Drug eluting stent
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Muhammad Saad, M.B.B.S.[2]
Overview
A drug-eluting stent (DES) is a coronary stent placed into narrowed, diseased coronary arteries that slowly releases an antiproliferative drug to inhibit neointimal hyperplasia and prevent in-stent restenosis.[1] DES consist of three components: a metallic scaffold (platform), a polymer carrier coating, and an antiproliferative drug.[2] More than 500,000 DES are implanted annually in the United States alone.[1]
The 2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization provides a Class 1, Level of Evidence A recommendation that DES should be used in preference to bare metal stents (BMS) in patients undergoing percutaneous coronary intervention (PCI) to reduce the risk of restenosis, myocardial infarction, and stent thrombosis.[3] An individual patient data meta-analysis of 20 randomized controlled trials (26,616 patients) confirmed that DES significantly reduce myocardial infarction (HR 0.79; 95% CI 0.71–0.88), definite stent thrombosis (HR 0.63; 0.50–0.80), and target-vessel revascularization (HR 0.55; 0.50–0.60) compared with BMS, although all-cause mortality is not significantly different (HR 0.96; 0.88–1.05).[4]
DES technology has evolved through several generations. First-generation DES (sirolimus-eluting Cypher and paclitaxel-eluting Taxus stents) dramatically reduced restenosis compared with BMS but raised concerns about late stent thrombosis. Second-generation DES (e.g., everolimus-eluting and zotarolimus-eluting stents) with thinner struts, improved polymers, and more potent antiproliferative agents have further reduced stent thrombosis and myocardial infarction rates.[1][2] Contemporary cobalt-chromium everolimus-eluting stents have been associated with lower rates of definite stent thrombosis than both other DES types and even BMS, representing a paradigm shift in stent safety.[5]
Structure
Components
Drug-eluting stents consist of three integrated components:[2][1]
Metallic scaffold (platform): The expandable framework that provides structural support. Early stents used stainless steel (316L); contemporary platforms use cobalt-chromium (CoCr) or platinum-chromium (PtCr) alloys, which allow thinner struts while maintaining radial strength. Strut thickness has decreased from 130–140 μm in first-generation DES to 60–81 μm in current ultrathin-strut devices.
Polymer carrier coating: The polymer matrix that controls drug release kinetics. Three categories exist:
Durable (permanent) polymers: Remain on the stent indefinitely (e.g., fluoropolymer on Xience, BioLinx on Resolute)
Biodegradable polymers: Gradually degrade after drug release is complete (e.g., poly-L-lactic acid [PLLA] on Orsiro, PLGA on Synergy)
Polymer-free coatings: Use alternative drug delivery mechanisms without polymers
Antiproliferative drug: Inhibits smooth muscle cell proliferation to prevent neointimal hyperplasia. Contemporary DES exclusively use limus-family analogues (sirolimus, everolimus, zotarolimus, biolimus A9) that inhibit the mammalian target of rapamycin (mTOR) pathway, causing G1 cell cycle arrest. Paclitaxel, which stabilizes microtubules and arrests cell division at the M phase, was used in first-generation DES but has fallen out of use on stent platforms due to local toxicity.[2]
Mechanism of Action
Sirolimus (rapamycin) and its analogues bind to the immunophilin FKBP-12. The resulting complex inhibits mTOR, preventing the cell from duplicating its genetic material and blocking the cell cycle at the G1→S transition.[6] This inhibits both vascular smooth muscle cell proliferation and migration, significantly reducing neointimal hyperplasia. Studies in porcine models demonstrated that rapamycin reduces the arterial proliferative response after angioplasty by increasing the level of the cyclin-dependent kinase inhibitor p27(kip1) and inhibiting retinoblastoma protein (pRb) phosphorylation within the vessel wall.[6]
