PCI After Fibrinolysis or for Patients Not Undergoing Primary Reperfusion...277

6. Ancillary Therapy for Patients Undergoing PCI for STEMI...278

7. Antiplatelet Therapy...278

8. Bare-Metal and Drug-Eluting Stents...281

   8.1. Selection of a Bare-Metal or Drug-Eluting Stent...281

9. Secondary Prevention...283

References...288

Appendix 1...293

Appendix 2...293

	Preamble

Top Introduction Preamble 1. Introduction 2. Patients With Unstable... 3. Facilitated PCI 4. Rescue PCI 5. PCI After Fibrinolysis... 6. Ancillary Therapy for... 7. Antiplatelet Therapy 8. Bare-Metal and Drug-Eluting... 9. Secondary Prevention Staff References

 
A primary challenge in the development of clinical practice guidelines is keeping pace with the stream of new data upon which recommendations are based. In an effort to respond more quickly to new evidence, the American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines has created a new "focused update" process to revise the existing guideline recommendations that are affected by evolving data or opinion. Before the initiation of this focused approach, periodic updates and revisions of existing guidelines required up to 3 years to complete. Now, however, new evidence will be reviewed in an ongoing fashion to more efficiently respond to important science and treatment trends that could have a major impact on patient outcomes and quality of care. Evidence will be reviewed at least twice a year, and updates will be initiated on an as needed basis as quickly as possible while maintaining the rigorous methodology that the ACC and AHA have developed during their more than 20 years of partnership.

These updated guideline recommendations reflect a consensus of expert opinion following a thorough review primarily of late-breaking clinical trials identified through a broad-based vetting process as important to the relevant patient population and of other new data deemed to have an impact on patient care (see Section 1.1 for details regarding this focused update). It is important to note that this focused update is not intended to represent an update based on a full literature review from the date of the previous guideline publication. Specific criteria/considerations for inclusion of new data include:

• Publication in a peer-reviewed journal
  
• Large, randomized, placebo-controlled trial(s)
  
• Nonrandomized data deemed important on the basis of results that impact current safety and efficacy assumptions
  
• Strengths/weakness of research methodology and findings
  
• Likelihood of additional studies influencing current findings
  
• Impact on current performance measure(s) and/or likelihood of the need to develop new performance measure(s)
  
• Requests and requirements for review and update from the practice community, key stakeholders, regulatory agencies, and other sources free of relationships with industry or other potential bias
  
• Number of previous trials showing consistent results
  
• Need for consistency with other new guidelines or guideline revisions
  

In analyzing the data and developing updated recommendations and supporting text, the focused update writing group used evidence-based methodologies developed by the ACC/AHA Task Force on Practice Guidelines, which are described elsewhere.^1,2

The schema for class of recommendation and level of evidence is summarized in Table 1, which also illustrates how the grading system provides estimates of the size of the treatment effect and the certainty of the treatment effect. Note that a recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in guidelines do not lend themselves to clinical trials. Although randomized trials may not be available, there may be a very clear clinical consensus that a particular test or therapy is useful and effective. Both the class of recommendation and level of evidence listed in the focused updates are based on consideration of the evidence reviewed in previous iterations of the guidelines as well as the focused update. Of note, the implications of older studies that have informed recommendations but have not been repeated in contemporary settings are carefully considered.

View larger version (70K): [in this window] [in a new window]   Table 1. Applying Classification of Recommendations and Level of Evidence *Data available from clinical trials or registries about the usefulness/efficacy in different subpopulations, such as gender, age, history of diabetes, history of prior myocardial infarction, history of heart failure, and prior aspirin use. A recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in the guidelines do not lend themselves to clinical trials. Even though randomized trials are not available, there may be a very clear clinical consensus that a particular test or therapy is useful or effective. In 2003, the ACC/AHA Task Force on Practice Guidelines developed a list of suggested phrases to use when writing recommendations. All guideline recommendations have been written in full sentences that express a complete thought, such that a recommendation, even if separated and presented apart from the rest of the document (including headings above sets of recommendations), would still convey the full intent of the recommendation. It is hoped that this will increase readers’ comprehension of the guidelines and will allow queries at the individual recommendation level.

The ACC/AHA practice guidelines address patient populations (and health care providers) residing in North America. As such, drugs that are not currently available in North America are discussed in the text without a specific class of recommendation. For studies performed in large numbers of subjects outside of North America, each writing committee reviews the potential impact of different practice patterns and patient populations on the treatment effect and on the relevance to the ACC/AHA target population to determine whether the findings should form the basis of a specific recommendation.

The ACC/AHA practice guidelines are intended to assist health care providers in clinical decision making by describing a range of generally acceptable approaches for the diagnosis, management, and prevention of specific diseases or conditions. The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment regarding care of a particular patient must be made by the health care provider and patient in light of all the circumstances presented by that patient. Thus, there are circumstances in which deviations from these guidelines may be appropriate. Clinical decision making should consider the quality and availability of expertise in the area where care is provided. These guidelines may be used as the basis for regulatory or payer decisions, but the ultimate goal is quality of care and serving the patient’s best interests.

Prescribed courses of treatment in accordance with these recommendations are only effective if they are followed by the patient. Because lack of patient adherence may adversely affect treatment outcomes, health care providers should make every effort to engage the patient in active participation with prescribed treatment.

The ACC/AHA Task Force on Practice Guidelines makes every effort to avoid any actual, potential, or perceived conflict of interest arising from industry relationships or personal interests of a writing committee member. All writing committee members and peer reviewers were required to provide disclosure statements of all such relationships pertaining to the trials and other evidence under consideration (see Appendixes 1 and 2). Final recommendations were balloted to all writing committee members. Writing committee members with significant (greater than $10 000) relevant relationships with industry (RWI) were required to recuse themselves from voting on that recommendation. Writing committee members who did not participate are not listed as authors of this focused update.

