Your activity: 20 p.v.
your limit has been reached. plz Donate us to allow your ip full access, Email: sshnevis@outlook.com

Percutaneous coronary intervention with intracoronary stents: Overview

Percutaneous coronary intervention with intracoronary stents: Overview
Authors:
J Dawn Abbott, MD, FACC
Donald Cutlip, MD
Section Editor:
Stephan Windecker, MD
Deputy Editor:
Nisha Parikh, MD, MPH
Literature review current through: Nov 2022. | This topic last updated: Jun 03, 2020.

INTRODUCTION — Percutaneous coronary intervention (PCI) is a minimally invasive nonsurgical procedure performed to improve blood flow in one or more segments of the coronary circulation. Coronary revascularization with PCI primarily involves the use of balloon angioplasty and intracoronary stenting with either drug-eluting stents (DES) or bare metal stents (BMS); other tools to improve coronary blood flow include atherectomy and radiation.

DES reduce the rate of restenosis and (accordingly) target lesion revascularization compared with BMS, which are no longer commonly used. The majority of DES consist of a metallic alloy stent, a polymer coating (which may be durable or bioabsorbable), and an antirestenotic drug that is mixed within the polymer and is released over a period of weeks to months after implantation to reduce the local proliferative healing response. DES types currently approved in the United States for use in the coronary circulation are shown in a table (table 1).

This topic will present an overview of the use of stents and DES in particular, including issues related to stent deployment, periprocedural medication use, and a few procedural and safety issues. Other relevant topics include:

(See "Drug-eluting intracoronary stents: Stent types".)

(See "Periprocedural complications of percutaneous coronary intervention".)

(See "Bioresorbable scaffold coronary artery stents".)

(See "Specialized revascularization devices in the management of coronary heart disease".)

(See "Antithrombotic therapy for elective percutaneous coronary intervention: General use".)

BENEFITS OF STENTING — Late lumen loss and restenosis after non-stent interventions such as balloon angioplasty are caused by a combination of acute recoil, negative remodeling (arterial contraction) of the treated segment, and local neointimal hyperplasia (growth of tissue into the stent). In contrast, late lumen loss after stenting is due solely to in-stent neointimal hyperplasia; the main benefit of stents is to prevent recoil and negative remodeling. Stents retain a larger acute lumen diameter that offsets the reduction in lumen diameter from neointimal hyperplasia. Drug-eluting stents (DES) reduce local neointimal hyperplasia. (See "Intracoronary stent restenosis", section on 'Pathogenesis'.)

Drug-eluting stents — DES reduce local neointimal hyperplasia. There is strong evidence from randomized trials and large PCI registry databases that DES significantly lower the rate of target lesion revascularization compared with BMS. With regard to safety, the preponderance of evidence suggests that current-generation DES have similar rates of death and myocardial infarction (MI) to BMS. The risk of stent thrombosis with current-generation DES is similar to or possibly lower than BMS [1-3].

Sirolimus is a macrocyclic triene antibiotic that has immunosuppressive and antiproliferative properties, and inhibits the intracellular mammalian target of rapamycin, thereby affecting cell cycle regulation. Sirolimus-eluting stents were first-generation devices developed to prevent the proliferation of smooth muscle cells and other cell types seen with restenosis after PCI. Sirolimus is incorporated into investigational stents, including polymer-free and bioabsorbable polymer devices.

Biologic characteristics of the four commercially available antirestenotic drugs (all of which are derivatives of sirolimus) that have been used in DES include [4]:

Everolimus is a semi-synthetic sirolimus derivative in which the hydroxyl group at position C40 of sirolimus has been alkylated with a 2-hydroxyethyl group and that was shown in early small studies to be effective at preventing restenosis [5]. It is slightly more lipophilic than sirolimus, and therefore it is more rapidly absorbed into the arterial wall. Everolimus is in use in durable polymer and bioabsorbable polymer devices.

Zotarolimus is a derivative of sirolimus, in which the C40 position is modified by a tetrazole ring, resulting in a shorter circulating half-life of the drug. It is an equipotent analogue of sirolimus in vitro and in vivo and was specifically developed for delivery from DES. Similar to everolimus, the compound is highly lipophilic, which is favorable for cellular uptake.

Ridaforolimus is a lipophilic sirolimus analogue.

Biolimus A9 is a highly lipophilic sirolimus analogue.

The length of time over which the drugs are eluted varies from 2 to 12 weeks and is presented in table form (table 1).

Role for bare metal stents — BMS are uncommonly used to treat coronary artery lesions, as DES are preferred for most patients. (See "Coronary artery stent thrombosis: Incidence and risk factors", section on 'Comparison of DES and BMS'.)