Currently Available Devices
Contemporary DES platforms in widespread clinical use include:[7][8]
| Device | Manufacturer | Platform (Alloy) | Strut Thickness (μm) | Polymer Type | Drug |
|---|---|---|---|---|---|
| Xience Alpine/Sierra | Abbott | CoCr (L-605) | 81 | Durable fluoropolymer (PVDF-HFP) | Everolimus |
| Promus Premier/Elite | Boston Scientific | PtCr | 81 | Durable fluoropolymer (PVDF-HFP) | Everolimus |
| Resolute Integrity/Onyx | Medtronic | Co-alloy | 81–91 | Durable BioLinx (C10/C19/PVP) | Zotarolimus |
| Synergy | Boston Scientific | PtCr | 74 | Biodegradable (PLGA), abluminal | Everolimus |
| Orsiro | Biotronik | CoCr (L-605) | 60 | Biodegradable (PLLA) | Sirolimus |
| Ultimaster | Terumo | CoCr | 80 | Biodegradable (PDLLA-PCL), abluminal | Sirolimus |
History
The first procedural method to treat blocked coronary arteries was coronary artery bypass graft (CABG) surgery. In 1977, Andreas Grüntzig introduced percutaneous transluminal coronary angioplasty (PTCA), in which a catheter was introduced through a peripheral artery and a balloon expanded to compress the obstructive plaque.[9]
As equipment and techniques improved, the use of PTCA rapidly increased. However, PTCA had a high rate (30–40% in six months) of restenosis, and approximately 3% of patients required emergency bypass surgery. In 1964, Dotter and Judkins had suggested using prosthetic devices inside arteries to maintain blood flow, and in 1986, Puel and Sigwart implanted the first coronary stent in humans.[10] Several trials in the 1990s demonstrated the superiority of stent placement over simple balloon angioplasty, and stent placement reached 84% of percutaneous interventions by 1999.[10]
Initial difficulties included blood clotting and occluding the stent in the hours or days after placement. Using high balloon pressures to tightly fix the stent against the vessel wall and administering aspirin and clopidogrel as antiplatelet agents were established; these changes eliminated most of the difficulty with early stent thrombosis.[10]
Difficulties still remained with neointimal hyperplasia inside the stent. The stent itself was a logical choice for delivering medication directly to the target site, providing high local drug concentrations while avoiding systemic side effects. The first successful trials were of sirolimus-eluting stents. A successful trial in 2002 led to approval of the Cypher stent in Europe, followed by FDA approval in the United States in 2003.[10] Soon thereafter, a series of trials of paclitaxel-eluting stents led to FDA approval of the Taxus stent in 2004.
Generational Evolution
| Generation | Era | Examples | Key Features | Limitations |
|---|---|---|---|---|
| First-generation DES | 2003–2008 | Cypher (sirolimus), Taxus (paclitaxel) | Dramatic reduction in restenosis vs. BMS (angiographic restenosis reduced from ~30% to ~5–10%); thick struts (132–140 μm); durable polymers | Increased late and very late stent thrombosis; polymer-related chronic inflammation; delayed arterial healing |
| Second-generation DES | 2008–2015 | Xience/Promus (everolimus), Resolute (zotarolimus) | Thinner struts (81–91 μm); improved polymers (fluoropolymer, BioLinx); more potent limus-family drugs; reduced stent thrombosis and MI vs. first-generation DES | Permanent polymer remains after drug elution |
| Newer-generation DES | 2015–present | Orsiro (sirolimus), Synergy (everolimus), Ultimaster (sirolimus) | Ultrathin struts (60–80 μm); biodegradable polymers or abluminal-only coating; further reduction in target lesion failure | Long-term (>5 year) advantages over second-generation DES remain under investigation |
Drug-Eluting Stents Versus Bare-Metal Stents
Summary of Evidence
The superiority of DES over BMS for reducing restenosis and repeat revascularization is firmly established across multiple large-scale randomized controlled trials and meta-analyses.
