The results of 4 meta-analyses have found that vascular closure devices decrease time to hemostasis compared with manual compression but do not decrease vascular complica- tions, bleeding complications, or the need for blood transfu- sions.256,789,791,793 Future studies of vascular closure devices need to be randomized, include high-risk patients and high-risk anatomy, use blinded endpoint adjudication as much as possible, use well-defined and comprehensive com- plication endpoints, and be adequately powered to detect clinically important endpoints, particularly bleeding and vas- cular complications. 6. Postprocedural Considerations Postprocedural considerations in patients undergoing PCI are discussed below and summarized in Table 14. Some recom- mendations and text regarding DAPT in Section 5.7.2 are intentionally repeated in this section for reader ease of use. 6.1. Postprocedural Antiplatelet Therapy: Recommendations Class I 1. After PCI, use of aspirin should be continued indef- initely.560 563 (Level of Evidence: A) 2. The duration of P2Y12 inhibitor therapy after stent implantation should generally be as follows: a. In patients receiving a stent (BMS or DES) dur- ing PCI for ACS, P2Y12 inhibitor therapy should be given for at least 12 months. Options include (Level of Evidence: B) b. In patients receiving DES for a non-ACS indica- tion, clopidogrel 75 mg daily should be given for at least 12 months if the patient is not at high risk of bleeding.208,212,571 (Level of Evidence: B) c. In patients receiving BMS for a non-ACS indica- tion, clopidogrel should be given for a minimum of 1 month and ideally up to 12 months (unless the patient is at increased risk of bleeding; then it should be given for a minimum of 2 weeks).572 (Level of Evidence: B) 3. Patients should be counseled on the importance of compliance with DAPT and that therapy should not be discontinued before discussion with their cardi- ologist.208 (Level of Evidence: C) Levine et al 2011 ACCF/AHA/SCAI PCI Guideline e613 Table 14. Postprocedural Recommendations for Patients Undergoing PCI Recommendations COR LOE References Aspirin After PCI, use of aspirin should be continued indefinitely. I A 560 563 After PCI, it is reasonable to use aspirin 81 mg/d in preference to higher maintenance doses. IIa B 302,573 576 In patients receiving a stent (BMS or DES) during PCI for ACS, P2Y12 inhibitor therapy should be given for at least 12 mo. Options include clopidogrel 75 mg/d, prasugrel 10 mg/d, and ticagrelor 90 mg twice daily. I B 567,568,570 In patients receiving DES for a non-ACS indication, clopidogrel 75 mg/d should be given for at least 12 mo if patients are not at high risk of bleeding. I B 208,212,571 In patients receiving BMS for a non-ACS indication, clopidogrel should be given for a minimum of 1 mo and ideally up to 12 mo (unless the patient is at increased risk of bleeding; then it should be given for a minimum of 2 wk). I B 572 Patients should be counseled on the importance of compliance with DAPT and that therapy should not be discontinued before discussion with their cardiologist. I C 208 PPIs should be used in patients with a history of prior GI bleeding who require DAPT. I C 794 If the risk of morbidity from bleeding outweighs the anticipated benefit afforded by a recommended duration of P2Y12 inhibitor therapy after stent implantation, earlier discontinuation (eg, 12 mo) of P2Y12 inhibitor therapy is reasonable. IIa C N/A Use of PPIs is reasonable in patients with an increased risk of GI bleeding (eg, advanced age, concomitant use of warfarin, steroids, NSAIDs, Helicobacter pylori infection) who require DAPT. IIa C 794 Continuation of clopidogrel, prasugrel, or ticagrelor beyond 12 mo may be considered in patients undergoing placement of DES. IIb C N/A Routine use of a PPI is not recommended for patients at low risk of GI bleeding, who have much less potential to benefit from prophylactic therapy. III: No Benefit C 794 Exercise testing For patients entering a formal cardiac rehabilitation program after PCI, treadmill exercise testing is reasonable. IIa C 567,568 Routine periodic stress testing of asymptomatic patients after PCI without specific clinical indications should not be performed. III: No Benefit C 795 Cardiac rehabilitation Medically supervised exercise programs (cardiac rehabilitation) should be recommended to patients after PCI, particularly for patients at moderate to high risk, for whom supervised exercise training is warranted. I A 796 804 Secondary prevention (recommendations included from the 2011 AHA/ACCF Secondary Prevention and Risk Reduction Therapy Guideline)805 Lipid management with lifestyle modification and lipid-lowering pharmacotherapy Lifestyle modification I B 806,807 Statin therapy I A 344,806,808 810,810a Statin therapy which lowers LDL cholesterol to 100 mg/dL and achieves at least a 30% lowering of LDL cholesterol I C 344,806,808 810,810a Statin therapy which lowers LDL cholesterol to 70 mg/dL in very high-risk* patients