With the exception of the recommendations presented in this statement, the full guidelines remain current. Only the recommendations from the affected section(s) of the full guidelines are included in this focused update. For easy reference, all recommendations from any section of guidelines impacted by a change are presented with a notation as to whether they remain current, are new, or have been modified. When evidence impacts recommendations in more than 1 set of guidelines, those guidelines are updated concurrently.

The recommendations in this focused update will be considered current until they are superseded by another focused update or the full-text guidelines are revised. This focused update is published in the January 15, 2008, issue of the Journal of the American College of Cardiology, the January 15, 2008, issue of Circulation, and e-published in Catheterization and Cardiovascular Interventions as an update to the full-text guidelines and is posted on the ACC (www.acc.org), AHA (my.americanheart.org), and Society for Angiography and Interventions (SCAI) (www.scai.org) Web sites. Copies of the focused update are available from all organizations.

Sidney C. Smith, Jr., MD, FACC, FAHA

Chair, ACC/AHA Task Force on Practice Guidelines

Alice K. Jacobs, MD, FACC, FAHA

Vice-Chair, ACC/AHA Task Force on Practice Guidelines

	1. Introduction

Top Introduction Preamble 1. Introduction 2. Patients With Unstable... 3. Facilitated PCI 4. Rescue PCI 5. PCI After Fibrinolysis... 6. Ancillary Therapy for... 7. Antiplatelet Therapy 8. Bare-Metal and Drug-Eluting... 9. Secondary Prevention Staff References

 
1.1. Evidence Review
Selected late-breaking clinical trials presented at the 2005 and 2006 annual scientific meetings of the ACC, AHA, and European Society of Cardiology, as well as selected other data, were reviewed by the standing guideline writing committee along with the parent Task Force and other experts to identify those trials and other key data that might impact guideline recommendations. On the basis of the criteria/considerations noted above, recent trial data and other clinical information were considered important enough to prompt a focused update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention.^3–13

To provide clinicians with a comprehensive set of data, whenever possible, the exact event rates in various treatment arms of clinical trials are presented to permit calculation of the absolute risk difference (ARD) and number needed to treat (NNT) or harm (NNH); the relative treatment effects are described either as odds ratio (OR), relative risk (RR), or hazard ratio (HR), depending on the format in the original publication.

Consult the full-text version or executive summary of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention for policy on clinical areas not covered by the focused update.^13a Individual recommendations updated in this focused update will be incorporated into future revisions and/or updates of the full-text guidelines.

1.2. Organization of Committee and Relationships With Industry
For this focused update, all members of the 2005 PCI writing committee were invited to participate; those who agreed (referred to as the 2007 focused update writing group) were required to disclose all RWI relevant to the data under consideration.² Focused update writing group members who had no significant relevant RWI wrote the first draft of the focused update; the draft was then reviewed and revised by the full writing group. Each recommendation required a confidential vote by the writing group members before external review of the document. Any writing committee member with a significant (greater than $10 000) RWI relevant to the recommendation was recused from voting on that recommendation.

1.3. Review and Approval
This document was reviewed by 2 outside reviewers nominated by each cosponsoring organization (ACC, AHA, and SCAI) and 24 individual content reviewers. All reviewer RWI information was collected and distributed to the writing committee and is published in this document (see Appendix 2 for details).

This document was approved for publication by the governing bodies of the American College of Cardiology Foundation, AHA, and SCAI.

	2. Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction

Top Introduction Preamble 1. Introduction 2. Patients With Unstable... 3. Facilitated PCI 4. Rescue PCI 5. PCI After Fibrinolysis... 6. Ancillary Therapy for... 7. Antiplatelet Therapy 8. Bare-Metal and Drug-Eluting... 9. Secondary Prevention Staff References

 
This 2007 PCI Focused Update section regarding patients with unstable angina (UA)/non–ST-elevation myocardial infarction (NSTEMI) is based on recommendations from the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction,¹⁴ which emphasize the importance of assessing risk of cardiovascular events as a guide to therapeutic decision making and the need for interventional therapy (see Table 2).

View this table: [in this window] [in a new window]   Table 2. Updates to Section 5.3: Initial Conservative Versus Initial Invasive Strategies (Patients With UA/NSTEMI)

View this table: [in this window] [in a new window]   Table 2. Continued

View this table: [in this window] [in a new window]   Table 2. Continued

Because of the importance of several new changes in the ACC/AHA 2007 UA/NSTEMI Guidelines, selected text from the guidelines is included in the following paragraphs and summarized in Table 2.

A number of risk-assessment tools have been developed to assist in assessing risk of death and ischemic events in patients with UA/NSTEMI, thereby providing a basis for therapeutic decision making. It should be recognized that the predictive ability of these commonly used risk assessment scores for risk of nonfatal coronary heart disease (CHD) is only moderate.

The Thrombolysis in Myocardial Infarction (TIMI) risk score¹⁵ is a simple tool composed of 7 (1-point) risk indicators rated on presentation (Table 4). The composite end points (all-cause mortality, new or recurrent myocardial infarction [MI], or severe recurrent ischemia prompting urgent revascularization within 14 days) increase as the TIMI risk score increases. The TIMI risk score has been validated internally within the TIMI IIB trial and 2 separate cohorts of patients from the ESSENCE (Efficacy and Safety of Subcutaneous Enoxaparin in Unstable Angina and Non–Q-Wave Myocardial Infarction) trial.¹⁶ The model remained a significant predictor of events and appeared relatively insensitive to missing information, such as knowledge of previously documented coronary stenosis of 50% or greater. The model’s predictive ability remained intact, with a cutoff of 65 years of age. The TIMI risk score was recently studied in an unselected emergency department population with chest pain syndrome; its performance was similar to that in the acute coronary syndrome (ACS) population from which it was derived and validated.¹⁷ The TIMI risk calculator is available at www.timi.org. The TIMI risk index, a modification of the TIMI risk score that uses the variables age, systolic blood pressure, and heart rate, has not only been shown to predict short-term mortality in ST-elevation myocardial infarction (STEMI) but also has been useful in prediction of 30-day and 1-year mortality rates across the spectrum of patients with ACS, including UA/NSTEMI.¹⁸