Individual Patient Data Meta-Analysis (Piccolo et al., Lancet, 2019)
A systematic review and individual patient data meta-analysis of 20 randomized controlled trials enrolling 26,616 patients compared newer-generation DES with BMS.[4] Key findings:
DES reduced the composite primary outcome of all-cause death, myocardial infarction, or target-vessel revascularization (HR 0.84; 95% CI 0.78–0.90; P<0.001)
DES reduced myocardial infarction (HR 0.79; 95% CI 0.71–0.88; P<0.001)
DES reduced definite stent thrombosis (HR 0.63; 95% CI 0.50–0.80; P<0.001)
DES reduced target-vessel revascularization (HR 0.55; 95% CI 0.50–0.60; P<0.001)
All-cause death was not significantly different (HR 0.96; 95% CI 0.88–1.05; P=0.358)
The treatment effect was time-dependent, with benefit primarily in the first year
NORSTENT Trial (Bønaa et al., NEJM, 2016)
The largest single RCT comparing DES with BMS enrolled 9,013 patients in Norway.[11] At 6 years:
No significant difference in the composite of death or nonfatal spontaneous myocardial infarction (16.6% DES vs. 17.1% BMS; HR 0.98; 95% CI 0.88–1.09; P=0.66)
Repeat revascularization was significantly lower with DES (16.5% vs. 19.8%; HR 0.76; 95% CI 0.69–0.85; P<0.001)
Definite stent thrombosis was lower with DES (0.8% vs. 1.2%; P=0.0498)
Mixed-Treatment Comparison Meta-Analysis (Bangalore et al., Circulation, 2012)
A network meta-analysis of 76 randomized controlled trials encompassing 117,762 patient-years of follow-up compared all available stent types.[12] Key findings:
All DES reduced long-term target-vessel revascularization by 39%–61% compared with BMS
Efficacy ranking: everolimus-eluting stents (EES) ≈ sirolimus-eluting stents (SES) ≈ Resolute zotarolimus-eluting stents (ZES-R) > paclitaxel-eluting stents (PES) ≈ Endeavor zotarolimus-eluting stents (ZES) > BMS
EES was the safest stent (>86% probability), with significant reduction in myocardial infarction and stent thrombosis vs. BMS (rate ratio 0.51; 95% CrI 0.35–0.73)
Early DES vs. BMS Data
An early hierarchical Bayesian meta-analysis of randomized controlled trials of first-generation DES demonstrated the following comparative outcomes:[13]
| Outcome | DES (%) | BMS (%) |
|---|---|---|
| Death | 0.9 | 0.9 |
| Myocardial infarction | 2.7 | 2.9 |
| Target lesion revascularization | 4.2 | 13.2 |
| MACE | 7.8 | 16.4 |
| Angiographic restenosis | 8.9 | 29.3 |
| Edge restenosis | 3.0 | 1.9 |
| Stent thrombosis | 0.7 | 0.5 |
| Late incomplete stent apposition | 8.5 | 5.1 |
These early data demonstrated that while first-generation DES dramatically reduced restenosis and target lesion revascularization, they were associated with slightly higher rates of edge restenosis, stent thrombosis, and late incomplete stent apposition compared with BMS — limitations that have been largely overcome with newer-generation DES.[13][5]
First-Generation Versus Second-Generation Drug-Eluting Stents
Second-generation DES have demonstrated significant improvements in safety over first-generation devices.
