Percutaneous Coronary Intervention

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Chapter 20

Percutaneous Coronary Intervention

1. What does the term percutaneous coronary intervention mean?

    Percutaneous coronary intervention (PCI) is a common term used to describe both percutaneous transluminal coronary angioplasty (PTCA), which implies the use of balloon angioplasty but not stenting, and coronary stent placement. The first successful balloon angioplasty procedure in humans was performed by Dr. Andreas Gruentzig in 1977. Since then, there has been tremendous development in the field of interventional cardiology. The development of coronary stents was a major boost to interventional cardiology, addressing many of the complications and limitations associated with balloon angioplasty. Eighty percent of the PCIs performed currently involve stent placement. PCI has become one of the most commonly performed medical procedures in the United States, with more than about 600,000 procedures performed annually. PCI is performed for coronary revascularization in patients with stable coronary disease, as well as those with acute coronary syndromes (ACS) in the appropriate clinical settings.

2. Which patients with chronic stable angina benefit from PCI?

    The goals of treatment in patients with coronary artery disease are to:

Multiple clinical trials of PCI plus medical therapy or medical therapy alone involving patients with chronic stable angina over the last two decades have consistently shown improvement in angina, exercise duration, and quality of life with PCI. However, they have not demonstrated any difference in death and MI between treatment with PCI plus medical therapy compared to medical therapy alone. In contrast, the use of PCI in patients with ACS has been shown to decrease recurrent ischemia, nonfatal MI, and death.

In general, patients with chronic stable angina in whom PCI should be considered are those with symptom-limiting angina, one or more significant coronary arteries stenoses, a high likelihood of technical success, and a low risk of complications.

In patients with 3-vessel coronary artery disease (CAD), particularly if they have complex and/or extensive CAD (reflected in a high SYNTAX score or diabetes), bypass surgery is generally preferred over multivessel PCI. Unprotected left main PCI can be considered in those with a stenosis that has a high likelihood of procedural success and long-term durability, especially in cases in which the patient is at high risk for surgery (reflected by a high Society of Thoracic Surgeons [STS] risk score).

3. Which patients with unstable angina/non–ST elevation myocardial infarction (UA/NSTEMI) should undergo a strategy of early cardiac catheterization and revascularization?

    Two major strategies, conservative (medical therapy without an initial strategy of catheterization and revascularization) and early invasive, are employed in treating patients with UA/NSTEMI. The early invasive approach involves performing diagnostic angiography with intent to perform PCI along with administering the usual antiischemic, antiplatelet, and anticoagulant medications. Evidence from clinical trials suggests that an early invasive approach with UA/NSTEMI leads to a reduction in adverse cardiovascular outcomes, such as death and nonfatal MI, especially in high-risk patients. Several risk-assessment tools are available that assign a score based upon the patient’s clinical characteristics (e.g., TIMI and GRACE scores). Patients who present with UA/NSTEMI should be risk stratified to identify those who would benefit most from an early invasive approach. Patients with the following clinical characteristics indicative of high risk should be taken for early coronary angiography with intent to perform revascularization:

Initially stabilized patients without the above risk factors (low-risk patients) may be treated with an initial conservative (or selective invasive) strategy. An early invasive approach should not be undertaken in patients with extensive comorbidities, organ failure, or advanced cancer, in which the risk of revascularization is greater than the benefit, or in patients who do not consent to the procedure.

4. What are the contraindications to PCI and the predictors of adverse outcomes?

    The only absolute contraindication to PCI is lack of any vascular access or active severe bleeding, which precludes the use of anticoagulation and antiplatelet agents. Relative contraindications include the following:

Patients generally should not undergo PCI if the following conditions are present:

Clinical predictors of poor outcomes include older age, an unstable condition (ACS, acute MI, decompensated CHF, cardiogenic shock), LV dysfunction, multivessel coronary disease, diabetes mellitus, renal insufficiency, small body size, and peripheral artery disease.