View this table: [in this window] [in a new window]   Table 4. TIMI Risk Score for Unstable Angina/Non–ST-Elevation Myocardial Infarction

The PURSUIT (Platelet Glycoprotein IIb-IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy) trial risk model,¹⁹ based on patients enrolled in the PURSUIT trial, is another useful tool to guide the clinical decision-making process when the patient is admitted to the hospital. In the PURSUIT risk model, critical clinical features associated with an increased 30-day incidence of death and the composite of death or myocardial (re)infarction were (in order of strength) age, heart rate, systolic blood pressure, ST-segment depression, signs of heart failure (HF), and cardiac enzymes.¹⁹

The GRACE (Global Registry of Acute Coronary Events) study risk model, which predicts in-hospital mortality (and death or MI), can be useful to clinicians to guide treatment type and intensity.^20,21 The GRACE risk tool was developed on the basis of 11 389 patients in GRACE and validated in subsequent GRACE and GUSTO (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) IIb cohorts and predicts in-hospital death in patients with STEMI, NSTEMI, or UA (C statistic=0.83). The 8 variables used in the GRACE risk model are older age (OR 1.7 per 10 years), Killip class (OR 2.0 per class), systolic blood pressure (OR 1.4 per 20 mm Hg decrease), ST-segment deviation (OR 2.4), cardiac arrest during presentation (OR 4.3), serum creatinine level (OR 1.2 per 1 mg per dL increase), positive initial cardiac markers (OR 1.6), and heart rate (OR 1.3 per 30-bpm increase). The sum of scores is applied to a reference nonogram to determine the corresponding all-cause mortality from hospital discharge to 6 months. The GRACE clinical application tool can be downloaded to a handheld PDA (personal digital assistant) to be used at the bedside and is available at www.outcomes-umassmed.org/grace (Figure 1).²¹ An analysis comparing the 3 risk scores (TIMI, GRACE, and PURSUIT) concluded that all 3 demonstrated good predictive accuracy for death and MI at 1 year, thus identifying patients who might be likely to benefit from aggressive therapy, including early myocardial revascularization.²²

View larger version (35K): [in this window] [in a new window]   Figure 1. GRACE Prediction Score Card and Nomogram for All-Cause Mortality From Discharge to 6 Months. Reprinted with permission.20 Copyright © 2004 American Medical Association.

The electrocardiogram (ECG) provides unique and important diagnostic and prognostic information (see also Section 2.1 below). Accordingly, ECG changes have been incorporated into quantitative decision aids for the triage of patients who present with chest discomfort.²³ Although ST elevation carries the highest early risk of death, ST depression on the presenting ECG portends the highest risk of death at 6 months, with the degree of ST-segment depression showing a strong relationship to outcome.²⁴

The recommendations in the ACC/AHA 2007 UA/NSTEMI Guidelines¹⁴ recognize recent data from the ACUITY (Acute Catheterization and Urgent Intervention Triage strategY) trial, which showed that in patients with ACS who were undergoing invasive treatment, bivalirudin alone was associated with rates of ischemia similar to those treated with glycoprotein (GP) IIb/IIIa inhibitors plus heparin and significantly less bleeding.²⁵

The ACC/AHA 2007 UA/NSTEMI Guidelines cite a progressively greater benefit from newer, more aggressive therapies such as low-molecular-weight heparin (LMWH),^16,26 platelet GP IIb/IIIa inhibition,²⁷ and an invasive strategy²⁸ with increasing risk score.

2.1. Electrocardiogram
The ECG lies at the center of the decision pathway for the evaluation and management of patients with acute ischemic discomfort (Table 5). The diagnosis of MI is confirmed with serial cardiac biomarkers in more than 90% of patients who present with ST-segment elevation greater than or equal to 1 mm (0.1 mV) in at least 2 contiguous leads, and such patients should be considered candidates for acute reperfusion therapy. Patients who present with ST-segment depression are initially considered to have either UA or NSTEMI; the distinction between the 2 diagnoses is ultimately based on the detection of markers of myocardial necrosis in the blood.^29–31

View this table: [in this window] [in a new window]   Table 5. Likelihood That Signs and Symptoms Represent an Acute Coronary Syndrome Secondary to CAD

Up to 25% of patients with NSTEMI and elevated CK-MB go on to develop Q-wave MI during their hospital stay, whereas the remaining 75% have non–Q-wave MI. Acute fibrinolytic therapy is contraindicated for ACS patients without ST-segment elevation, except for those with electrocardiographic true posterior MI manifested as ST-segment depression in 2 contiguous anterior precordial leads and/or isolated ST-segment elevation in posterior chest lead.^32–34 Inverted T waves may also indicate UA/NSTEMI. In patients suspected of having ACS on clinical grounds, marked (greater than or equal to 2 mm [0.2 mV]) symmetrical precordial T-wave inversion strongly suggests acute ischemia, particularly that associated with a critical stenosis of the left anterior descending coronary artery (LAD).³⁵ Patients with this ECG finding often exhibit hypokinesis of the anterior wall and are at high risk if given medical treatment alone.³⁶ Revascularization will often reverse both the T-wave inversion and wall-motion disorder.³⁷ Nonspecific ST-segment and T-wave changes, usually defined as ST-segment deviation less than 0.5 mm (0.05 mV) or T-wave inversion less than or equal to 2 mm (0.2 mV), are less diagnostically helpful than the foregoing findings. Established Q waves greater than or equal to 0.04 second are also less helpful in the diagnosis of UA, although by suggesting prior MI, they do indicate a high likelihood of significant coronary artery disease (CAD). Isolated Q waves in lead III may be a normal finding, especially in the absence of repolarization abnormalities in any of the inferior leads. A completely normal ECG in a patient with chest pain does not exclude the possibility of ACS, because 1% to 6% of such patients eventually are proven to have had an MI (by definition, NSTEMI), and at least 4% will be found to have UA.^38–40

In addition to the presence or absence of ST-segment deviation or T-wave inversion patterns noted earlier, there is evidence that the magnitude of the ECG abnormality provides important prognostic information. Thus, Lloyd-Jones et al.⁴¹ reported that the diagnosis of acute non–Q-wave MI was 3 to 4 times more likely in patients with ischemic discomfort who had at least 3 ECG leads that showed ST-segment depression and maximal ST depression of greater than or equal to 0.2 mV. Investigators from the TIMI III Registry⁴² reported that the 1-year incidence of death or new MI in patients with at least 0.5 mm (0.05 mV) of ST-segment deviation was 16.3% compared with 6.8% for patients with isolated T-wave changes and 8.2% for patients with no ECG changes.