Pooled Analysis of 16 RCTs (Colmenarez et al., EuroIntervention, 2014)
A pooled analysis of 16 randomized controlled trials enrolling 25,427 patients found that second-generation DES were associated with:[14]
26% relative risk reduction in myocardial infarction (RR 0.74; 95% CI 0.61–0.90)
30% relative risk reduction in stent thrombosis (RR 0.70; 95% CI 0.55–0.89)
Strut thickness ≤91 μm was associated with significantly lower MI risk (RR 0.54; 95% CI 0.51–0.86)
STEMI Population (Chichareon et al., JACC, 2019)
In patients with ST-segment elevation myocardial infarction (STEMI), second-generation DES demonstrated superior outcomes:[15]
Second-generation DES vs. BMS: adjusted HR for definite/probable stent thrombosis 0.61 (95% CI 0.42–0.89)
Second-generation DES vs. first-generation DES: adjusted HR for definite/probable stent thrombosis 0.56 (95% CI 0.36–0.88)
Sirolimus-Eluting Versus Paclitaxel-Eluting Stents
Among first-generation DES, sirolimus-eluting stents demonstrated superior efficacy over paclitaxel-eluting stents. A meta-analysis of 6 randomized controlled trials (3,669 patients) found that sirolimus-eluting stents had lower target lesion revascularization (5.1% vs. 7.8%; OR 0.64; 95% CI 0.49–0.84; P=0.001) and lower angiographic restenosis (9.3% vs. 13.1%; OR 0.68; 95% CI 0.55–0.86; P=0.001), with no differences in stent thrombosis, death, or death/MI.[16]
A head-to-head RCT of 1,012 patients confirmed a 44% reduction in MACE at 9 months with sirolimus-eluting stents compared with paclitaxel-eluting stents (6.2% vs. 10.8%; HR 0.56; P=0.009), driven by lower target lesion revascularization (4.8% vs. 8.3%).[17]
Ultrathin-Strut Drug-Eluting Stents
Strut thickness is a critical determinant of stent performance. Thinner struts reduce vessel wall injury, inflammation, and thrombogenicity, and promote faster endothelial healing.
Meta-Analysis of 10 RCTs (Bangalore et al., Circulation, 2018)
A meta-analysis of 10 randomized controlled trials enrolling 11,658 patients compared ultrathin-strut DES (<70 μm) with thicker-strut second-generation DES:[18]
16% reduction in target lesion failure (RR 0.84; 95% CI 0.72–0.99)
20% reduction in myocardial infarction (RR 0.80; 95% CI 0.65–0.99)
Qualitatively lower stent thrombosis (RR 0.72; 95% CI 0.51–1.01)
Network Meta-Analysis by Strut Thickness (Iantorno et al., Am J Cardiol, 2018)
A network meta-analysis of 69 randomized controlled trials (80,885 patients) stratified by strut thickness found that ultrathin struts compared with thick struts were associated with significantly less stent thrombosis (OR 0.43; CrI 0.27–0.68) and myocardial infarction (OR 0.73; CrI 0.62–0.92).[19]
Long-Term Follow-Up (Hassan et al., Eur J Med Res, 2024)
A large-scale meta-analysis of 19 randomized controlled trials and 2 registries (103,101 patients) demonstrated that ultrathin-strut DES showed benefit in target lesion failure at ≥1, ≥2, and ≥3 years of follow-up, but no significant difference at ≥5 years compared with thicker-strut second-generation DES.[20]
Biodegradable Polymer Versus Durable Polymer Drug-Eluting Stents
Biodegradable polymer DES were developed to eliminate the chronic inflammatory stimulus of a permanent polymer coating after drug elution is complete, theoretically promoting better long-term arterial healing.
BIOSCIENCE Trial 5-Year Outcomes (Pilgrim et al., Lancet, 2018)
The BIOSCIENCE trial compared ultrathin-strut biodegradable-polymer sirolimus-eluting stents (Orsiro) with durable-polymer everolimus-eluting stents (Xience) and found similar safety and efficacy during 5-year follow-up.[21]
BIO-RESORT Trial (von Birgelen et al., Lancet, 2016)
The BIO-RESORT trial enrolled 3,514 patients and demonstrated that very thin strut biodegradable polymer everolimus-eluting and sirolimus-eluting stents were noninferior to durable polymer zotarolimus-eluting stents for target vessel failure at 1 year (5% in each group).[22]
Mixed-Treatment Comparison Meta-Analysis (Bangalore et al., BMJ, 2013)
A comprehensive network meta-analysis of 126 randomized controlled trials (258,544 patient-years) found that biodegradable polymer DES were superior to first-generation DES but not to newer-generation durable polymer DES. Cobalt-chromium everolimus-eluting stents were the safest, with significant reductions in definite stent thrombosis (rate ratio 0.35; 95% CrI 0.21–0.53), myocardial infarction (rate ratio 0.65; 0.55–0.75), and death (rate ratio 0.72; 0.58–0.90) compared with BMS.[23]
Polymer-Free Drug-Eluting Stents
Polymer-free DES were developed to eliminate polymer-related complications entirely. However, current evidence suggests they may be inferior to polymer-coated DES for restenosis prevention.