Circumstances in which implantation of a BMS may be reasonable:

Patients for whom it is known at the time of PCI that dual antiplatelet therapy (DAPT) cannot be used for at least 30 days. In this setting, some of our experts choose BMS while others place DES. There are no studies assessing safety of DES with less than 30 days of DAPT, but the use of DES in this setting is acceptable to some experts. The rationale is based on experimental data showing thromboresistance with current generation polymers, and with everolimus-eluting stents in particular, and extrapolation from the high bleeding risk trials showing at least similar safety of DES with only 30 days of DAPT.

Patients that require noncardiac surgery within four to six weeks of PCI. Within this interval, there is increased risk after BMS or DES. Some of our experts place BMS, while others place DES with temporary interruption of DAPT at the time of required surgery.

Patients with active bleeding at the time of PCI or those at very high risk of bleeding while taking DAPT even for 30 days.

USE FOR SPECIFIC LESIONS OR PATIENTS — The role of drug-eluting stents (DES) has been evaluated in specific clinical situations and populations. These are discussed separately:

Left main coronary artery disease or left anterior descending disease. (See "Left main coronary artery disease" and "Management of significant proximal left anterior descending coronary artery disease".)

Multivessel revascularization, ostial lesions, chronic total occlusion, long lesions (that may require overlapping stents), diffuse disease, bifurcation lesions, small coronary arteries, and intermediate (<50 percent stenosis) lesions. (See "Percutaneous coronary intervention of specific coronary lesions".)

PCI for ST-elevation MI (STEMI). (See "Primary percutaneous coronary intervention in acute ST-elevation myocardial infarction: Periprocedural management", section on 'Selection of stent type'.)

Non-ST elevation acute coronary syndrome. (See "Non-ST-elevation acute coronary syndromes: Revascularization", section on 'Percutaneous coronary intervention versus coronary artery bypass graft surgery'.)

Saphenous vein graft stenosis. (See "Coronary artery bypass graft surgery: Prevention and management of vein graft stenosis", section on 'Outcomes with PCI'.)

Patients with diabetes. (See "Coronary artery revascularization in stable patients with diabetes mellitus", section on 'Stent type'.)

Women. (See "Management of coronary heart disease in women".)

Patients at high risk of bleeding. (See "High bleeding risk patients undergoing percutaneous coronary intervention".)

OPTIMAL STENTING TECHNIQUE — Coronary stents are delivered and deployed on balloon catheters (figure 1), which are inserted via the femoral, radial, or less commonly the brachial artery. Optimal stent deployment is necessary to minimize the likelihood of procedure complications and stent restenosis. When restenosis does occur with drug-eluting stents (DES), it is often a consequence of balloon barotrauma to the artery in areas not covered by the stent, gaps in stent coverage, inadequate stent expansion, or inability of the drug to limit neointimal hyperplasia [6-12]. The incidence and risk factors for DES restenosis are discussed separately. (See "Intracoronary stent restenosis", section on 'Predictors in DES' and "Intracoronary stent restenosis", section on 'Incidence of restenosis'.)

Coronary artery characteristics may interfere with optimal stent deployment:

Arterial diameter. Vessels smaller than 2 mm are not suitable for stenting.

Tortuous, angulated, and calcified arterial segments. These may prevent delivery of the stent to the target lesion, and severe calcification may prevent optimal stent expansion.

The single most important contribution to stenting efficacy is to achieve full expansion of the arterial lumen (so-called optimal stenting). Attainment of a large luminal diameter minimizes the risk of both stent thrombosis and restenosis [13,14]. Suboptimal luminal dilation is due to inadequate balloon expansion. This may be related to plaque characteristics, poor technique, or to elastic recoil, which is associated with stent design and resistance [15].

Another principle in the deployment of DES is to cover the entire lesion, as well as sites of balloon predilation, to cover all areas of balloon barotrauma. Multiple overlapping stents are sometimes required for diffusely diseased segments that cannot be treated adequately with a single stent. On the other hand, overlapping stents and longer total stent length are associated with an increased risk for restenosis. (See "Percutaneous coronary intervention of specific coronary lesions", section on 'Overlapping stents'.)

The following sections describe some components of stent delivery, deployment, and evaluation.

Predilation — Predilation of the lesion is performed in most cases. Direct stenting without predilation, an alternative, may be reasonable based upon anticipated ease of delivery and deployment. Should predilation suggest that the lesion is not "dilatable," an alternative strategy such as atherectomy, high-pressure noncompliant balloon dilation, cutting or scoring balloons, or not placing a stent needs to be considered. Angiographic predictors of inability to predilate include moderate or severe coronary calcification, heavy plaque burden, or diffuse coronary artery disease.