Cardiogenic shock can occur in the setting of both STEMI and NSTEMI, and there is high mortality and morbidity in each. The SHOCK (SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK) study⁴³ found that approximately 20% of all cardiogenic shock complicating MI was associated with NSTEMI. The GUSTO-II⁴⁴ and PURSUIT⁴⁵ trials found that cardiogenic shock occurs in up to 5% of patients with NSTEMI and that mortality rates are greater than 60%. Thus, hypotension and evidence of organ hypoperfusion can occur and constitute a medical emergency in NSTEMI.

2.1.1. Comparison of Early Invasive and Initial Conservative Strategies for UA/NSTEMI
Prior meta-analyses concluded that routine invasive therapy (the "invasive" or "early" strategy triages patients to undergo an invasive diagnostic evaluation without first getting a noninvasive stress test or without failing medical treatment [i.e., an initial conservative diagnostic strategy or sometimes now known as the "selective invasive strategy"]¹⁴) is better than an initial conservative or selectively invasive approach (the "initial conservative strategy" [also referred to as "selective invasive management"] calls for proceeding with an invasive evaluation only for those patients who fail medical therapy [refractory angina or angina at rest or with minimal activity despite rigorous medical therapy] or in whom objective evidence of ischemia [dynamic ECG changes, high-risk stress test] is identified¹⁴). Mehta et al⁴⁷ concluded that the routine invasive strategy resulted in an 18% relative reduction in death or MI, including a significant reduction in MI alone. The routine invasive arm was associated with higher in-hospital mortality (1.8% versus 1.1%), but this disadvantage was more than compensated for by a significant reduction in mortality between discharge and the end of follow-up (3.8% versus 4.9%). In those analyses, the invasive strategy was associated with less angina and fewer rehospitalizations than the conservative pathway. Patients undergoing routine invasive treatment also had improved quality of life.

In contrast to these findings, other studies, most recently ICTUS (Invasive versus Conservative Treatment in Unstable coronary Syndromes), have favorably highlighted a strategy of selective invasive therapy.⁴⁸ In ICTUS, 1200 high-risk ACS patients without ST-segment elevation were randomized to receive routine invasive versus selective invasive management and followed up for 1 year with respect to the combined incidence of death, MI, and ischemic rehospitalization. All patients were treated with optimal medical therapy that included aspirin, clopidogrel, LMWH, and lipid-lowering therapy; abciximab was given to those undergoing revascularization. At the end of 1 year, there was no significant difference in the composite end point between groups. This study suggests that a selective invasive strategy could be reasonable for ACS patients. A possible explanation for the lack of benefit of the invasive approach in this trial (and other trials)⁴⁹ could be related to the relatively high rate of revascularization actually performed in patients treated in the selective invasive arm (47%), thereby reducing observed differences between treatment strategies,²² and to the lower event rate (lower-risk population) than in other studies. Results were unchanged during longer-term follow-up.^50,51 Nevertheless, ICTUS required troponin positivity for entry. Thus, troponin alone might no longer be an adequate criterion for strategy selection, especially with increasingly sensitive troponin assays. The degree of troponin elevation and other high-risk clinical factors taken together should be considered in selecting a treatment strategy. The ICTUS trial was relatively underpowered for hard end points, and it used a controversial definition for post procedural MI (i.e., even minimal asymptomatic CK-MB elevation).^48,50,51

Additionally, 1-year follow-up may be inadequate to fully realize the long-term impact and benefit of the routine invasive strategy. In the RITA-3 trial (Third Randomized Intervention Trial of Angina), 5-year but not 1-year event rates favored the early invasive arm (see Figure 2 and text below).⁵² In ICTUS, however, results were maintained during a 3-year follow-up.⁵³

View larger version (18K): [in this window] [in a new window]   Figure 2. Cumulative Risk of Death or Myocardial Infarction in RITA-3. Top: Cumulative risk of death or myocardial infarction in the RITA-3 trial of patients with non-ST acute coronary syndrome. Bottom: Cumulative risk of death in the RITA-3 trial of patients with non-ST acute coronary syndromes. Reprinted with permission.52

Thus, the 2007 UA/NSTEMI Guidelines¹⁴ recommend that in initially stabilized UA/NSTEMI patients, an initial conservative (selective invasive) strategy may be considered as an alternative treatment option. The writing committee also believes that additional comparative trials of the selective invasive with the routine initial invasive strategies are indicated, using aggressive contemporary medical therapies in both arms, including routine dual antiplatelet therapy (DAT) in medically treated patients as well as aggressive lipid lowering and other updated secondary prevention measures.