A meta-analysis of 10 randomized controlled trials (9,020 patients) comparing polymer-free DES with biodegradable polymer DES found that polymer-free DES had significantly higher target lesion revascularization at 12 months (2.08% vs. 1.36%; RR 1.55; P=0.02) and at 24 months (RR 2.01; P<0.0001), with no differences in stent thrombosis, myocardial infarction, or mortality.[24]
A separate meta-analysis of 12 randomized controlled trials (6,927 patients) confirmed that when using the same antiproliferative drugs, polymer-free DES had increased risk of restenosis (increased late lumen loss and long-term target lesion revascularization) compared with polymer-coated DES.[25]
Stent Thrombosis: The Paradigm Shift
Early concerns about late and very late stent thrombosis with first-generation DES prompted extensive investigation. Contemporary evidence demonstrates that newer-generation DES have fundamentally changed the stent thrombosis landscape.
A comprehensive analysis demonstrated that cobalt-chromium everolimus-eluting stents may be associated with lower rates of definite stent thrombosis than other DES and even lower than BMS, representing a paradigm shift in stent safety. Contributing factors include the thin-strut structure, thromboresistant fluoropolymer, and reduced polymer and drug load.[5]
A network meta-analysis of 60 randomized controlled trials (63,242 patients) confirmed that everolimus-eluting and Resolute zotarolimus-eluting stents offered the highest safety profiles among all stent types.[26]
Placement
Treating a blocked coronary artery with a drug-eluting stent follows the same steps as other angioplasty procedures. The interventional cardiologist uses angiography to assess the location and estimate the size of the blockage by injecting a contrast medium through the guide catheter and viewing the flow of blood through the downstream coronary arteries. Intravascular ultrasound (IVUS) or optical coherence tomography (OCT) may be used to assess the lesion's characteristics including calcification.
Common practice is to predilate the blockage before delivering the stent. Predilation is accomplished by threading the lesion with an ordinary balloon catheter and expanding it to the vessel's original diameter. The physician then threads the stent on its balloon catheter through the lesion and expands the balloon, which deforms the metal stent to its expanded size. The cardiologist may optimize the fit of the stent using intravascular imaging (IVUS or OCT) to guide the work. It is critically important that the framework of the stent be in direct contact with the walls of the vessel to minimize potential complications such as stent thrombosis and restenosis.
Dual Antiplatelet Therapy After Drug-Eluting Stent Implantation
Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor (typically clopidogrel, prasugrel, or ticagrelor) is mandatory after DES implantation to prevent stent thrombosis.