IIa B 345,808 810,810a,811,812 Blood pressure control (with a blood pressure goal of 140/90 mm Hg) Lifestyle modification I B 813 817 Pharmacotherapy I A 813,818,819 Diabetes management (eg, lifestyle modification and pharmacotherapy) coordinated with the patient s primary care physician and/or endocrinologist I C N/A Complete smoking cessation I A 820 823 *Presence of established cardiovascular disease plus 1) multiple major risk factors (especially diabetes), 2) severe and poorly controlled risk factors (especially continued cigarette smoking), 3) multiple risk factors of the metabolic syndrome (especially high triglycerides 200 mg/dL plus non HDL cholesterol 130 mg/dL with low HDL cholesterol [ 40 mg/dL]), and 4) acute coronary syndromes. ACS indicates acute coronary syndromes; BMS, bare-metal stent(s); COR, class of recommendation; DAPT, dual antiplatelet therapy; DES, drug-eluting stent(s); GI, gastrointestinal; HDL, high-density lipoprotein; LDL, low-density lipoprotein; LOE, level of evidence; N/A, not applicable; NSAID, nonsteroidal anti-inflammatory drug; PCI, percutaneous coronary intervention; and PPI, proton pump inhibitor. Class IIa 1. After PCI, it is reasonable to use aspirin 81 mg per day in preference to higher maintenance dos- es.302,573 576 (Level of Evidence: B) 2. If the risk of morbidity from bleeding outweighs the anticipated benefit afforded by a recommended du- ration of P2Y12 inhibitor therapy after stent implan- tation, earlier discontinuation (eg, <12 months) of P2Y12 inhibitor therapy is reasonable. (Level of Evidence: C) Class IIb 1. Continuation of clopidogrel, prasugrel, or ticagrelor beyond 12 months may be considered in patients undergoing placement of DES.567,568 (Level of Evi- dence: C) Continued treatment with the combination of aspirin and a P2Y12 inhibitor antagonist after PCI appears to reduce MACE.570,572 On the basis of RCT protocols, secondary prevention measures, and expert consensus opinion, aspirin 81 mg daily should be given indefinitely after PCI. Likewise, P2Y12 inhibitors should be given for a minimum of 1 month after BMS (minimum 2 weeks for patients at significant increased risk of bleeding)580 and for 12 months after DES and ideally in all patients who are not at high risk of bleeding. The 2009 STEMI/PCI guidelines update10 listed the rec- ommendation if the risk of morbidity because of bleeding outweighs the anticipated benefit afforded by thienopyridine therapy, earlier discontinuation should be considered as a Class I recommendation, although the language used, in part, was consistent with a Class IIa recommendation. To clarify the intent of the recommendation, as well as to acknowledge the inherent difficulties in weighing bleeding and stent thrombosis risks, the recommendation is designated a Class IIa recommendation, using the phrase earlier discontinuation is reasonable. Recommendations regarding P2Y12 inhibitor discontinuation before elective or urgent CABG are provided in the 2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery. 824 6.1.1. PPIs and Antiplatelet Therapy: Recommendations Class I 1. PPIs should be used in patients with a history of prior gastrointestinal (GI) bleeding who require DAPT.794 (Level of Evidence: C) Class IIa 1. Use of PPIs is reasonable in patients with an in- creased risk of GI bleeding (eg, advanced age, concomitant use of warfarin, steroids, nonsteroidal anti-inflammatory drugs, Helicobacter pylori infec- tion) who require DAPT.794 (Level of Evidence: C) Class III: NO BENEFIT 1. Routine use of a PPI is not recommended for pa- tients at low risk of GI bleeding, who have much less potential to benefit from prophylactic therapy.794 (Level of Evidence: C) See Online Data Supplement 31 for additional data regarding the clopidogrel PPI interaction. PPIs are often prescribed prophylactically when clopidogrel is started to prevent GI complications such as ulceration and bleeding due to DAPT.825 There is pharmacodynamic evidence that omeprazole interferes with clopidogrel metabolism,826,827 but there is no clear evidence implicating other PPIs. However, even with omeprazole, there are no convincing data supporting an important clinical drug drug interaction.826 The FDA com- munication about an ongoing safety review of clopidogrel advises that healthcare providers avoid the use of clopidogrel in patients with impaired CYP2C19 function due to known genetic variation or drugs that inhibit CYP2C19 activity. The FDA notes that there is no evidence that other drugs that reduce stomach acid, such as histamine-2 receptor antagonists (except cimeti- dine) or antacids, interfere with clopidogrel responsiveness. The COGENT (Clopidogrel and the Optimization of Gastrointestinal Events) trial randomized patients with DAPT to clopidogrel and omeprazole or clopidogrel and placebo, and while there was no difference in cardiovascular events between the 2 groups, GI events were halved in those randomized to omeprazole.828 It is reasonable to carefully evaluate the