Intracoronary Stents

Anatomy and Physiology

Coronary stents are expandable, tubular mesh-like scaffolds designed to restore and maintain vessel patency following PCI. Structurally, stents consist of 3 key anatomical components—the platform, the polymer coating (in DES), and the antiproliferative drug. The platform provides radial strength to prevent vessel recoil while maintaining flexibility for navigating through complex coronary anatomy. Early-generation stents were made of stainless steel, but advancements have led to thinner struts composed of cobalt-chromium or platinum-chromium alloys. These improvements enhance deliverability and mechanical performance while reducing vessel trauma. The polymer coating acts as a reservoir to regulate the release of antiproliferative agents, with hydrophobic, hydrophilic, or bioabsorbable properties designed to improve biocompatibility and minimize inflammation.

The drug component, historically either sirolimus or paclitaxel, inhibits SMC proliferation to prevent neointimal hyperplasia and reduce the risk of in-stent restenosis. Studies suggest that sirolimus and similar agents are more effective than paclitaxel in reducing neointimal hyperplasia and restenosis, although both carry similar risks of thrombosis and myocardial infarction.[9] Most newer-generation DES utilize sirolimus analogs such as everolimus, zotarolimus, biolimus, or novolimus, further enhancing efficacy while optimizing safety profiles.[10]

Physiologically, coronary stents serve as scaffolds that keep the vessel open, seal dissection flaps caused by balloon angioplasty, and prevent negative remodeling. Their deployment restores blood flow to the myocardium, reducing ischemia. However, stent implantation initiates a vascular healing response, necessitating reendothelialization of the stent struts to minimize thrombogenicity. DES helps balance this process by suppressing excessive SMC proliferation while allowing essential endothelial recovery.

Vessel anatomy and lesion characteristics are critical factors in determining stent deployment strategy and success. Stent sizing is determined based on the maximal diameter of the distal reference segment to avoid under- or oversizing, which can lead to complications such as stent malapposition or vessel injury. In heavily calcified vessels, preprocedural intracoronary imaging (eg, intravascular ultrasound [IVUS] or optical coherence tomography [OCT]) may be warranted to characterize plaque morphology better and determine the need for adjunctive plaque-modifying techniques such as rotational, orbital, or laser atherectomy. Additionally, careful consideration is given to potential side-branch impingement and plaque shift during stent deployment, particularly in bifurcation lesions, where specialized strategies may be required to preserve side-branch flow.[5] Together, the anatomical, mechanical, and pharmacological characteristics of coronary stents, along with patient-specific vessel considerations, support their physiological role in treating CAD, preventing restenosis, and improving clinical outcomes. Ongoing innovations continue to refine stent design, optimizing safety, deliverability, and long-term vessel healing.

Indications

Coronary stents are widely used in the treatment of CAD, particularly in patients with ACS, including ST-elevation myocardial infarction (STEMI), non-ST-elevation myocardial infarction (NSTEMI), and unstable angina. Primary PCI with stent placement is the preferred approach in these cases, as it improves myocardial perfusion, reduces infarct size, and enhances survival outcomes. Coronary stents are also commonly utilized in stable ischemic heart disease when symptoms persist despite optimal medical therapy or when noninvasive testing indicates significant myocardial ischemia.

Intracoronary stent placement is routinely performed following successful balloon angioplasty of a significant lesion or as part of acute myocardial infarction management. Balloon angioplasty alone can cause endothelial injury and small plaque dissections, increasing the risk of acute vessel thrombosis. Without stent placement, restenosis rates after balloon angioplasty alone can reach up to 50%. In contrast, both BMS and DES significantly reduce restenosis rates, target vessel failure, and the need for future revascularization procedures.[11] Please see StatPearls' companion resource, "Acute ST-Segment Elevation Myocardial Infarction (STEMI)," for more information.

Coronary angioplasty with stent placement is indicated in several scenarios:

• STEMI or NSTEMI/ACS requiring urgent revascularization.
• Stable angina refractory to guideline-directed medical therapy.
• Patients experiencing anginal equivalents such as dyspnea, arrhythmia, dizziness, or syncope.
• Objective evidence of medium-to-large areas of ischemia on noninvasive testing.[12][13][14][15]

The circumstances in which BMS may be reasonable have significantly decreased since the advent of DES.[16] Although BMS use has declined, it may still be considered in specific situations, such as for patients requiring noncardiac surgery within 4 to 6 weeks of PCI, those at high risk of bleeding on DAPT, or patients unlikely to comply with prolonged antiplatelet therapy. Evidence shows improved outcomes with newer-generation DES compared to early-generation DES and BMS.[17] For most other patients, current-generation DES are preferred due to their superior outcomes, reduced restenosis rates, and improved biocompatibility.