Angiographic predictors of poor outcomes include the presence of thrombus, degenerated bypass graft, unprotected left main disease, long lesions (more than 20 mm), excessive tortuosity of proximal segment, extremely angulated lesions (more than 90 degrees), a bifurcation lesion with involvement of major side branches, or chronic total occlusion.

5. What are the major complications related to PCI?

    The incidence of major complications has constantly decreased over the last two decades as a result of the use of activated clotting time to measure degree of anticoagulation, better antithrombotic and antiplatelet agents, advanced device technology, more skilled operators, and superior PCI strategies. These factors have particularly lowered the incidence of MI and the need for emergent CABG. Major complications of PCI include the following:

Death: The overall in-hospital mortality rate is 1.27% ranging from 0.65% in elective PCI to 4.81% in ST elevation myocardial infarction (STEMI) (based on the National Cardiac Data Registry [NCDR] CathPCI database of patients undergoing PCI between 2004 and 2007).

MI: The incidence of PCI-related MI is 0.4% to 4.9%; the incidence varies depending on the acuity of symptoms, lesion morphology, definition of MI, and frequency of measurement of biomarkers.

Stroke: The incidence of PCI-related stroke is 0.22%. In-hospital mortality in patients with PCI-related stroke is 25% to 30% (based on a contemporary analysis from the NCDR).

Emergency CABG: The need to perform emergency CABG in the stent era is extremely low (between 0.1% and 0.4%).

Vascular complications: The incidence of vascular complications ranges from 2% to 6%. These include access-site hematoma, retroperitoneal hematoma, pseudoaneurysm, arteriovenous fistula, and arterial dissection. In randomized trials, closure devices were only beneficial in reducing time to hemostasis but did not reduce the incidence of vascular complications.

Radial artery access complications: There is significant reduction of vascular complications with the use of radial arterial access as compared to femoral artery access. Complications include loss of the radial pulse in fewer than 5% of cases, compartment syndrome, pseudoaneurysm in fewer than 0.01% of cases, sterile abscess, and radial artery spasm.

Other complications associated with PCI: Other complications include transient ischemic attack (TIA), renal insufficiency, and anaphylactoid reactions to contrast agents.

6. When should cardiac biomarkers be assessed in patients undergoing PCI?

    The American College of Cardiology/American Heart Association (ACC/AHA) guidelines recommend measuring the myocardium-associated isozyme of creatine kinase (CK-MB), or troponin I or T in all patients who have signs or symptoms suggestive of MI during or after PCI, and in those who undergo complicated procedures. Currently, there are no compelling data to support routinely measuring cardiac biomarkers for all PCI procedures.

7. What is abrupt vessel closure?

    Abrupt vessel closure is when the artery becomes completely occluded within hours of the PCI procedure. This can be due to stent thrombosis, dissection flap, vessel spasm, or side-branch occlusion. The incidence has decreased to less than 1% in the modern era of stents and antiplatelet therapies.

8. What is stent thrombosis?

    Stent thrombosis is when there is complete occlusion of the artery due to thrombus formation in the stent. This may occur in the first 24 hours after stent deployment (acute stent thrombosis); in the first month after implantation (subacute stent thrombosis); between 1 and 12 months after implantation (late stent thrombosis); or even more than 1 year after implantation, most notably after drug-eluting stent (DES) implantation (very late stent thrombosis). Most instances of stent thrombosis occur in the first thirty days after implantation, at a rate of less than 1% per year. Beyond 30 days, the incidence is 0.2% to 0.6% per year depending on patient characteristics and type of stent used. Stent thrombosis is a potentially catastrophic event and often presents as STEMI, requiring emergency revascularization. Stent thrombosis carries a mortality rate of 20% to 45%. The primary factors contributing to stent thrombosis are inadequate stent deployment, incomplete stent apposition, residual stenosis, unrecognized dissection impairing blood flow, and noncompliance with dual antiplatelet therapy (DAPT). Noncompliance to DAPT is the most common cause of stent thrombosis. Resistance to aspirin and clopidogrel, and hypercoagulable states, such as those associated with malignancy, are additional, less common causes of stent thrombosis.