Direct stenting without predilation — The availability of low-profile stent-delivery systems has led to the consideration of direct stenting (ie, without predilation). Although stenting reduces the incidence of restenosis after percutaneous transluminal coronary angioplasty, the classic approach of predilation, stent deployment, and high-pressure post-dilation is associated with increased procedure duration, more radiation exposure and contrast use, and increased cost compared with direct stenting [16,17].

Settings in which direct stenting might be considered include [16]:

Vessel ≥2.5 mm in diameter

Proximal lesion location

Absence of severe coronary calcification

Absence of significant angulation (bend >45°)

Absence of very severe lesions and bifurcation lesions

STEMI

Saphenous vein grafts

A number of randomized clinical trials (BET, SWIBAP, PREDICT, CONVERTIBLE, and TRENDS) have compared direct stenting with stenting after balloon dilation [18-22]. Major outcomes were similar, including procedural success (although 6 to 14 percent of patients in the direct stenting group required predilation because of an inability to cross the lesion), adverse effects, and major cardiac events at follow-up. The authors of PREDICT concluded that direct stenting was safe and successful, but offered only modest cost savings and no reduction in late restenosis [20].

We favor predilation in most lesions. One possible exception is in degenerated saphenous vein grafts. In this situation, each balloon dilation is associated with a risk of embolization of degenerated graft material and obstruction of the coronary microcirculation and its consequences. If direct stenting is contemplated and it is unclear if the lesion is suitable or the correct stent sizing cannot be determined, intracoronary imaging such as intravascular ultrasound (IVUS) or optical coherence tomography (OCT) can be performed to assist in decision making.

High pressure balloon dilation — A major strategy to attain optimal stent deployment is high-pressure balloon dilation during or after stent deployment. Initial studies showed clear improvement in stent expansion and apposition with high-pressure dilation post-stenting [23-25]. These observations provided the basis for modern stenting techniques using routine high-pressure dilation in addition to antiplatelet therapy to prevent stent thrombosis. (See "Antithrombotic therapy for elective percutaneous coronary intervention: Clinical studies".)

Stents are usually deployed with a high-pressure technique utilizing ≥12 to 16 atmospheres (atm). Lower pressure deployment (8 to 14 atm) is indicated when there is significant vessel tapering or when proximal edge injury is a concern. In most cases, we perform high-pressure post-dilation with an appropriately sized noncompliant balloon at a minimum of 12 to 16 atm to achieve full stent expansion.

Intravascular ultrasound — Intravascular ultrasound (IVUS; also called intracoronary ultrasound) is a diagnostic procedure that allows the operator to plan the stent procedure by determining the reference vessel diameter and lesion length, visualizing how well a stent is deployed by assessing stent expansion, and surveying for complications that occur at the edge of stents such as dissection [23,26]. Several studies have assessed the benefit of routine IVUS. (See "Intravascular ultrasound, optical coherence tomography, and angioscopy of coronary circulation", section on 'Intravascular ultrasound'.)

Early studies of patients who received bare metal stents (BMS) suggested a reduction in the need for target vessel revascularization from routine IVUS guidance [24,27], but the results from subsequent randomized trials are conflicting [28-32].

With regard to early DES, multiple meta-analyses of predominantly small, observational studies have suggested that IVUS-guided implantation improves outcomes compared with angiographic guidance [33-35]. In these meta-analyses, the large majority of patients received BMS or early generation DES. A mortality benefit was suggested in a large meta-analysis of randomized and observational data [36].  

The optimal use of IVUS after stent placement is unknown and remains controversial. Due to the added time and expense and lack of availability in many interventional laboratories, IVUS tends to be performed in only a small proportion of patients, although use varies considerably between centers. It is most useful when underexpansion is suspected on coronary angiography, with long lesions, when the final size goal is uncertain, or when stent expansion is expected to be difficult, as with calcified lesions or a lesion in the left main coronary artery [37]. There is evidence that intracoronary imaging to help guide optimal PCI results in improved outcomes. Certainly, techniques to optimize stent results should be routine. Post-deployment high pressure dilation may meet this goal in most cases, but it is advisable that PCI operators are trained and have IVUS or OCT available for cases where optimal stent expansion or sizing is uncertain.

In patients with prior stent placement, IVUS or OCT is recommended if stent failure is identified. Mechanisms of restenosis or thrombosis can be determined, including stent underexpansion, intimal hyperplasia, neoatherosclerosis, malapposition, edge dissection, or adjacent inflow or outflow lesions related to disease progression. Treatment is guided by the findings and may include balloon angioplasty, DES, drug-eluting balloon (if available), atherectomy, brachytherapy, or coronary artery bypass grafting.

Optical coherence tomography — OCT has a higher spatial resolution than IVUS and is more useful for assessing stent apposition and strut coverage during follow-up imaging. Both techniques may be useful for guiding optimal stent deployment [38]. (See "Intravascular ultrasound, optical coherence tomography, and angioscopy of coronary circulation", section on 'Optical coherence tomography'.)  