indication for PPI therapy in patients treated with clopidogrel, based on the presence or absence of the risk factors discussed above.794 The need for GI protection increases with the number of risk factors for bleeding. Prior upper GI bleeding is the strongest and most consistent risk factor for GI bleeding on antiplatelet therapy. Patients with ACS and prior upper GI bleeding are at substantial cardiovascular risk, so DAPT with concomitant use of a PPI may provide the optimal balance of risk and benefit. It should be noted that PPIs, by decreasing adverse GI effects related to clopidogrel, might decrease patients discontinuation of clopidogrel. In patients in whom there is a clear indication for PPI therapy, some clinicians may choose to use a PPI other than omeprazole. 6.1.2. Clopidogrel Genetic Testing: Recommendations Class IIb 1. Genetic testing might be considered to identify whether a patient at high risk for poor clinical outcomes is predisposed to inadequate platelet inhi- bition with clopidogrel.829 (Level of Evidence: C) 2. When a patient predisposed to inadequate platelet inhibition with clopidogrel is identified by genetic testing, treatment with an alternate P2Y12 inhibitor (eg, prasugrel or ticagrelor) might be considered.829 (Level of Evidence: C) Class III: NO BENEFIT 1. The routine clinical use of genetic testing to screen patients treated with clopidogrel who are undergoing PCI is not recommended.829 (Level of Evidence: C) On March 12, 2010, the FDA approved a new label for clopidogrel with a boxed warning about the diminished effectiveness of clopidogrel in patients with impaired ability to convert the drug into its active metabolite.829 Patients with decreased CYP2C19 function because of genetic polymor- phisms metabolize clopidogrel poorly and have higher rates of cardiovascular events after ACS and PCI than patients with Levine et al 2011 ACCF/AHA/SCAI PCI Guideline e615 normal CYP2C19 function. The warning also notes that tests are available to identify patients with genetic polymorphisms and that alternative treatment strategies should be considered for patients who are poor metabolizers. The clopidogrel boxed warning leaves the issue of whether to perform CYP2C19 testing up to the individual physician. It does not specifically require genetic testing or other changes in evaluation or treatment and does not imply that there are solid evidence-based reasons for such actions. Rather, it serves to inform clinicians of genetic variations in response to clopidogrel and to emphasize that clinicians should use this knowledge to make decisions about how to treat individual patients. At the present time, the evidence base is insufficient to recommend routine genetic testing in patients undergoing PCI. There may be a potential role for genetic testing for patients undergoing elective high-risk PCI procedures (eg, unprotected left main, bifurcating left main, or last patent coronary artery). 6.1.3. Platelet Function Testing: Recommendations Class IIb 1. Platelet function testing may be considered in pa- tients at high risk for poor clinical outcomes.829 (Level of Evidence: C) 2. In patients treated with clopidogrel with high plate- let reactivity, alternative agents, such as prasugrel or ticagrelor, might be considered.829 (Level of Evi- dence: C) Class III: NO BENEFIT 1. The routine clinical use of platelet function testing to screen patients treated with clopidogrel who are undergoing PCI is not recommended.829 (Level of Evidence: C) Platelet function testing to tailor antiplatelet therapy has received considerable interest. The GRAVITAS (Gauging Responsiveness With A VerifyNow Assay-Impact On Thrombosis And Safety) trial and several other ongoing trials test the concept that tailoring antiplatelet therapy based on platelet responsiveness assessed in an ex vivo P2Y12 assay will improve cardiovascular outcomes.830 In GRAVITAS, treatment with high-dose clopidogrel for 6 months in patients with high platelet reactivity on standard-dose clopidogrel was not beneficial. At the present time, the evidence base is insufficient to recommend routine platelet function testing. The results of 2 ongoing trials (DANTE [Dual Antiplatelet Therapy Tailored on the Extent of Platelet Inhibition] and ARCTIC [Double Randomization of a Monitoring Adjusted Antiplatelet Treatment Versus a Common Antiplatelet Treat- ment for DES Implantation, and Interruption Versus Contin- uation of Double Antiplatelet Therapy, One Year After Stenting]) will provide further information on the issue (www.clinicaltrials.gov). 