9. What do the terms slow-flow and no-reflow mean?

    Slow-flow is the term applied when contrast agent injection of the coronary artery reveals delayed clearing of the contrast down the coronary artery; no-reflow is the more extreme form, when the contrast does not appear to flow down the coronary artery at all. These entities are caused by vasospasm, distal embolization, and microvascular plugging resulting in impaired epicardial blood flow, quantified as abnormal TIMI frame rates and myocardial blush scores. It occurs more commonly in the setting of atherectomy, thrombus, or degenerated saphenous vein graft (SVG) PCI. Another form of no-reflow is seen when reperfusion in the infarct-related artery is suboptimal. The etiology includes myocardial edema and endothelial injury, in addition to vasospasm and embolization.

10. Are bleeding complications related to PCI clinically important?

    A bleeding complication is an independent predictor of early and late mortality in patients undergoing elective or urgent PCI. The potential for bleeding complications is always present, due to the routine use of potent antithrombin and antiplatelet agents during PCI. Bleeding can adversely affect a patient, not only due to ensuing severe anemia, but also due to the potential of ischemic events when anticoagulation is reversed. Additionally, accumulating data suggest a possible direct link between blood transfusion and poor outcomes. Proinflammatory and prothrombotic effects of red blood cell transfusion have been demonstrated. Use of a restrictive transfusion policy has been associated with improved outcomes.

    Factors contributing towards the risk of bleeding include advanced age, low body mass index, renal insufficiency, anemia at baseline, difficult vascular access, site and condition of access vessel, sheath size, and degree of anticoagulation and platelet inhibition. Measures to reduce the bleeding complications include using weight-based anticoagulation regimens, frequent assessment of anticoagulation status to prevent over-anticoagulation, use of bivalirudin, and adjustment of the dosing of certain medications when chronic kidney disease is present. Use of the radial access may also decrease bleeding complications.

11. What are the important complications that can occur at the access site?

    Potential complications of vascular access include retroperitoneal bleeding, pseudoaneurysm, arteriovenous fistula, arterial dissection, thrombosis, distal artery embolization, groin hematoma, infection and/or abscess, and femoral neuropathy. Risk factors for access-site complications include older age, female gender, morbid obesity or low body weight, hypertension, low platelet count, peripheral artery disease, larger sheath size, prolonged sheath time, intraaortic balloon pump use, concomitant venous sheath, over-anticoagulation, thrombolytic therapy use, and repeat intervention. Patients with a femoral puncture site above the most inferior border of the inferior epigastric artery are at an increased risk for retroperitoneal bleeding. Conversely, development of pseudoaneurysm and arteriovenous fistula are associated with a puncture site at or below the level of the femoral bifurcation.

    Arteriotomy closure devices (vascular closure devices) have emerged as an alternative to mechanical compression for achieving rapid vascular hemostasis. These devices are categorized based on the principle mechanism of hemostasis, which includes biodegradable plug, suture, or staples. Although arteriotomy closure devices offer advantages over mechanical compression (shorter time to hemostasis and patient ambulation, high rate of patient satisfaction, and greater cost effectiveness), no prospective randomized study has been able to show a clear-cut reduction in vascular complications with these devices.

12. What are some treatment options for various vascular complications?

Pseudoaneurysm: For small pseudoaneurysms, observation is recommended. For larger pseudoaneurysms, ultrasound-guided compression or percutaneous thrombin injection under ultrasound guidance is the treatment of choice. For pseudoaneurysms with a large neck, simultaneous balloon inflation to occlude the entry site can be helpful. In cases of thrombin failure, surgical repair should be considered. Endovascular repair with stent-graft implantation can also be used in the treatment of pseudoaneurysms.