Standard Duration
The 2016 ACC/AHA Guideline Focused Update on Duration of DAPT established that the standard duration of DAPT after DES implantation is at least 6 months for patients with stable coronary artery disease and at least 12 months for patients presenting with acute coronary syndrome.[27]
Extended DAPT
Extended DAPT (18–48 months) after DES resulted in approximately 1%–2% absolute decrease in late stent thrombosis and ischemic complications and approximately 1% absolute increase in bleeding.[27] In the DAPT trial, 30-month vs. 12-month DAPT after DES reduced very late stent thrombosis by 0.7%, myocardial infarction by 2.0%, and MACE by 1.6%, but increased moderate/severe bleeding by 0.9%. For everolimus-eluting stents specifically, extended DAPT resulted in 0.4% absolute reduction in stent thrombosis, 1.1% reduction in MI, and 1.2% increase in moderate/severe bleeding.[27]
Shortened DAPT
Seven randomized controlled trials have suggested that 6-month or even 3-month DAPT may be as effective and safer than 12-month DAPT after DES. The benefit-risk ratio of prolonged DAPT appears better in patients with MI than without prior MI. A personalized approach is advisable.[28]
The STOPDAPT-2 trial (3,045 patients) demonstrated that 1-month DAPT followed by clopidogrel monotherapy was noninferior to 12-month DAPT after contemporary DES for the composite of cardiovascular death, myocardial infarction, definite stent thrombosis, stroke, or major bleeding at 12 months.[29]
Complications
Risks Due to Cardiac Catheterization
As with all cardiac catheterization, there are several risks. Patients may exhibit severe allergic reaction to the contrast agents used to visualize the coronary arteries, and occasionally, the peripheral entry artery fails to properly heal after the catheter is removed, causing a hematoma.
Coronary Artery Perforation
Rarely, a coronary artery can be perforated while the catheter is advanced or during stent placement.
In-Stent Restenosis
In-stent restenosis (ISR) remains a clinical concern despite the significant reductions achieved with DES. ISR occurs in approximately 5% to 10% of patients undergoing PCI with DES, compared with 20–30% with BMS. The primary mechanism is neointimal hyperplasia. Restenosis after DES implantation is generally more focal than following BMS placement. Risk factors include stent underexpansion, stent fracture, lesion complexity, small vessel diameter, diabetes mellitus, and chronic kidney disease.[3][1]
Management of ISR is discussed in detail on the PCI complications: restenosis page.
Stent Thrombosis
Stent thrombosis is classified by timing:[3]
Acute stent thrombosis: Within 24 hours of implantation
Subacute stent thrombosis: 24 hours to 30 days
Late stent thrombosis: 30 days to 1 year
Very late stent thrombosis: Beyond 1 year
Early stent thrombosis is usually due to residual target-lesion thrombus, stent underexpansion or malapposition, or nonadherence to dual antiplatelet therapy. Late stent thrombosis is usually associated with inadequate neointimal coverage, incomplete healing, or premature discontinuation of DAPT.[3]
With contemporary newer-generation DES, the risk of definite stent thrombosis has decreased to <1% at 1 year and <0.5% per year thereafter.[5] Both sirolimus and paclitaxel-eluting first-generation stents were associated with a small but statistically higher risk of thrombosis after the first year compared to BMS; this limitation has been largely overcome with second-generation and newer-generation DES.[5][12]
Allergic Reaction
Rarely, a type of hypersensitivity reaction to the drug or polymer may occur. Episodes of hypersensitivity-related late coronary thrombosis have been reported, particularly with first-generation sirolimus-eluting stents.[30]
DES Versus CABG for Left Main and Multivessel Disease
The choice between PCI with DES and CABG for patients with left main or multivessel coronary artery disease remains an area of active investigation.