6.2. Stent Thrombosis The majority of stent thrombosis occurs early (0 to 30 days after PCI). In broad clinical practice, the expected rate of early stent thrombosis is 1%, and beyond 30 days it is 0.2% to 0.6% per year.210,831 Acute stent thrombosis often presents as STEMI, and emergency revascularization is indicated. Acute stent thrombosis is associated with mortality rates of 20% to 45%.832 Survivors are also at risk of recurrent stent Mechanical and pharmacological factors are the most frequent cause of acute stent thrombosis. After the usual measures to restore flow in the infarct-related artery, it is important to consider the etiology of stent thrombosis as it pertains to further therapy and avoidance of recurrence. IVUS may identify factors such as an undersized stent, incomplete stent apposition, residual stenosis, or dissection and can guide subsequent treatment. The most common cause of acute stent thrombosis is nonadherence to DAPT; however, resistance to aspirin or thienopyridines and prothrombotic states such as congenital or acquired thrombophilic states (malignancy) are additional risk factors.834,835 Given the poor prognosis of stent thrombosis and the uncertainties surrounding treatment, the importance of pre- vention must be emphasized. This includes ensuring compli- ance with DAPT and adequate stent sizing and expansion.836 6.3. Restenosis: Recommendations Class I 1. Patients who develop clinical restenosis after balloon angioplasty should be treated with BMS or DES if anatomic factors are appropriate and if the patient is able to comply with and tolerate DAPT.837 (Level of Evidence: B) 2. Patients who develop clinical restenosis after BMS should be treated with DES if anatomic factors are appropriate and the patient is able to comply with and tolerate DAPT.838 840 (Level of Evidence: A) Class IIa 1. IVUS is reasonable to determine the mechanism of stent restenosis.495 (Level of Evidence: C) Class IIb 1. Patients who develop clinical restenosis after DES may be considered for repeat PCI with balloon angioplasty, BMS, or DES containing the same drug or an alternative antiproliferative drug if anatomic factors are appropriate and the patient is able to comply with and tolerate DAPT.495 (Level of Evi- dence: C) 6.3.1. Background and Incidence After balloon angioplasty, mechanisms contributing to reste- nosis include smooth muscle cell migration and proliferation, platelet deposition, thrombus formation, elastic recoil, and negative arterial remodeling. Stents block elastic recoil and negative remodeling, and the predominant mechanism for restenosis after stent implantation is neointimal hyperplasia. Restenosis rates vary, depending on whether angiographic restenosis (defined as 50% diameter stenosis at follow-up angiography) or clinical restenosis (symptomatic and requir- ing target-lesion revascularization or target-vessel revascular- ization) is measured, as well as on patient characteristics, coronary anatomy considerations, and device type (balloon angioplasty, BMS, or DES). The incidence of angiographic restenosis rates for uncomplicated lesions treated in RCTs ranges from 32% to 42% after balloon angioplasty463,464 and from 16% to 32% after BMS,463,464 and is generally 10% after DES.454,841 Less than half of patients with angiographic restenosis present with symptomatic, clinically relevant reste- nosis at 1-year follow-up, and a pooled analysis of 6186 patients from 6 trials of BMS showed target-lesion revascu- larization was performed in 12% and target-vessel revascu- larization in 14% at 1 year.842,843 Patients with clinical restenosis typically present with recurrent exertional angina, but 5% to 10% of patients present with acute MI and 25% Factors associated with an increased risk of restenosis in various models include clinical setting (STEMI, ACS, daily angina), patient characteristics (diabetes, age 55 to 60 years, prior PCI, male sex, multivessel CAD), lesion location (unprotected left main, SVG), and procedural characteristics (minimum stent diameter 2.5 mm, total stent length PCI strategies for treating restenosis after balloon angio- plasty, BMS, and DES are reviewed in the following sections. In addition to repeat PCI, intensified medical therapy or CABG are often also reasonable strategies, dependent on initial treatment (eg, balloon angioplasty, BMS), pattern of restenosis, likelihood of recurrent restenosis, ability to inten- sify medical therapy, suitability for CABG, and patient preference. Repeat PCI with BMS or DES is not appropriate if the patient is not able to comply with and tolerate DAPT. 6.3.2. Restenosis After Balloon Angioplasty For clinical restenosis after balloon angioplasty, stent implan- tation is superior to repeat balloon angioplasty or atheroab- lation devices. The REST (REstenosis STent) study showed that target-lesion revascularization rates were 10% for stent- treated patients and 27% for balloon-treated patients 6.3.3. Restenosis After BMS In-stent restenosis is classified according to these angio- graphic characteristics: Pattern I includes focal lesions 10 mm in length; Pattern II is in-stent restenosis 10 mm within the stent; Pattern III includes in-stent restenosis 10 mm extending outside the stent; and Pattern IV is totally occluded in-stent restenosis.847 Treatment of in-stent resteno- sis with balloon angioplasty, repeat BMS, or atheroablation devices for Patterns I to IV resulted in 