Coronary flow reserve measurements — Coronary artery Doppler measurements can be used to assess whether optimal stenting has been achieved. Two measurements have been evaluated: the relative coronary flow velocity reserve and the coronary pressure-derived myocardial fractional flow reserve (FFRmyo). Although these methods are useful to predict optimal stent results and predict future events, they are seldom used for this purpose. Most operators rely on angiographic appearance or IVUS. (See 'Intravascular ultrasound' above.)

The coronary pressure-derived FFRmyo compares the intracoronary pressure distal to the stented site (measured with a specially designed angioplasty guidewire) with the aortic root pressure measured through the guiding catheter during maximal hyperemic flow produced by bolus intracoronary adenosine injection or a continuous intravenous infusion. It is an easy, inexpensive, and rapidly obtainable index. (See "Clinical use of coronary artery pressure flow measurements".)

The prognostic effect of the FFRmyo has been demonstrated in several studies [39-41]. In the largest series, FFRmyo was measured in 750 patients who had undergone apparently satisfactory stent implantation [39]. At six months, adverse cardiac events occurred in 10 percent, primarily target vessel revascularization (70 percent) and MI (25 percent). By multivariate analysis, the FFR was the major independent predictor of adverse events. At a normal FFR (>0.95), adverse events occurred in 4.9 percent compared with 6.2, 20.3, and 29.5 percent, respectively, for FFR between 0.90 and 0.95 (<0.9 and <0.80).

The potential value of the routine use of FFRmyo before PCI on all lesions deemed to require PCI using angiographic criteria is discussed separately. (See "Clinical use of coronary artery pressure flow measurements", section on 'Multivessel disease'.)

ADJUNCTIVE MEDICAL THERAPY

Antithrombotic therapy — All patients undergoing PCI are given combined anticoagulant and antiplatelet therapy [37,42]. The data supporting the use of these drugs and the recommended regimen are presented elsewhere. (See "Antithrombotic therapy for elective percutaneous coronary intervention: Clinical studies" and "Antithrombotic therapy for elective percutaneous coronary intervention: General use".)

Almost all patients are discharged on dual antiplatelet therapy (DAPT) after placement of an intracoronary stent. After a period of DAPT, most patients continue on single antiplatelet therapy. (See "Long-term antiplatelet therapy after coronary artery stenting in stable patients", section on 'Our approach'.)

Statin therapy — Statin therapy improves the outcome of patients with either stable or unstable coronary disease treated medically. (See "Management of low density lipoprotein cholesterol (LDL-C) in the secondary prevention of cardiovascular disease" and "Low density lipoprotein-cholesterol (LDL-C) lowering after an acute coronary syndrome".)

A benefit from statin therapy at the time of PCI has also been demonstrated, as established below.

Before percutaneous coronary intervention — Benefit from statin therapy prior to PCI, as evidenced by a reduction in periprocedural MI, has been shown in multiple randomized trials [43-48]:

The benefit from initiation of statin therapy prior to PCI in patients with acute coronary syndrome was evaluated in the ARMYDA-ACS trial of 171 patients with non-ST elevation MI scheduled to undergo urgent (but not emergent) PCI [48]. The patients were randomly assigned to either 80 mg of atorvastatin 12 hours before the procedure with an additional preprocedural dose of 40 mg, or to matching placebo; all patients received 40 mg of atorvastatin daily thereafter. The primary outcome of 30-day major adverse cardiac events (eg, death, MI, or unplanned revascularization) occurred significantly less often in the early atorvastatin group (5 versus 17 percent, odds ratio 0.12, 95% CI 0.05-0.50). The difference was due almost entirely to a lowering of the incidence of MI, defined as important creatine kinase MB fraction (CK-MB) elevation.

In the ARMYDA trial, 153 stable patients were randomly assigned to atorvastatin 40 mg/day or placebo starting seven days before the procedure [43]. Cardiac biomarkers were measured at baseline and at 8 and 24 hours after the procedure. Patients pretreated with atorvastatin had a significantly lower incidence of myocardial injury as detected by elevation in serum CK-MB (12 versus 35 percent) and troponin I (20 versus 48 percent).

In the open label NAPLES II trial, 668 stable, statin-naive patients were randomly assigned to either atorvastatin 80 or no therapy 24 hours before PCI [47]. Cardiac biomarkers were measured at baseline and at 8 and 24 hours after the procedure. The primary end point of periprocedural MI (CK-MB elevation >3 X upper limit of normal) was significantly lower in the atorvastatin group (9.5 versus 15.8 percent; odds ratio 0.56, 95% CI 0.36-0.89).