EXCEL Trial
The EXCEL trial randomized 1,905 patients with left main coronary artery disease (SYNTAX score ≤32) to PCI with second-generation everolimus-eluting stents versus CABG. There was no difference in the primary composite endpoint (death, stroke, myocardial infarction) at 3 years. At 5 years, CABG was associated with lower all-cause mortality and repeat revascularization.[3]
NOBLE Trial
The NOBLE trial enrolled 1,201 patients with left main coronary artery disease. At 5 years, CABG was superior to PCI for the composite MACCE endpoint, with lower rates of nonprocedural myocardial infarction and repeat revascularization. There was no difference in all-cause mortality.[31]
2021 ACC/AHA/SCAI Guideline Recommendations: Choice of Stent Type
| Class 1 Recommendation, Level of Evidence: A[3] |
| In patients undergoing PCI, DES are recommended in preference to BMS to reduce the risk of restenosis, myocardial infarction, and acute stent thrombosis. |
| Class 1 Recommendation, Level of Evidence: A[3] |
| In patients undergoing PCI with DES, the safety ranking of stent types is: durable-polymer DES ≥ biodegradable-polymer DES > BMS. |
Landmark Clinical Trials: Long-Term Outcomes
The following table summarizes 5-year outcomes from landmark randomized controlled trials comparing first-generation DES with BMS:[32]
| Trial | DES Type | TLR (DES vs. BMS) | MACE (DES vs. BMS) |
|---|---|---|---|
| RAVEL (5-year) | Sirolimus-eluting | 10.3% vs. 26.0% (P<0.001) | 25.8% vs. 35.2% (P=0.03) |
| SIRIUS (5-year) | Sirolimus-eluting | 9.4% vs. 24.4% (P<0.001) | 20.3% vs. 33.5% (P<0.001) |
| TAXUS IV (5-year) | Paclitaxel-eluting | 16.9% vs. 27.4% (P<0.001) | 24.0% vs. 32.8% (P<0.001) |
References
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- ↑ 2.0 2.1 2.2 2.3 Byrne RA, Stone GW, Ormiston J, Kastrati A (2017). "Coronary balloon angioplasty, stents, and scaffolds". Lancet. 390 (10096): 781–792. doi:10.1016/S0140-6736(17)21754-5. PMID 28872850.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Lawton JS, Tamis-Holland JE, Bangalore S, Bates ER, Beckie TM, Bischoff JM, Bittl JA, Cohen MG, DiMaio JM, Don CW, Fremes SE, Gaudino MF, Goldberger ZD, Grant MC, Jasber JB, Kurlansky PA, Mehran R, Metkus TS, Nnacheta LC, Rao SV, Sellke FW, Sharma G, Yong CM, Zwischenberger BA (2022). "2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines". J Am Coll Cardiol. 79 (2): e21–e129. doi:10.1016/j.jacc.2021.09.006. PMID 34895950 Check
|pmid=value (help). - ↑ 4.0 4.1 Piccolo R, Bonaa KH, Efthimiou O, Varber O, Connolly SJ, Eikelboom JW, Gibson CM, Tendera M, Valgimigli M, Windecker S, Jüni P (2019). "Drug-eluting or bare-metal stents for percutaneous coronary intervention: a systematic review and individual patient data meta-analysis of randomised clinical trials". Lancet. 393 (10190): 2503–2510. doi:10.1016/S0140-6736(19)31272-8. PMID 31056295.
- ↑ 5.0 5.1 5.2 5.3 5.4 Palmerini T, Biondi-Zoccai G, Della Riva D, Mariani A, Sabaté M, Smits PC, Kaiser C, D'Ascenzo F, Frati G, Mancone M, Genereux P, Stone GW (2013). "Stent thrombosis with drug-eluting stents: is the paradigm shifting?". J Am Coll Cardiol. 62 (21): 1915–1921. doi:10.1016/j.jacc.2013.08.725. PMID 24036027.
- ↑ 6.0 6.1 Gallo R, Padurean A, Jayaraman T, Marx S, Roque M, Adelman S, Chesebro J, Fallon J, Fuster V, Marks A, Badimon JJ (1999). "Inhibition of intimal thickening after balloon angioplasty in porcine coronary arteries by targeting regulators of the cell cycle". Circulation. 99 (16): 2164–2170. doi:10.1161/01.cir.99.16.2164. PMID 10217658.
- ↑ Marlevi D, Edelman ER (2021). "Vascular lesion-specific drug delivery systems: JACC state-of-the-art review". J Am Coll Cardiol. 77 (19): 2413–2431. doi:10.1016/j.jacc.2021.03.312.