Nevertheless, a meta-analysis of contemporary randomized trials in NSTEMI, including ICTUS, currently support long-term mortality and morbidity benefits of an early invasive compared with an initial conservative strategy.⁵⁴ Nonfatal MI at 2 years (7.6% vs. 9.1%, respectively; RR 0.83 [95% CI 0.72 to 0.96]; p = 0.012) and hospitalization (at 13 months; RR = 0.69 [95% CI 0.65 to 0.74]; p less than 0.0001) also were reduced by an early invasive strategy (Figure 3). A separate review of contemporary randomized trials in the stent era using the Cochrane Database arrived at similar conclusions.⁵⁵ Details of selected contemporary trials of invasive versus conservative strategies may be found in the ACC/AHA 2007 UA/NSTEMI Guidelines.¹⁴

View larger version (15K): [in this window] [in a new window]   Figure 3. Relative Risk of Outcomes With Early Invasive Versus Conservative Therapy in UA/NSTEMI. A: Relative risk of all-cause mortality for early invasive therapy compared with conservative therapy at a mean follow-up of 2 years. B: Relative risk of recurrent nonfatal myocardial infarction for early invasive therapy compared with conservative therapy at a mean follow-up of 2 years. C: Relative risk of recurrent unstable angina resulting in rehospitalization for early invasive therapy compared with conservative therapy at a mean follow-up of 13 months.54 CI indicates confidence interval; FRISC-II, FRagmin and fast Revascularization during InStability in Coronary artery disease; ICTUS, Invasive versus Conservative Treatment in Unstable coronary Syndromes; ISAR-COOL, Intracoronary Stenting with Antithrombotic Regimen COOLing-off; RITA-3, Third Randomized Intervention Trial of Angina; RR, relative risk; TIMI-18, Thrombolysis In Myocardial Infarction-18; TRUCS, Treatment of Refractory Unstable angina in geographically isolated areas without Cardiac Surgery; UA/NSTEMI, unstable angina/non-ST-segment elevation myocardial infarction: Open multicenter randomized trial. Modified with permission.54

Thus, the FRISC-II (Fragmin and Fast Revascularisation during InStability in Coronary artery disease)⁵⁶ and TACTICS (Treat Angina with Aggrastat and Determine Cost of Therapy with an Invasive or Conservative Strategy)-TIMI 18²⁸ trials showed a benefit in patients assigned to invasive strategy. In contrast to earlier trials, a large majority of patients undergoing percutaneous coronary intervention (PCI) in these 2 trials received coronary stenting as opposed to balloon angioplasty alone. Also, there was a differential rate of thienopyridine use between the 2 arms; only stented patients were treated. In FRISC-II, the invasive strategy involved treatment with LMWH, aspirin, nitrates, and beta blockers for an average of 6 days in the hospital before coronary angiography, an approach that would be difficult to adopt in US hospitals. In TACTICS-TIMI 18, treatment included the GP IIb/IIIa antagonist tirofiban, which was administered for an average of 22 hours before coronary angiography. The routine use of the GP IIb/IIIa inhibitor in this trial may have eliminated the excess risk of early (within 7 days) MI in the invasive arm, a risk that was observed in FRISC-II and other trials in which there was no routine "upstream" use of a GP IIb/IIIa blocker. Therefore, an invasive strategy is associated with a better outcome in UA/NSTEMI patients at high risk as defined in Table 3 and as demonstrated in TACTICS-TIMI 18 when a GP IIb/IIIa inhibitor is used.²⁸ Although the benefit of intravenous GP IIb/IIIa inhibitors is established for UA/NSTEMI patients undergoing PCI, the optimal time to start these drugs before the procedure has not been established. In the PURSUIT trial,⁴⁵ in patients with UA/NSTEMI who were admitted to community hospitals, the administration of eptifibatide was associated with a reduced need for transfer to tertiary referral centers and improved outcomes.⁵⁷

View this table: [in this window] [in a new window]   Table 3. Selection of Initial Treatment Strategy: Invasive Versus Conservative Strategy

The RITA-3 trial⁵² compared early and conservative therapy in 1810 moderate-risk patients with ACS. Patients with positive cardiac biomarkers (CK-MB greater than 2 times the upper limit of normal at randomization) were excluded from randomization, as were those with new Q waves, MI within 1 month, PCI within 1 year, and any prior coronary artery bypass graft (CABG). The combined end point of death, nonfatal MI, and refractory angina was reduced from 14.5% to 9.6% by early invasive treatment. The benefit was driven primarily by a reduction in refractory angina. There was a late divergence of the curves, with reduced 5-year death and MI in the early invasive arm (Figure 2).

In the VINO trial (Value of first day angiography/ angioplasty In evolving Non-ST segment elevation myocardial infarction: Open multicenter randomized trial),⁵⁸ 131 patients with NSTEMI were randomized to cardiac catheterization on the day of admission versus conservative therapy. Despite the fact that 40% of the conservatively treated patients crossed over to revascularization by the 6-month follow-up, there was a significant reduction in death or reinfarction for patients assigned to early angiography and revascularization (6% versus 22%).

The ISAR-COOL (Intracoronary Stenting with Antithrombotic Regimen Cooling-off) trial⁵⁹ randomized 410 intermediate- to high-risk patients to very early angiography and revascularization versus a delayed invasive strategy. All patients were treated with intensive medical therapy that included aspirin, heparin, clopidogrel (600-mg loading dose), and the intravenous GP IIb/IIIa receptor inhibitor tirofiban. In the very early arm, patients underwent cardiac catheterization at a mean time of 2.4 hours versus 86 hours in the delayed invasive arm. The very early invasive strategy was associated with significantly better outcome at 30 days, as measured by reduction in death and large MI (5.9% versus 11.6%). More importantly, the benefit seen was attributable to a reduction in events before cardiac catheterization, which raises the possibility that there is a hazard associated with a "cooling-down" period.

2.1.2. Selection for Coronary Angiography
In contrast to the noninvasive tests, coronary angiography provides detailed structural information to allow assessment of prognosis and provide direction for appropriate management. When combined with left ventricular (LV) angiography, it also allows an assessment of global and regional LV function. Indications for coronary angiography are interwoven with indications for possible therapeutic plans, such as PCI or CABG.