Arteriovenous fistula: For small arteriovenous fistulae, observation is recommended; most close spontaneously or remain stable. For a large fistula or when significant shunting is present, options include ultrasound-guided compression, covered stent, or surgical repair.

Dissection: If there is no effect on blood flow, a conservative approach is indicated. In the presence of flow impairment (distal limb ischemia), angioplasty, stenting, and surgical repair are the treatment options.

Retroperitoneal bleeding: This should always be suspected with unexplained hypotension, marked decrease in hematocrit, flank/abdominal or back pain, and high arterial sticks. Treatment includes intravascular volume replacement, reversal of anticoagulation, blood transfusion, and, occasionally, vasopressor agents and monitoring in the intensive care unit with serial hemoglobin and hematocrit checks. Endovascular management with covered stents, prolonged balloon inflation, or surgical repair are options, but are rarely necessary.

13. What is contrast nephropathy?

    Contrast nephropathy is a worsening in renal function, as assessed by creatinine levels, due to administration of intravascular iodinated contrast agent, such as is used during cardiac catheterization and PCI. Contrast nephropathy usually first manifests clinically 48 hours after contrast administration, and peaks approximately 5 days after contrast administration. Contrast-induced nephropathy (CIN) has been associated with increased mortality and morbidity. Several predisposing factors for CIN have been identified, including chronic renal insufficiency (the risk of CIN is directly proportional to the severity of preexisting renal insufficiency), diabetes, CHF, intravascular volume depletion, multiple myeloma, and the use of a large volume of contrast. The most widely accepted measure to prevent CIN consists of assuring adequate hydration with isotonic saline (such as 1.0 to 1.5 mL/kg/hr for 3 to 12 hours before and continuing for 6 to 24 hours after the procedure). In patients with creatinine clearance of less than 60 mL/min, contrast volume should be kept to a minimum and adequate intravenous hydration initiated. Diuretics, nonsteroidal antiinflammatory agents, and other nephrotoxic drugs should be held before PCI.

    Both a recent meta-analysis and a recent large randomized trial assessing the efficacy of N-acetylcysteine for CIN found no benefit with N-acetylcysteine administration. Based upon these data, the 2011 ACC/AHA guidelines on PCI do not recommend the use of N-acetylcysteine for prevention of CIN, giving it a “class III–no benefit” indication. Studies of administration of bicarbonate or hemofiltration (ultrafiltration) have produced conflicting results.

14. What is restenosis?

    Restenosis is the process by which the treated stenosis in a coronary artery recurs over time. Restenosis usually clinically manifests itself over the 1 to 6 month period after PCI. Patients with restenosis present most commonly with exertional angina and less frequently with unstable angina or MI. The process of restenosis is driven by the following mechanisms:

Restenosis occurs more commonly in patients with diabetes, renal insufficiency, ostial, bifurcation or SVG locations, small vessels (less than 2.5 mm diameter), and long lesions (longer than 40 mm).

Angiographic restenosis rates after balloon PTCA range from 32% to 42%, based upon randomized controlled trials, and approximately half of these patients with restenosis require clinically driven repeat target lesion revascularization within the first year.

Coronary stents prevent vessel elastic recoil and negative remodeling, and significantly reduce both angiographic and clinical restenosis rates. The main factor leading to restenosis in coronary arteries treated with bare metal stents (BMS) is neointimal hyperplasia as a result of smooth muscle cell proliferation and extracellular matrix production. Angiographic restenosis rates with BMS range from 16% to 32% with a target lesion revascularization rate of 12% and target-vessel revascularization rate of 14% at 1 year. Similar to PTCA, restenosis after BMS typically occurs within the first 6 months.