- ↑ Nicolas J, Pivato CA, Chiarito M, Beerkens FJ, Cao D, Mehran R (2023). "Evolution of drug-eluting coronary stents: a back-and-forth journey from the bench to bedside". Cardiovasc Res. 119 (3): 631–646. doi:10.1093/cvr/cvac105. PMID 35788828 Check
|pmid=value (help). - ↑ Grüntzig AR, Senning A, Siegenthaler WE (1979). "Nonoperative dilatation of coronary-artery stenosis: percutaneous transluminal coronary angioplasty". N Engl J Med. 301 (2): 61–68. doi:10.1056/NEJM197907123010201. PMID 449946.
- ↑ 10.0 10.1 10.2 10.3 Serruys PW, Kutryk MJ, Ong AT (2006). "Coronary-artery stents". N Engl J Med. 354 (5): 483–495. doi:10.1056/NEJMra051091. PMID 16452560.
- ↑ Bønaa KH, Mannsverk J, Wiseth R, Aarber K, Grundvold I, Valborgland T, Fjeld JG, Steffensen GK, Slette GK, Steigen T, Trovik T, Myreng Y, Bøhmer E, Arnesen H, Kjeldsen SE, Moer R, Bendz B, Stavnes S, Jakobsen OJ, Jørgensen B, Endresen K, Andersen K, Forsdahl SH, Selfors A, Hanssen TA, Wiseth R (2016). "Drug-eluting or bare-metal stents for coronary artery disease". N Engl J Med. 375 (13): 1242–1252. doi:10.1056/NEJMoa1607991. PMID 27659749.
- ↑ 12.0 12.1 Bangalore S, Kumar S, Fusaro M, Amoroso N, Attubato MJ, Feit F, Bhatt DL, Slater J (2012). "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. 125 (23): 2873–2891. doi:10.1161/CIRCULATIONAHA.112.097014. PMID 22586281.
- ↑ 13.0 13.1 Babapulle MN, Joseph L, Bélisle P, Brophy JM, Eisenberg MJ (2004). "A hierarchical Bayesian meta-analysis of randomised clinical trials of drug-eluting stents". Lancet. 364 (9434): 583–591. doi:10.1016/S0140-6736(04)16850-5. PMID 15313358.
- ↑ Colmenarez H, Fernández C, Escaned J (2014). "Impact of technological developments in drug-eluting stents on patient-focused outcomes: a pooled direct and indirect comparison of randomised trials comparing first- and second-generation drug-eluting stents". EuroIntervention. 10 (2): 249–257. doi:10.4244/EIJV10I2A41. PMID 23771557.
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- ↑ Kastrati A, Dibra A, Eberle S, Mehilli J, Suárez de Lezo J, Goy JJ, Ulm K, Schömig A (2005). "Sirolimus-eluting stents vs paclitaxel-eluting stents in patients with coronary artery disease: meta-analysis of randomized trials". JAMA. 294 (7): 819–825. doi:10.1001/jama.294.7.819. PMID 16103034.
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- ↑ von Birgelen C, Kok MM, van der Heijden LC, ";";";";";"; Danse PW, ";";";";";";";";";";";";"; Löwik MM, van der Palen J, "; Munnink JT, "; Stoel MG, van Houwelingen KG, "; Alings FMW, Jansen J, Man F, Giannitsis E, Linssen G, Doggen C, von Birgelen C (2016). "Very thin strut biodegradable polymer everolimus-eluting and sirolimus-eluting stents versus durable polymer zotarolimus-eluting stents in allcomers with coronary artery disease (BIO-RESORT): a three-arm, randomised, non-inferiority trial". Lancet. 388 (10060): 2607–2617. doi:10.1016/S0140-6736(16)31920-1. PMID 27806897. Vancouver style error: punctuation (help)
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|pmid=value (help). - ↑ Chen YL, Fan J, Chen G, Zhu SH, Guo YH, Ye MX, Huang ZM (2019). "Polymer-free drug-eluting stents versus permanent polymer drug-eluting stents: an updated meta-analysis". Medicine (Baltimore). 98 (15): e15180. doi:10.1097/MD.0000000000015180. PMID 30985722.
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