Coronary angiography is usually indicated in patients with UA/NSTEMI who either have recurrent symptoms or ischemia despite adequate medical therapy or are at high risk as categorized by clinical findings (HF, serious ventricular arrhythmias) or noninvasive test findings (significant LV dysfunction: ejection fraction less than 0.35, large anterior or multiple perfusion defects) (Tables 6, 7, and 8). Patients with UA/NSTEMI who have had previous PCI or CABG also should generally be considered for early coronary angiography unless prior coronary angiography data indicate that further revascularization is not likely to be possible. The placement of an intra-aortic balloon pump (IABP) may allow coronary angiography and revascularization in those with hemodynamic instability. Patients with suspected Prinzmetal’s variant angina also are candidates for coronary angiography.

View this table: [in this window] [in a new window]   Table 6. Noninvasive Risk Stratification

View this table: [in this window] [in a new window]   Table 7. Noninvasive Test Results That Predict High Risk for Adverse Outcome (Left Ventricular Imaging)

View this table: [in this window] [in a new window]   Table 8. Noninvasive Test Results That Predict High Risk for Adverse Outcome on Stress Radionuclide Myocardial Perfusion Imaging

In all cases, the general indications for coronary angiography and revascularization are tempered by individual patient characteristics and preferences. Patient and physician judgments regarding risks and benefits are particularly important for patients who might not be candidates for coronary revascularization, such as very frail older adults and those with serious comorbid conditions (i.e., severe hepatic, pulmonary, or renal failure or active or inoperable cancer).

2.1.3. Chronic Kidney Disease
The following recommendations have been added to the PCI Focused Update in accordance with new recommendations appearing in the 2007 UA/NSTEMI Guidelines¹⁴ (Table 9). Supporting text from that guidelines statement is presented in the following paragraphs.

View this table: [in this window] [in a new window]   Table 9. Indications for Chronic Kidney Disease

Chronic kidney disease (CKD) is not only a coronary risk equivalent for ascertainment of coronary risk but also a risk factor for the development and progression of cardiovascular disease (CVD).⁶³ CKD constitutes a risk factor for adverse outcomes after MI,⁶⁴ including NSTEMI and other coronary patient subsets. In the highly validated GRACE risk score, serum creatinine is 1 of 8 independent predictors of death.^20,65 In 1 recent study, even early CKD constituted a significant risk factor for cardiovascular events and death.^64,66 CKD also predicts an increase in recurrent cardiovascular events.⁶⁷ Cardiovascular death is 10 to 30 times higher in dialysis patients than in the general population. The underrepresentation of patients with renal disease in randomized controlled trials of CVD is a concern.⁶⁸ Current opinion and most of the limited evidence available suggest that when appropriately monitored, cardiovascular medications and interventional strategies can be applied safely in those with renal impairment and provide therapeutic benefit.⁶⁴ However, not all recent evidence is consistent with this premise: atorvastatin did not significantly reduce the primary end point of cardiovascular death, nonfatal MI, or stroke in a prospective randomized trial of patients with diabetes and end-stage CKD who were undergoing hemodialysis.⁶⁹ The preference for primary PCI has also been questioned.⁷⁰

Particularly in the setting of ACS, bleeding complications are higher in this patient subgroup because of platelet dysfunction and dosing errors; benefits of fibrinolytic therapy, antiplatelet agents, and anticoagulants can be negated or outweighed by bleeding complications; and renin-angiotensin-aldosterone inhibitors can impose a greater risk because of the complications of hyperkalemia and worsening renal function in the patient with CKD. Angiography carries an increased risk of contrast-induced nephropathy; the usual benefits of PCI can be lessened or abolished; and PCI in patients with CKD is associated with a higher rate of early and late complications of bleeding, restenosis, and death.⁶⁸ Thus, identification of CKD is important in that it represents an ACS subgroup with a far more adverse prognosis but for whom interventions have less certain benefit.

Coronary arteriography is a frequent component of the care of ACS patients. As such, contrast-induced nephropathy can constitute a serious complication of diagnostic and interventional procedures. In patients with CKD or CKD and diabetes, isosmolar contrast material lessens the rise in creatinine and is associated with lower rates of contrast-induced nephropathy than low-osmolar contrast media. This has been documented in a randomized clinical trial (RECOVER [Renal Toxicity Evaluation and Comparison Between Visipaque (Iodixanol) and Hexabrix (Ioxaglate) in Patients With Renal Insufficiency Undergoing Coronary Angiography]) comparing iodixanol with ioxaglate⁷¹ and in a meta-analysis of 2727 patients from 16 randomized clinical trials.⁷²

Identification of patients with CKD as recommended in the AHA Science Advisory on Detection of CKD in patients with or at increased risk of CVD should guide the use of isosmolar contrast agents.⁶³ The advisory, which was developed in collaboration with the National Kidney Foundation, recommends that all patients with CVD be screened for evidence of kidney disease by estimating glomerular filtration rate, testing for microalbuminuria, and measuring the albumin-to-creatinine ratio. A glomerular filtration rate of less than 60 ml per min per 1.73 square meters of body surface should be regarded as abnormal. Furthermore, the albumin-to-creatinine ratio should be used to screen for the presence of kidney damage in adult patients with CVD, with values greater than 30 mg of albumin per 1 g of creatinine considered abnormal.

A diagnosis of renal dysfunction is critical to proper medical therapy for UA/NSTEMI. Many cardiovascular drugs used in patients with UA/NSTEMI are renally cleared; their doses should be adjusted for estimated creatinine clearance [see also Section 3 of the 2007 UA/NSTEMI Guidelines¹⁴]. In a large community-based registry study, 42% of patients with UA/NSTEMI received excessive initial dosing of at least 1 antiplatelet or antithrombin agent (unfractionated heparin [UFH], LMWH, or GP IIb/IIIa inhibitor).⁷³ Renal insufficiency was an independent predictor of excessive dosing. Dosing errors predicted an increased risk of major bleeding. Clinical studies and labeling that defines adjustments for several of these drugs have been based on the Cockcroft-Gault formula for estimating creatinine clearance, which is not identical to the Modification of Diet and Renal Disease (MDRD) formula. Use of the Cockcroft-Gault formula to generate dose adjustments is recommended. The impact of renal dysfunction on biomarkers of necrosis (i.e., troponin) is discussed in Section 2.2.8.2.1 of the 2007 UA/NSTEMI Guidelines.¹⁴

To increase the meager evidence base and to optimize care for this growing high-risk population, the recognition of CKD patients with or at risk of CVD and the inclusion and reporting of renal disease in large CVD trials must be increased in the future.