1-year target-lesion tively. For clinical restenosis after BMS, repeat stenting with DES is preferred. Studies have demonstrated lower recurrent restenosis rates with DES compared with BMS or vascular 6.3.4. Restenosis After DES Clinical restenosis after placement of DES is becoming increasingly common due to the large numbers of patients who have been treated with DES. The predominant angio- graphic pattern for DES in-stent restenosis is focal ( 10 mm in length). Several biologic, mechanical, and technical factors may contribute to DES in-stent restenosis, including drug resistance, hypersensitivity, stent underexpansion, stent strut fracture, nonuniform stent strut coverage, gap in stent cover- age, and residual uncovered atherosclerotic lesion. IVUS might be considered to determine the cause for in-stent restenosis and help guide treatment strategy. Interventionists may treat focal DES restenosis with balloon angioplasty and treat nonfocal DES restenosis with BMS, CABG, or repeat DES with the same or an alternative antiproliferative drug.848,849 Small, observational cohort studies have demon- strated angiographic restenosis rates of 25% to 30% with repeat DES either with the same or an alternative drug.495,849,850 There are no RCTs, and the most appropriate treatment of restenosis of DES remains unknown. 6.4. Clinical Follow-Up At the time of discharge, patients are instructed to contact their physician or seek immediate medical attention if symp- toms recur. Most physicians will give the patient instructions on return to work and timing of return to full activities. The importance of strict compliance with aspirin and P2Y12 inhibitor therapy is ideally emphasized to the patient at the time of discharge and during follow-up visits. Secondary prevention measures after PCI are an essential part of long-term therapy, reducing both future morbidity and mortality associated with CAD, and are discussed in Section 6.5. A follow-up visit after PCI is usually scheduled to assess the patient s clinical status, the patient s compliance with secondary prevention therapies, and the success of secondary prevention measures (eg, blood pressure control, low-density lipoprotein levels, smoking cessation). Routine, periodic stress testing of asymptomatic patients is not considered part of standard patient follow-up. 6.4.1. Exercise Testing: Recommendations Class IIa 1. In patients entering a formal cardiac rehabilitation program after PCI, treadmill exercise testing is reasonable. (Level of Evidence: C) Class III: NO BENEFIT 1. Routine periodic stress testing of asymptomatic pa- tients after PCI without specific clinical indications should not be performed.795 (Level of Evidence: C) Treadmill exercise testing before cardiac rehabilitation pro- vides information about peak exercise capacity and heart rate, helping to stratify patients for the level of supervision during training, and seems reasonable for this purpose851; nuclear imaging to assess ischemia in this context usually adds little. The role of exercise testing to evaluate restenosis is much less certain. Although the presence of symptoms may not be a reliable means of detecting restenosis, there is no evidence that the detection of silent restenosis leads to improved outcome.852,853 Routine testing of all patients after PCI will also lead to many false-positive tests, particularly in the era of DES. As restenosis rates decline from 30% to 10%, the false-positive rate of stress imaging increases from 37% to 77%.854 A recent analysis of a national health insurance claims database and accompanying editorial find that stress testing after PCI is likely overused and rarely leads to repeat revascularization.855,856 In summary, there is no proven ben- Levine et al 2011 ACCF/AHA/SCAI PCI Guideline e617 efit or indication for routine periodic stress testing in patients after PCI, and, thus, it is not indicated.8,851 In cases in which there is a clear clinical indication for stress testing in a patient after PCI, exercise ECG alone is an insensitive predictor of restenosis857,858; therefore, stress imaging is the preferred stress test.8 In cases of recurrent angina after PCI in which the pretest likelihood of restenosis is high and repeat revascular- ization based on symptoms is likely indicated, most practi- tioners will proceed directly to cardiac catheterization rather than first obtain stress imaging. 