Drug-eluting stents (DES) are coated with a polymer that contains antirestenotic (antiproliferative) medication that is slowly released over a period of weeks. Restenosis after DES ranges from 5% to 10%, depending on the type of DES, stent size, length, lesion morphology, and presence of diabetes. Compared with BMS, DES significantly reduce the rates of target lesion revascularization (approximately 6.2% versus 16.6%), without any effect on all-cause mortality.

Options to treat restenosis include aggressive medical therapy, repeat PCI and CABG. Patient factors such as compliance with DAPT, the type of intervention (PTCA, BMS, or DES) initially performed, chances of recurrence of restenosis, and appropriateness of CABG should be considered when addressing restenotic lesions. For restenosis after PTCA, stent placement is recommended; for restenosis after BMS, repeat stenting with DES is the preferred treatment. For DES restenosis, there is a lack of robust clinical data for the most appropriate therapy. In current interventional practice, focal DES restenosis is treated mostly by PTCA. For diffuse DES restenosis, repeat DES placement, and CABG can be considered, taking into account patient and angiographic characteristics.

15. What are the recommendations regarding antiplatelet therapy after PCI?

    Patients undergoing PCI should receive dual antiplatelet therapy with aspirin and a P2Y12 inhibitor. The duration of antiplatelet therapy depends upon the type (PTCA, BMS or DES) and setting (elective vs. ACS) of intervention performed.

    Recommendations for aspirin:

Recommendations for P2Y12 receptor inhibitors:

image A loading dose of a P2Y12 inhibitor should be given prior to PCI with stent placement. The loading doses for the three recommended drugs are clopidogrel 600 mg, prasugrel 60 mg, and ticagrelor 180 mg.

image Following a loading dose of a P2Y12 inhibitor, a maintenance dose is continued. The recommendations for dose and duration are as follows:

Prior to PCI, the ability of the patient to comply with DAPT should be assessed and therapy tailored accordingly.

16. What steps should be taken to prevent premature discontinuation of dual antiplatelet therapy?

    Although stent thrombosis most commonly occurs in the first month after stent implantation, numerous cases of late stent thrombosis (1 month to 1 year) or even very late stent thrombosis (after 1 year) have been reported, particularly in patients who have been treated with DES.

    Premature discontinuation of antiplatelet therapy markedly increases the risk of stent thrombosis, and with this, MI or death. Factors contributing to premature cessation of P2Y12 therapy include drug cost, inadequate patient and health care provider understanding about the importance of continuing therapy, and requests to discontinue therapy before noncardiac procedures.

    To eliminate premature discontinuation of P2Y12 therapy, the following recommendations should be followed:

image Patients should be clearly educated about the rationale for not stopping antiplatelet therapy and the potential consequences of stopping such therapy. Each should be instructed to call their cardiologist if bleeding develops or if another physician advises them to stop antiplatelet therapy.

image Health care providers who perform invasive or surgical procedures and are concerned about periprocedural bleeding must be made aware of the potentially catastrophic risks of premature discontinuation of P2Y12 therapy. The professionals who perform these procedures should contact the patient’s cardiologist to discuss optimal patient management strategy.

image Any elective procedure for which there is significant risk of perioperative bleeding should be deferred until patients have completed an appropriate course of P2Y12 therapy (12 months after DES implantation if they are not at high risk of bleeding, and a minimum of 1 month for BMS implantation).

image For patients treated with DES who are to undergo procedures that mandate discontinuation of P2Y12 therapy, aspirin should be continued if at all possible, and thienopyridine restarted as soon as possible after the procedure.

17. What should be the management of a patient with a DES who requires urgent noncardiac surgery?

    If at all possible, elective surgery should be avoided until the patient has received a minimum of 1 year of dual antiplatelet therapy after DES. Aspirin should not be discontinued in the perioperative period unless a significant bleeding situation arises (and continuation of P2Y12 therapy is also preferred). Use of heparin or short-acting GP IIb/IIIa inhibitors is not routinely recommended in patients being withdrawn from P2Y12 therapy, because of lack of evidence and concern for rebound platelet hyperactivity, especially in absence of aspirin, with or without clopidogrel treatment.