	3. Facilitated PCI

Top Introduction Preamble 1. Introduction 2. Patients With Unstable... 3. Facilitated PCI 4. Rescue PCI 5. PCI After Fibrinolysis... 6. Ancillary Therapy for... 7. Antiplatelet Therapy 8. Bare-Metal and Drug-Eluting... 9. Secondary Prevention Staff References

 
Facilitated PCI refers to a strategy of planned immediate PCI after administration of an initial pharmacological regimen intended to improve coronary patency before the procedure. These regimens have included high-dose heparin, platelet GP IIb/IIIa inhibitors, full-dose or reduced-dose fibrinolytic therapy, and the combination of a GP IIb/IIIa inhibitor with a reduced-dose fibrinolytic agent (e.g., fibrinolytic dose typically reduced 50%). Facilitated PCI should be differentiated from primary PCI without fibrinolytic therapy, from primary PCI with a GP IIb/IIIa inhibitor started at the time of PCI, from early or delayed PCI after successful fibrinolytic therapy, and from rescue PCI after unsuccessful fibrinolytic therapy. Potential advantages of facilitated PCI include earlier time to reperfusion, smaller infarct size, improved patient stability, lower infarct artery thrombus burden, greater procedural success rates, higher TIMI flow rates, and improved survival rates. Potential risks include increased bleeding complications, especially in older patients; potential limitations include added cost.

Despite the potential advantages, clinical trials of facilitated PCI have not demonstrated any benefit in reducing infarct size or improving outcomes. The largest of these was the ASSENT-4 (Assessment of the Safety and Efficacy of a New Treatment Strategy with Percutaneous Coronary Intervention) PCI trial,⁵ in which 1667 patients were randomized to full-dose tenecteplase and PCI versus primary PCI. The trial was terminated prematurely because of a higher in-hospital mortality rate in the facilitated PCI group (6% vs. 3%, p = 0.01). The primary end point, a composite of death, shock, and congestive heart failure within 90 days, was significantly higher with facilitated PCI than with primary PCI (18.6% vs. 13.4%; p = 0.0045), and there was a trend toward higher 90-day mortality (6.7% vs. 4.9%; p = 0.14). Defenders of the facilitated PCI strategy point out that the absence of an infusion of heparin after bolus administration and of a loading dose of clopidogrel, plus prohibition of GP IIb/IIIa inhibitors except in bail-out situations, made adjunctive antithrombotic therapy suboptimal for the facilitated PCI group. Moreover, the median treatment delay between tenecteplase and PCI was only 104 minutes, and mortality rates with facilitated PCI were higher in PCI centers. Whether earlier (pre-hospital) administration of fibrinolytic therapy, better antithrombotic therapy, longer delays to PCI, or selective use of PCI as a rescue strategy would make the facilitated PCI strategy beneficial is unclear and requires further study. On the basis of these data, however, facilitated PCI offered no clinical benefit.

Keeley and coworkers performed a quantitative review of 17 trials that compared facilitated PCI and primary PCI⁷⁴ (Figure 4). Included were 9 trials with GP IIb/IIIa inhibitors alone (n = 1148), 6 trials with fibrinolytic therapy (including ASSENT-4 PCI) (n = 2953), and 2 trials with a fibrinolytic agent plus a GP IIb/IIIa inhibitor (n = 399). Facilitated PCI with fibrinolytic therapy had significantly higher rates of mortality, nonfatal reinfarction, urgent target vessel revascularization, total and hemorrhagic stroke, and major bleeding compared with primary PCI. There were no differences in efficacy or safety when facilitated PCI with a GP IIb/IIIa inhibitor was compared with primary PCI.

View larger version (29K): [in this window] [in a new window]   Figure 4. Short-Term Death in Patients Treated With Facilitated Or Primary PCI. Trials were classified by facilitated regimen. Diamonds and squares indicate odds ratios. Lines indicate 95% confidence intervals. Reprinted with permission.74

A planned reperfusion strategy using full-dose fibrinolytic therapy followed by immediate PCI may be harmful (Table 10). Nevertheless, selective use of the facilitated strategy with regimens other than full-dose fibrinolytic therapy in high-risk subgroups of patients (large MI or hemodynamic or electrical instability) with low bleeding risk who present to hospitals without PCI capability might be performed when transfer delays for primary PCI are anticipated. Although the quantitative analysis showed no advantage for pretreatment with a GP IIb/IIIa inhibitor, neither did it document any major disadvantage. The use of GP IIb/IIIa inhibitors, particularly abciximab, during primary PCI is well established. Further trials of reduced-dose fibrinolytic therapy, with or without GP IIb/IIIa inhibitors, are in progress and may yield different efficacy and/or safety results. For further clarification, please see Section 6.3.1.6.2.1 of the 2004 ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction.⁷⁵

View this table: [in this window] [in a new window]   Table 10. Updates to Section 5.4.3: PCI for STEMI in Conjunction With Concomitant Fibrinolytic Therapy

Pharmacological reperfusion with full-dose fibrinolysis is not uniformly successful in restoring antegrade flow in the infarct artery. In such situations, a strategy of prompt coronary angiography with intent to perform PCI is frequently contemplated. In certain patients, such as those with cardiogenic shock (especially in those less than 75 years of age), severe congestive heart failure/pulmonary edema, or hemodynamically compromising ventricular arrhythmias (regardless of age), a strategy of coronary angiography with intent to perform PCI is a useful approach regardless of the time since initiation of fibrinolytic therapy, provided further invasive management is not considered futile or unsuitable given the clinical circumstances (Table 11). Further discussion of the management of such patients may be found in Section 5.4.4 (which has been updated in this document) of the 2005 PCI Guideline Update.^13a