6.4.2. Activity and Return to Work The timing of return to physical activity depends on the presenting condition as well as previous functional status. For STEMI, for example, daily walking is encouraged immedi- ately, and driving can begin within 1 week after uncompli- cated MI if allowed by local motor vehicle laws.859 Sexual activity usually can be resumed within days, provided exer- cise tolerance is adequate, normally assessed by the ability to climb a fiight of stairs.859 Similar recommendations have been issued for UA/NSTEMI.860 Patients with UA who have undergone successful revascularization and are otherwise doing well may return to physical activity on an accelerated schedule, usually within a few days.860 Return to work is more complex. Return to work rates after MI range from 63% to 94% and are confounded by factors such as job satisfaction, financial stability, and company policies.861 The physical demands and degree of stress of a particular job require that recommendations be individual- ized. In the PAMI-2 (Primary Angioplasty in Myocardial Infarction) trial, patients were encouraged to return to work 2 weeks after primary PCI for STEMI, and no adverse events were reported.862 In the RITA (Randomized Intervention Treatment of Angina) trial, revascularization with PCI led to earlier return to work compared with CABG, and subsequent employment rates were associated with relief of angina.105 Many practitioners use graded exercise treadmill testing to determine the safety of activity and return to work by measuring the metabolic equivalent of task (MET) level achieved and comparing that level to energy levels required to perform different activities.863 6.4.3. Cardiac Rehabilitation: Recommendation Class I 1. Medically supervised exercise programs (cardiac rehabilitation) should be recommended to patients after PCI, particularly for moderate- to high-risk patients for whom supervised exercise training is warranted.796 804 (Level of Evidence: A) Participation in cardiac rehabilitation is associated with sig- nificant reductions in all-cause mortality (OR: 0.80, 95% CI: 0.68 to 0.93) and cardiac mortality.796,797 Reports from community-based surveys, which in general enroll older and higher-risk patients than clinical trials, have confirmed that participation in comprehensive rehabilitation is indepen- dently associated with a reduction in recurrent MI and reduced mortality.799 Cardiac rehabilitation is also associated with improvements in exercise tolerance, cardiac symptoms, lipid levels, cigarette smoking cessation rates (in conjunction with a smoking cessation program), stress levels, improved medical regimen compliance, and improved psychosocial well- being.800 Cardiac rehabilitation is cost-effective as well.864 Phy- sician referral may be the most powerful predictor of patient participation in a cardiac rehabilitation program.865 6.5. Secondary Prevention The treatment of the patient does not end with PCI; secondary prevention measures are a critical component of patient management. Important secondary prevention measures were presented in detail in the 2006 AHA/ACC Guidelines for Secondary Prevention for Patients With Coronary and Other Atherosclerotic Vascular Disease 562 and have recently been updated in the AHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease: 2011 Update. 805 The reader is referred to this document for detailed discussions of secondary prevention. Among the important recommendations are the following: Lipid management with lifestyle modification (Class I; Level of Evidence: B)805 807 and statin therapy are recommended. (Level of Evidence: A)344,806,808 810,810a An adequate statin dose should be employed which reduces low-density lipoprotein cholesterol to 100 mg/dL AND achieves at least a 30% lowering of low-density lipoprotein cholesterol. (Class I; Level of Evidence: C)806 810,810a It is reasonable to treat patients with statin therapy which lowers low-density lipoprotein cholesterol to 70 mg/dL in very high risk* patients. (Class IIa; Level of Evidence: C)345,808 810,810a,811,812 Patients who have triglycerides 200 mg/dL should be treated with statins to lower non high-density lipoprotein cholesterol to 130 mg/dL. (Class I; Level of Evidence: B)344,809,810,866 In patients who are very high risk* and have triglycerides 200 mg/dL, a non high-density lipoprotein cholesterol goal of 100 mg/dL is reasonable. (Class IIa; Level of Evidence: C)344,809,810,866 Blood pressure control with lifestyle modification (Class I; Level of Evidence: B)813 817 and pharmacotherapy (Class I; Level of Evidence: A),805,813,818,819 with the goal of blood pressure 140/90 mm Hg. Diabetes management (eg, lifestyle modification and pharmacotherapy), coordinated with the patient s pri- mary care physician and/or endocrinologist. (Class I; Level of Evidence: C)805 Advising patients on the need for complete smoking cessation. (Class I; Level of Evidence: A)805,820 823 7. Quality and Performance Considerations 7.1. Quality and Performance: Recommendations Class I 1. Every PCI program should operate a quality- improvement program that routinely 1) reviews Presence of established cardiovascular disease plus 1) multiple major risk factors (especially diabetes), 2) severe and poorly controlled risk factors (especially continued cigarette smoking), 3) multiple risk factors of the metabolic syndrome (especially high triglycerides 200 mg/dL plus non high-density lipoprotein cholesterol 130 mg/dL with low high-density lipoprotein cholesterol [ 40 mg/dL]), and 4) acute coronary syndromes. quality and outcomes of the