    Surgery should be performed in an institution with 24-hour catheterization laboratory availability, in case of stent thrombosis; emergency PCI is strongly preferred over thrombolysis in cases of stent thrombosis, and thrombolytic therapy is contraindicated in patients with recent surgery.

Bibliography, Suggested Readings, and Websites

1. Investigators, A.C.T. Acetylcysteine for prevention of renal outcomes in patients undergoing coronary and peripheral vascular angiography. main results from the randomized Acetylcysteine for Contrast-Induced Nephropathy Trial (ACT). Circulation. 2011;124:1250–1259.

2. Anderson, J.L., Adams, C.D., Antman, E.M., et al. ACCF/AHA Focused Update Incorporated Into the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011;123:e426–e579. 2011

3. Bavry, A.A., Kumbhani, D.J., Rassi, A.N., Bhatt, D.L., Askari, A.T. Benefit of early invasive therapy in acute coronary syndromes a meta-analysis of contemporary randomized clinical trials. J Am Coll Cardiol. 2006;48:1319–1325.

4. Boden, W.E., O’Rourke, R.A., Teo, K.K., et al. Optimal medical therapy with or without PCI for stable coronary disease. N Engl J Med. 2007;356:1503–1516.

5. Gonzales, D.A., Norsworthy, K.J., Kern, S.J., et al. A meta-analysis of N-acetylcysteine in contrast-induced nephrotoxicity: unsupervised clustering to resolve heterogeneity. BMC Med. 2007;5:32.

6. Grines, C.L., Bonow, R.O., Casey, D.E., et al. Prevention of premature discontinuation of dual antiplatelet therapy in patients with coronary artery stents. J Am Coll Cardiol. 2007;49:734–739.

7. Keeley, E.C., Boura, J.A., Grines, C.L. Comparison of primary and facilitated percutaneous coronary interventions for ST-elevation myocardial infarction: quantitative review of randomised trials. Lancet. 2006;367:579–588.

8. Levine, G.N., Bates, E.R., Blankenship, J.C., et al. ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. J Am Coll Cardiol. 2011;58:e44–e122.

9. Levine, G.N., Kern, M.J., Berger, P.B., et al. For the American Heart Association Diagnostic and Interventional Cardiac Catheterization Committee: management of patients undergoing percutaneous coronary revascularization. Ann Intern Med. 2003;139:123–136.

10. Patel, M.R., Dehmer, G.J., Hirshfeld, J.W., Smith, P.K., Spertus, J.A. ACCF/SCAI/STS/AATS/AHA/ASNC/HFSA/SCCT 2012 Appropriate use criteria for coronary revascularization focused update: a report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, Society for Cardiovascular Angiography and Interventions, Society of Thoracic Surgeons, American Association for Thoracic Surgery, American Heart Association, American Society of Nuclear Cardiology, and the Society of Cardiovascular Computed Tomography. J Am Coll Cardiol. 2012;59:857–881.

11. Shaw, L.J., Berman, D.S., Maron, D.J., et al. Optimal Medical Therapy With or Without Percutaneous Coronary Intervention to Reduce Ischemic Burden Results From the Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) Trial Nuclear Substudy. Circulation. 2008;117:1283–1291.

12. Serruys, P.W., Morice, M.C., Kappetein, A.P., et al. Percutaneous Coronary Intervention versus Coronary-Artery Bypass Grafting for Severe Coronary Artery Disease. N Engl J Med. 2009;360:961–972.

13. Stergiopoulos, K., Brown, D.L. Initial coronary stent implantation with medical therapy vs medical therapy alone for stable coronary artery disease: meta-analysis of randomized controlled trials. Arch Intern Med. 2012;172:312–319.

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