View this table: [in this window] [in a new window]   Table 11. Updates to Section 5.4.4: PCI After Failed Fibrinolysis (All 2005 Recommendations Provided for Clarity)

	4. Rescue PCI

Top Introduction Preamble 1. Introduction 2. Patients With Unstable... 3. Facilitated PCI 4. Rescue PCI 5. PCI After Fibrinolysis... 6. Ancillary Therapy for... 7. Antiplatelet Therapy 8. Bare-Metal and Drug-Eluting... 9. Secondary Prevention Staff References

 
In other patients who do not exhibit the clinical instability noted above, PCI may also be reasonable if there is clinical suspicion of failure of fibrinolysis. This is referred to as rescue PCI. Critical to the success of rescue PCI is the initial clinical identification of patients who are suspected of having failed reperfusion with full-dose fibrinolysis. Because the presence or absence of ischemic discomfort may be unreliable for identifying failed reperfusion, clinicians should search for evidence of inadequate ST-segment resolution on the 12-lead ECG. Operationally, the 12-lead ECG should be scrutinized after adequate time has elapsed before making the judgment that fibrinolytic therapy has not been effective. Although earlier periods have been used in some studies, the writing committee felt that 90 minutes after initiation of fibrinolysis provided the best time for evaluating the need for rescue PCI: hence, if there is less than 50% ST resolution in the lead showing the greatest degree of ST-segment elevation at presentation, fibrinolytic therapy has likely failed to produce reperfusion.

The 2005 PCI Guideline Update^13a recommendations for rescue PCI were based on observational data and 2 small randomized clinical trials (n = 179) from the early 1990s.^94,95 More recently, MERLIN (Middlesbrough Early Revascularization to Limit Infarction) (n = 307) and REACT (Rescue Angioplasty versus Conservative Treatment or Repeat Thrombolysis) (n = 427) and 3 meta-analyses have refocused attention on rescue PCI.^96–100 This subject has been studied with fewer than 1000 patients enrolled in randomized trials.

In the period between trials studying rescue PCI, there was a transition between angiographic and electrocardiographic diagnosis to detect failed reperfusion. Importantly, in the earlier studies, rescue PCI was performed in infarct arteries with TIMI 0/1 flow, often after a protocol-mandated 90-minute angiogram. In MERLIN and REACT, however, patients were randomized if they had less than 50% ST-segment elevation resolution at 60 or 90 minutes, respectively. Many patients had patent infarct arteries at angiography; only 54% of patients in MERLIN and 74% of patients in REACT (which required less than TIMI grade 3 flow for PCI) actually underwent PCI. From a procedural standpoint, stents have replaced balloon angioplasty, antiplatelet therapy has improved with the addition of a thienopyridine agent and often a GP IIb/IIIa receptor antagonist, and procedural success rates are higher.

Despite these historical differences, recent data support the initial observation that rescue PCI decreases adverse clinical events compared with medical therapy. In the Wijeysundera meta-analysis¹⁰⁰) (Figure 5, there was a trend toward reduced mortality rates with rescue PCI from 10.4% to 7.3% (RR 0.69 [95% CI 0.46 to 1.05]; p = 0.09), reduced reinfarction rates from 10.7% to 6.1% (RR 0.58 [95% CI 0.35 to 0.97]; p = 0.04), and reduced HF rates from 17.8% to 12.7% (RR 0.73 [95% CI 0.54 to 1.00]; p = 0.05). These event rates suggest that high-risk patients were selected for enrollment, so these data do not define the role of rescue PCI in lower-risk patients. Also, the benefits of rescue PCI need to be balanced against the risk. There was an excess occurrence of stroke in 2 trials (10 events versus 2 events), but the majority were thromboembolic rather than hemorrhagic, and the sample size was small, so more data are required to define this risk. There was also an increase of 13% in absolute risk of bleeding, suggesting that adjustments in antithrombotic medication dosing are needed to improve safety. It should be noted that the majority of patients who underwent rescue PCI received streptokinase as fibrinolytic therapy.

View larger version (36K): [in this window] [in a new window]   Figure 5. Efficacy End Points for Rescue PCI Versus Conservative Therapy. CI indicates confidence interval; MERLIN, Middlesbrough Early Revascularization to Limit Infarction trial; NNT, number needed to treat; PCI, percutaneous coronary intervention; REACT, Rescue Angioplasty versus Conservative Treatment or Repeat Thrombolysis trial; RESCUE, Randomized Comparison of Rescue Angioplasty with Conservative Management of Patients with Early Failure of Thrombolysis for Acute Anterior Myocardial Infarction trial; RR, relative risk; and TAMI, Thrombolysis and Angioplasty in Myocardial Infarction study. Reprinted with permission.100

Given the association between bleeding events and subsequent ischemic events,¹⁰³ it might be reasonable to select moderate- and high-risk patients for PCI after fibrinolysis and to treat low-risk patients with medical therapy. As noted above, patients with cardiogenic shock, severe HF, or hemodynamically compromising ventricular arrhythmias are excellent candidates. An electrocardiographic estimate of potential infarct size in patients with persistent ST-segment elevation (less than 50% resolution at 90 minutes after initiation of fibrinolytic therapy in the lead showing the worst initial elevation) and ongoing ischemic pain is useful in selecting other patients for rescue PCI. Anterior MI or inferior MI with right ventricular involvement or precordial ST-segment depression usually predicts increased risk.¹⁰⁴ Conversely, patients with symptom resolution, improving ST-segment elevation (less than 50% resolution), or inferior MI localized to 3 ECG leads probably should not be referred for angiography. Likewise, it is doubtful that PCI of a branch artery (diagonal or obtuse marginal branch) will change prognosis in the absence of the high-risk criteria noted above.

	5. PCI After Fibrinolysis or for Patients Not Undergoing Primary Reperfusion

Top Introduction Preamble 1. Introduction