After percutaneous coronary intervention — Statin therapy has both short- and long-term benefits when administered after PCI with stenting [49-51]:

The PROVE-IT TIMI 22 trial demonstrated that the use of intensive statin therapy (atorvastatin 80 mg), as opposed to less intensive therapy (pravastatin 40 mg), after PCI in patients with acute coronary syndromes resulted in a significantly lower combined rate of all-cause mortality, MI, unstable angina, and revascularization after 30 days (21.5 versus 26.5 percent) [49]. (See "Low density lipoprotein-cholesterol (LDL-C) lowering after an acute coronary syndrome", section on 'Timing of initiation'.)

In the LIPS trial, 1677 patients with stable or unstable angina or silent ischemia with serum total cholesterol between 135 and 270 mg/dL (3.5 to 7.0 mmol/L) were randomly assigned to fluvastatin (80 mg/day) or placebo after successful completion of their first PCI [50]. At a median follow-up of 3.9 years, fluvastatin therapy was associated with a significant reduction in major adverse cardiac events, defined as any cardiac death, nonfatal MI, or a reintervention procedure (21.4 versus 26.7 percent). The benefit began at 1.5 years, was independent of baseline serum total cholesterol, and was seen in diabetics and those with multivessel disease.

There was no evidence of a reduction in restenosis in the LIPS trial. Thus, the benefit appeared to be unrelated to the stent site, and may have been due to actions (such as plaque stabilization) elsewhere in the coronary circulation. (See "Mechanisms of benefit of lipid-lowering drugs in patients with coronary heart disease".)

The issue of whether patients on chronic statin therapy scheduled to undergo PCI benefit from an acute dose of statin was addressed in the ARMYDA-RECAPTURE trial [52]. In this study, 383 patients (53 percent of whom had stable angina) were randomly assigned to either atorvastatin reload (80 mg 12 hours before the intervention, with a further 40 mg preprocedure dose) or placebo. The primary end point of 30-day major adverse cardiovascular events (eg, cardiac death, MI, or unplanned revascularization) occurred significantly less often in the atorvastatin reload group (3.7 versus 9.4 percent), driven mostly by a reduction in periprocedural MI. In subset analysis, the benefit was seen principally in patients with acute coronary syndrome (3.3 versus 14.8 percent), but not in those with stable angina (4.0 versus 4.9 percent). Whether routine reloading with a statin should be considered standard of care is yet to be determined. (See "Low density lipoprotein-cholesterol (LDL-C) lowering after an acute coronary syndrome".)

COMPLICATIONS — A variety of periprocedural complications (both cardiac and noncardiac) can occur after PCI with stenting. These issues are discussed separately. (See "Periprocedural complications of percutaneous coronary intervention".)

ANTIMICROBIAL PROPHYLAXIS — Placement of drug-eluting coronary stents is not an indication for antimicrobial prophylaxis before dental or invasive procedures [53].

TIMING OF DISCHARGE — We believe it is reasonable to discharge elective, lower-risk patients following uncomplicated, lower complexity PCI after four to eight hours of observation on the day of PCI if no complications or concerns have arisen.

A 2013 meta-analysis of five randomized trials (2039 patients) and eight observational studies (109,791 patients) with substantial heterogeneity compared same-day discharge (SDD) with overnight hospitalization (ON) [54]. Most patients were at low risk of a complication: Very few had an acute coronary syndrome, many had single vessel disease, and most did not have an intraprocedural complication [55]. The primary outcomes were the incidence of total complications, major adverse cardiovascular events, and rehospitalization within 30 days. With regard to the incidence of total complications within 30 days, there was no significant difference between SDD and ON in either the randomized trials or observational studies (odds ratio 1.2, 95% CI 0.82-1.74 and 0.67, 95% CI 0.27-1.66, comparing SDD with ON, respectively). There was no significant difference between the two approaches with regard to major adverse cardiovascular events or rehospitalization.

SAFETY OF MRI — Any ferromagnetic object within the body represents a potential hazard when exposed to the strong magnetic field of a magnetic resonance imaging (MRI) system. Based upon available evidence, it appears to be safe to perform an MRI at any time after placement of coronary artery stents of any type. The discussion of this issue is found elsewhere. (See "Patient evaluation for metallic or electrical implants, devices, or foreign bodies before magnetic resonance imaging", section on 'Arterial stents, coils, and clips'.)