entire program; 2) reviews results of individual operators; 3) includes risk adjustment; 4) provides peer review of difficult or complicated cases; and 5) performs random case reviews. (Level of Evidence: C) 2. Every PCI program should participate in a regional or national PCI registry for the purpose of bench- marking its outcomes against current national norms. (Level of Evidence: C) PCI quality and performance considerations are defined by attributes related to structure, processes, and risk-adjusted outcomes. Structural attributes include elements such as equipment, supplies, staffing, institutional and operator-level volumes, and the availability of electronic medical records. Processes include strategies for the appropriate patient, pro- tocols for pre- and postprocedural care, appropriate proce- dural execution and management of complications, and par- ticipation in databases and registries for benchmarking performance of the program and individual operator. Risk- adjusted outcomes are the end result of these structures and processes of care, and when available are more reliable measures of quality than the institutional and individual operator volumes discussed in Section 7.4. PCI process and outcomes assessments can be used for internal quality-improvement efforts and public reporting. Public reporting of institutional risk-adjusted outcomes is becoming more common. Although operator-level outcomes can be assessed and risk adjusted, the results are much less reliable due to lack of statistical power resulting from lower volumes. Any public reporting must use statistical methods that meet the high criteria established by the AHA Work The cognitive knowledge and technical skill required to perform PCI continue to grow. Details on the training required for interventional cardiology are found in the most recent ACCF Core Cardiology Training Statement.868 7.3. Certification and Maintenance of Certification: Recommendation Class IIa 1. It is reasonable for all physicians who perform PCI to participate in the American Board of Internal Medicine interventional cardiology board certifica- tion and maintenance of certification program. (Level of Evidence: C) The American Board of Internal Medicine established inter- ventional cardiology board certification in 1999 as an added qualification to the cardiovascular disease board certifica- tion. Since 1990 all certificates from the American Board of Internal Medicine are time limited for a 10-year period and require all diplomats to participate in maintenance of certifi- cation to maintain their board-certified status. Maintenance of certification in interventional cardiology requires physicians to document a minimum of 150 interventional cases over the 2 years before expiration of the current certification, complete self-assessment modules of their medical knowledge, partic- ipate in practice-based quality-improvement activities, and pass a secure, knowledge-based examination.869 871 For those who cannot meet the case volume requirement, an alternative option is to submit a log of 25 consecutive cases including patient characteristics and procedural outcomes. The mainte- nance of certification process is likely to change, as the American Board of Internal Medicine intends to evolve maintenance of certification from an episodic event that occurs once every 10 years to a more continuous process of continuous professional development. 7.4. Operator and Institutional Competency and Volume: Recommendations Class I 1. Elective/urgent PCI should be performed by opera- tors with an acceptable annual volume (>75 proce- dures) at high-volume centers (>400 procedures) with on-site cardiac surgery.872,873 (Level of Evi- dence: C) 2. Elective/urgent PCI should be performed by opera- tors and institutions whose current risk-adjusted outcomes statistics are comparable to those reported in contemporary national data registries. (Level of Evidence: C) 3. Primary PCI for STEMI should be performed by experienced operators who perform more than 75 elective PCI procedures per year and, ideally, at least 11 PCI procedures for STEMI per year. Ide- ally, these procedures should be performed in insti- tutions that perform more than 400 elective PCIs per year and more than 36 primary PCI procedures for STEMI per year.872,874 877 (Level of Evidence: C) Class IIa 1. It is reasonable that operators with acceptable vol- ume (>75 PCI procedures per year) perform elec- tive/urgent PCI at low-volume centers (200 to 400 PCI procedures per year) with on-site cardiac sur- gery.872 (Level of Evidence: C) 2. It is reasonable that low-volume operators (<75 PCI procedures per year) perform elective/urgent PCI at high-volume centers (>400 PCI procedures per year) with on-site cardiac surgery. Ideally, operators with an annual procedure volume of fewer than 75 procedures per year should only work at institutions with an activity level of more than 600 procedures per year. Operators who perform fewer than 75 procedures per