RISK OF EARLY NONCARDIAC SURGERY — Studies in patients receiving bare metal stents have shown that major noncardiac surgery within six weeks (and particularly within two weeks) of stenting is associated with an appreciable risk of stent thrombosis that is often associated with cessation of or a reduction in antiplatelet therapy to minimize bleeding risk. Limited data for drug-eluting stents suggest a similar risk. In contrast, balloon angioplasty alone appears to be associated with a low incidence of cardiac death or MI when performed a few weeks before noncardiac surgery. This issue is discussed separately. (See "Noncardiac surgery after percutaneous coronary intervention", section on 'Our approach'.)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

Basics topics (see "Patient education: Coping with high drug prices (The Basics)" and "Patient education: Stenting for the heart (The Basics)")

Beyond the Basics topics (see "Patient education: Angina treatment — medical versus interventional therapy (Beyond the Basics)" and "Patient education: Stenting for the heart (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Stents should be deployed with a goal of achieving minimal residual stenosis (so-called optimal stenting). Attainment of a large luminal diameter minimizes the risk of both stent thrombosis and restenosis. (See 'Optimal stenting technique' above.)

Although direct stenting has some advantages, predilation is recommended for the majority of lesions. (See 'Predilation' above.)

In most cases, we perform high-pressure stent deployment or post-dilation at 12 to 16 atm to achieve full stent expansion. (See 'High pressure balloon dilation' above.)

Intravascular ultrasound or optical coherence tomography can be a useful adjunct to guide stent placement. The routine use of one of these imaging tools (in addition to the use of a high-pressure balloon post-dilation) after second generation drug-eluting stent is uncertain, but it should be considered if there is any question about optimal results or for stent failure (thrombosis or restenosis). (See 'Intravascular ultrasound' above and 'Optical coherence tomography' above.)

Statin therapy improves the outcome of patients with either stable or unstable coronary disease treated medically. Virtually all patients undergoing percutaneous coronary intervention should be on chronic statin therapy. The role of statin reloading remains unclear. (See "Management of low density lipoprotein cholesterol (LDL-C) in the secondary prevention of cardiovascular disease" and "Low density lipoprotein-cholesterol (LDL-C) lowering after an acute coronary syndrome".)

Patients undergoing elective stent therapy are generally discharged within 24 hours after stent implantation following overnight observation and monitoring. Same-day discharge may be appropriate for elective patients who have an uncomplicated procedure and are at low risk of out-of-hospital complication.

  1. Räber L, Wohlwend L, Wigger M, et al. Five-year clinical and angiographic outcomes of a randomized comparison of sirolimus-eluting and paclitaxel-eluting stents: results of the Sirolimus-Eluting Versus Paclitaxel-Eluting Stents for Coronary Revascularization LATE trial. Circulation 2011; 123:2819.
  2. Baber U, Mehran R, Sharma SK, et al. Impact of the everolimus-eluting stent on stent thrombosis: a meta-analysis of 13 randomized trials. J Am Coll Cardiol 2011; 58:1569.
  3. Bangalore S, Kumar S, Fusaro M, et al. Short- and long-term outcomes with drug-eluting and bare-metal coronary stents: a mixed-treatment comparison analysis of 117 762 patient-years of follow-up from randomized trials. Circulation 2012; 125:2873.
  4. Stefanini GG, Holmes DR Jr. Drug-eluting coronary-artery stents. N Engl J Med 2013; 368:254.
  5. Grube E, Sonoda S, Ikeno F, et al. Six- and twelve-month results from first human experience using everolimus-eluting stents with bioabsorbable polymer. Circulation 2004; 109:2168.
  6. Costa MA, Simon DI. Molecular basis of restenosis and drug-eluting stents. Circulation 2005; 111:2257.
  7. Moses JW, Leon MB, Popma JJ, et al. Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery. N Engl J Med 2003; 349:1315.
  8. Schofer J, Schlüter M, Gershlick AH, et al. Sirolimus-eluting stents for treatment of patients with long atherosclerotic lesions in small coronary arteries: double-blind, randomised controlled trial (E-SIRIUS). Lancet 2003; 362:1093.
  9. Carrozza JP Jr. Sirolimus-eluting stents: does a great stent still need a good interventionalist? J Am Coll Cardiol 2004; 43:1116.
  10. Lemos PA, Saia F, Ligthart JM, et al. Coronary restenosis after sirolimus-eluting stent implantation: morphological description and mechanistic analysis from a consecutive series of cases. Circulation 2003; 108:257.
  11. Fujii K, Mintz GS, Kobayashi Y, et al. Contribution of stent underexpansion to recurrence after sirolimus-eluting stent implantation for in-stent restenosis. Circulation 2004; 109:1085.
  12. Takebayashi H, Kobayashi Y, Mintz GS, et al. Intravascular ultrasound assessment of lesions with target vessel failure after sirolimus-eluting stent implantation. Am J Cardiol 2005; 95:498.
  13. Fischman DL, Leon MB, Baim DS, et al. A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. Stent Restenosis Study Investigators. N Engl J Med 1994; 331:496.
  14. Serruys PW, de Jaegere P, Kiemeneij F, et al. A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. Benestent Study Group. N Engl J Med 1994; 331:489.
  15. Bermejo J, Botas J, García E, et al. Mechanisms of residual lumen stenosis after high-pressure stent implantation: a quantitative coronary angiography and intravascular ultrasound study. Circulation 1998; 98:112.
  16. Briguori C, Sheiban I, De Gregorio J, et al. Direct coronary stenting without predilation. J Am Coll Cardiol 1999; 34:1910.
  17. Wilson SH, Berger PB, Mathew V, et al. Immediate and late outcomes after direct stent implantation without balloon predilation. J Am Coll Cardiol 2000; 35:937.
  18. Carrié D, Khalifé K, Citron B, et al. Comparison of direct coronary stenting with and without balloon predilatation in patients with stable angina pectoris. BET (Benefit Evaluation of Direct Coronary Stenting) Study Group. Am J Cardiol 2001; 87:693.
  19. Le Breton H, Boschat J, Commeau P, et al. Randomised comparison of coronary stenting with and without balloon predilatation in selected patients. Heart 2001; 86:302.
  20. Baim DS, Flatley M, Caputo R, et al. Comparison of PRE-dilatation vs direct stenting in coronary treatment using the Medtronic AVE S670 Coronary Stent System (the PREDICT trial). Am J Cardiol 2001; 88:1364.
  21. Wijns W, Verheye S, Manoharan G, et al. Angiographic, intravascular ultrasound, and fractional flow reserve evaluation of direct stenting vs. conventional stenting using BeStent2 in a multicentre randomized trial. Eur Heart J 2005; 26:1852.
  22. Dawkins KD, Chevalier B, Suttorp MJ, et al. Effectiveness of "direct" stenting without balloon predilatation (from the Multilink Tetra Randomised European Direct Stent Study [TRENDS]). Am J Cardiol 2006; 97:316.
  23. Nakamura S, Colombo A, Gaglione A, et al. Intracoronary ultrasound observations during stent implantation. Circulation 1994; 89:2026.
  24. Colombo A, Hall P, Nakamura S, et al. Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance. Circulation 1995; 91:1676.
  25. Dirschinger J, Kastrati A, Neumann FJ, et al. Influence of balloon pressure during stent placement in native coronary arteries on early and late angiographic and clinical outcome: A randomized evaluation of high-pressure inflation. Circulation 1999; 100:918.
  26. Goldberg SL, Colombo A, Nakamura S, et al. Benefit of intracoronary ultrasound in the deployment of Palmaz-Schatz stents. J Am Coll Cardiol 1994; 24:996.
  27. Albiero R, Rau T, Schlüter M, et al. Comparison of immediate and intermediate-term results of intravascular ultrasound versus angiography-guided Palmaz-Schatz stent implantation in matched lesions. Circulation 1997; 96:2997.
  28. Fitzgerald PJ, Oshima A, Hayase M, et al. Final results of the Can Routine Ultrasound Influence Stent Expansion (CRUISE) study. Circulation 2000; 102:523.
  29. Frey AW, Hodgson JM, Müller C, et al. Ultrasound-guided strategy for provisional stenting with focal balloon combination catheter: results from the randomized Strategy for Intracoronary Ultrasound-guided PTCA and Stenting (SIPS) trial. Circulation 2000; 102:2497.