year should develop a defined men- toring relationship with a highly experienced oper- ator who has an annual procedural volume of at least 150 procedures per year. (Level of Evidence: C) Class IIb 1. The benefit of primary PCI for STEMI patients eligible for fibrinolysis when performed by an oper- ator who performs fewer than 75 procedures per year (<11 PCIs for STEMI per year) is not well established. (Level of Evidence: C) Levine et al 2011 ACCF/AHA/SCAI PCI Guideline e619 Class III: NO BENEFIT 1. It is not recommended that elective/urgent PCI be performed by low-volume operators (<75 proce- dures per year) at low-volume centers (200 to 400 procedures per year) with or without on-site cardiac surgery. An institution with a volume of fewer than 200 procedures per year, unless in a region that is underserved because of geography, should carefully consider whether it should continue to offer this service.872 (Level of Evidence: C) Older observational evidence supported a volume-outcome relationship in PCI at both the institutional and operator level.873 However, this relationship is complicated and may be inconsistent across low-volume institutions or operators. More recent data on primary PCI suggest that operator experience may modify the volume-outcome relationship at the institutional level.876,878 Risk-adjusted outcomes remain preferable to institutional and individual operator volumes as quality measures. Operator and hospital volume recommendations have been carried over from the 2005 PCI guideline. However, the writing committee recognizes that these volume recommen- dations are controversial. In addition, after extensive review of all relevant data, the writing committee believes that the LOE in support of all the above recommendations is best categorized as LOE C rather than LOE B as it has been in prior guidelines for some recommendations. We encourage the ACCF/AHA/ACP Clinical Competence and Training writing group for PCI and other expert writing groups to review this issue so that new recommendations can be considered by the next PCI guideline writing committee. 7.5. Participation in ACC NCDR or National Quality Database Assessment of PCI quality and outcomes is important both at the level of the entire program and at the level of the individual physician. This requires collection of clinical and procedural data for PCI that allows regular comparison of risk-adjusted outcomes and complications with national benchmarks. The ACC NCDR CathPCI Registry is an exam- ple of a national registry to fulfill the goals of assessing and benchmarking quality and outcomes. 8. Future Challenges Although this latest guideline reflects significant advance- ments in the field of PCI, there remain future challenges to the formulation and updating of guidelines for PCI. The proliferation of studies comparing the many newer drugs and devices with older therapies (or other newer therapies), often using different or novel study endpoints, endpoint definitions, and noninferiority designs, pose increasing challenges to objectively evaluating newer therapies and generating recom- mendations for their use. Numerous potential advances in the field of PCI, including intracoronary stem cell infusions for chronic and acute ischemic heart disease, designer drugs, novel intracoronary imaging technologies such as optical coherence tomography and virtual histology, new stent com- position and designs (eg, drug-eluting, biodegradable, bifur- cation), and drug-eluting balloons were considered for formal evaluation by the current writing committee, but it was thought that there were insufficient data at present to formu- late any formal recommendations on these topics. These and other emerging technologies and treatments will need to be addressed in future PCI guidelines. Finally, with this proliferation of new technology, the amount of data generated in the evaluation of these potential therapeutic advances will grow dramatically, adding signifi- cant challenges to future guideline generations. Of note, the Web site www.clinicaltrials.gov currently lists several hun- dred PCI-related clinical trials. Staff American College of Cardiology Foundation David R. Holmes, Jr, MD, FACC, President John C. Lewin, MD, Chief Executive Officer Janet Wright, MD, FACC, Senior Vice President, Science and Quality Charlene May, Senior Director, Science and Clinical Policy Erin A. Barrett, MPS, Senior Specialist, Science and Clinical Policy American College of Cardiology Foundation/American Heart Association Lisa Bradfield, CAE, Director, Science and Clinical Policy Sue Keller, BSN, MPH, Senior Specialist, Evidence-Based Medicine Jesse M. Welsh, Specialist, Science and Clinical Policy Debjani Mukherjee, MPH, Associate Director, Evidence- Based Medicine American Heart Association Ralph L. Sacco, MS, MD, FAAN, FAHA, President Nancy Brown, Chief Executive Officer Rose Marie Robertson, MD, FAHA, Chief Science Officer Gayle R. 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