  30. Schiele F, Meneveau N, Vuillemenot A, et al. Impact of intravascular ultrasound guidance in stent deployment on 6-month restenosis rate: a multicenter, randomized study comparing two strategies--with and without intravascular ultrasound guidance. RESIST Study Group. REStenosis after Ivus guided STenting. J Am Coll Cardiol 1998; 32:320.
  31. Mudra H, di Mario C, de Jaegere P, et al. Randomized comparison of coronary stent implantation under ultrasound or angiographic guidance to reduce stent restenosis (OPTICUS Study). Circulation 2001; 104:1343.
  32. Russo RJ, Silva PD, Teirstein PS, et al. A randomized controlled trial of angiography versus intravascular ultrasound-directed bare-metal coronary stent placement (the AVID Trial). Circ Cardiovasc Interv 2009; 2:113.
  33. Zhang Y, Farooq V, Garcia-Garcia HM, et al. Comparison of intravascular ultrasound versus angiography-guided drug-eluting stent implantation: a meta-analysis of one randomised trial and ten observational studies involving 19,619 patients. EuroIntervention 2012; 8:855.
  34. Ahn JM, Kang SJ, Yoon SH, et al. Meta-analysis of outcomes after intravascular ultrasound-guided versus angiography-guided drug-eluting stent implantation in 26,503 patients enrolled in three randomized trials and 14 observational studies. Am J Cardiol 2014; 113:1338.
  35. Jang JS, Song YJ, Kang W, et al. Intravascular ultrasound-guided implantation of drug-eluting stents to improve outcome: a meta-analysis. JACC Cardiovasc Interv 2014; 7:233.
  36. Buccheri S, Franchina G, Romano S, et al. Clinical Outcomes Following Intravascular Imaging-Guided Versus Coronary Angiography-Guided Percutaneous Coronary Intervention With Stent Implantation: A Systematic Review and Bayesian Network Meta-Analysis of 31 Studies and 17,882 Patients. JACC Cardiovasc Interv 2017; 10:2488.
  37. Levine GN, Bates ER, Blankenship JC, et al. 2011 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. Circulation 2011; 124:e574.
  38. Kubo T, Shinke T, Okamura T, et al. Optical frequency domain imaging vs. intravascular ultrasound in percutaneous coronary intervention (OPINION trial): one-year angiographic and clinical results. Eur Heart J 2017; 38:3139.
  39. Pijls NH, Klauss V, Siebert U, et al. Coronary pressure measurement after stenting predicts adverse events at follow-up: a multicenter registry. Circulation 2002; 105:2950.
  40. Fearon WF, Luna J, Samady H, et al. Fractional flow reserve compared with intravascular ultrasound guidance for optimizing stent deployment. Circulation 2001; 104:1917.
  41. Berger A, Botman KJ, MacCarthy PA, et al. Long-term clinical outcome after fractional flow reserve-guided percutaneous coronary intervention in patients with multivessel disease. J Am Coll Cardiol 2005; 46:438.
  42. Popma JJ, Ohman EM, Weitz J, et al. Antithrombotic therapy in patients undergoing percutaneous coronary intervention. Chest 2001; 119:321S.
  43. Pasceri V, Patti G, Nusca A, et al. Randomized trial of atorvastatin for reduction of myocardial damage during coronary intervention: results from the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) study. Circulation 2004; 110:674.
  44. Briguori C, Colombo A, Airoldi F, et al. Statin administration before percutaneous coronary intervention: impact on periprocedural myocardial infarction. Eur Heart J 2004; 25:1822.
  45. Herrmann J, Lerman A, Baumgart D, et al. Preprocedural statin medication reduces the extent of periprocedural non-Q-wave myocardial infarction. Circulation 2002; 106:2180.
  46. Patti G, Chello M, Pasceri V, et al. Protection from procedural myocardial injury by atorvastatin is associated with lower levels of adhesion molecules after percutaneous coronary intervention: results from the ARMYDA-CAMs (Atorvastatin for Reduction of MYocardial Damage during Angioplasty-Cell Adhesion Molecules) substudy. J Am Coll Cardiol 2006; 48:1560.
  47. Briguori C, Visconti G, Focaccio A, et al. Novel approaches for preventing or limiting events (Naples) II trial: impact of a single high loading dose of atorvastatin on periprocedural myocardial infarction. J Am Coll Cardiol 2009; 54:2157.
  48. Patti G, Pasceri V, Colonna G, et al. Atorvastatin pretreatment improves outcomes in patients with acute coronary syndromes undergoing early percutaneous coronary intervention: results of the ARMYDA-ACS randomized trial. J Am Coll Cardiol 2007; 49:1272.
  49. Gibson CM, Pride YB, Hochberg CP, et al. Effect of intensive statin therapy on clinical outcomes among patients undergoing percutaneous coronary intervention for acute coronary syndrome. PCI-PROVE IT: A PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22) Substudy. J Am Coll Cardiol 2009; 54:2290.
  50. Serruys PW, de Feyter P, Macaya C, et al. Fluvastatin for prevention of cardiac events following successful first percutaneous coronary intervention: a randomized controlled trial. JAMA 2002; 287:3215.
  51. Schömig A, Mehilli J, Holle H, et al. Statin treatment following coronary artery stenting and one-year survival. J Am Coll Cardiol 2002; 40:854.
  52. Di Sciascio G, Patti G, Pasceri V, et al. Efficacy of atorvastatin reload in patients on chronic statin therapy undergoing percutaneous coronary intervention: results of the ARMYDA-RECAPTURE (Atorvastatin for Reduction of Myocardial Damage During Angioplasty) Randomized Trial. J Am Coll Cardiol 2009; 54:558.
  53. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation 2007; 116:1736.
  54. Abdelaal E, Rao SV, Gilchrist IC, et al. Same-day discharge compared with overnight hospitalization after uncomplicated percutaneous coronary intervention: a systematic review and meta-analysis. JACC Cardiovasc Interv 2013; 6:99.
  55. Mavromatis K. Same-day discharge after percutaneous coronary intervention: are we ready? JACC Cardiovasc Interv 2013; 6:113.
Topic 1569 Version 33.0

References