Technological advancements have led to the development of self-expanding stents that better adapt to vessel size, particularly important in acute myocardial infarction, where vessel diameter may be challenging to assess due to thrombus burden or vessel wall contraction. Biodegradable stents and scaffolds are also being investigated to further reduce long-term complications. Complex lesions, such as bifurcation disease, may benefit from specific stenting techniques like the double-kissing crush technique, which has been shown to reduce stent-related adverse events.

PCI with stent placement is preferred over coronary artery bypass grafting (CABG) in select cases of single-vessel or 2-vessel disease involving the right coronary or circumflex arteries. However, the choice between PCI and CABG is individualized, taking into account anatomical complexity, comorbidities, diabetes status, and patient preferences. Coronary stents remain a cornerstone of modern interventional cardiology, offering essential revascularization options across a broad spectrum of CAD presentations.

Contraindications

Although coronary stenting is a well-established and commonly performed procedure for treating CAD, several absolute and relative contraindications must be carefully considered before proceeding. Most contraindications involve systemic conditions that pose a significant risk for procedural complications or prevent the safe use of essential post-procedural medications.

Absolute Contraindications

• Inability to take dual antiplatelet therapy: Successful stent implantation, particularly with DES, requires prolonged DAPT to prevent stent thrombosis. Patients unable to tolerate aspirin or P2Y12 inhibitors (clopidogrel, prasugrel, and ticagrelor) due to hypersensitivity, severe bleeding risk, or compliance issues are generally not candidates for stenting. Conditions such as active gastrointestinal bleeding, recent hemorrhagic stroke, or known bleeding disorders (eg, hemophilia) make DAPT unsafe.

• Severe anemia or thrombocytopenia: Significant baseline anemia or low platelet counts that impair clot formation increase the risk of procedural and post-procedural bleeding complications. These hematologic conditions may contraindicate both the stenting procedure and the required antiplatelet therapy.

• Diffuse, unstentable coronary artery disease: Extensive disease involving small-caliber vessels, diffuse atherosclerosis, or severe calcification that prevents safe stent deployment constitutes an anatomical contraindication.

• Severe comorbid conditions with limited life expectancy: Patients with terminal malignancies, end-stage organ failure, or advanced systemic disease in whom the risks of the procedure outweigh the potential benefits.

Relative Contraindications

• Active infection or sepsis: Sepsis with active bacteremia is considered a relative contraindication, as implanting a foreign body like a stent in the setting of systemic infection increases the risk of infection-related complications, including endovascular infection.

• Significant renal dysfunction: Severe chronic kidney disease (CKD) or acute kidney injury (AKI) raises the risk of contrast-induced nephropathy during the procedure. Strategies to minimize contrast load or alternative revascularization strategies may be preferred.

• Planned noncardiac surgery requiring interruption of antiplatelet therapy: If major surgery is scheduled within 4 to 6 weeks after PCI, the inability to safely maintain DAPT makes stenting risky. In such cases, consideration should be given to using BMS or deferring PCI.

• Significant bleeding diathesis or coagulopathy: Conditions that impair normal clotting mechanisms may increase the risk of severe bleeding during or after PCI.

• Pregnancy: PCI is generally avoided unless absolutely necessary due to concerns about radiation exposure, contrast-induced toxicity, and the need for antiplatelet therapy.

Additional Considerations

• Coronary anatomy not conducive to PCI: Complex lesions such as chronic total occlusions, ostial lesions, or severe tortuosity may have poor outcomes with stenting and may be better managed surgically.

• Hypersensitivity to contrast media or stent components: Allergy to contrast agents, stent metals (eg, nickel), polymers, or antiproliferative drugs may preclude stent use unless alternative materials or premedication strategies are available.

• Acute aortic dissection: Chest pain from an undiagnosed aortic dissection, mistaken for ACS, represents a contraindication to PCI and stenting.

Equipment

PCI with stent placement is a complex procedure requiring specialized equipment for vascular access, visualization, lesion crossing, stent delivery, and deployment. The procedure is performed in a catheterization laboratory equipped with a single- or biplane cine angiography system, intravascular ultrasound or optical coherence tomography, a motorized radiolucent procedure table, and hemodynamic monitoring systems to ensure patient stability throughout the intervention.

Vascular Access and Guiding Catheters

The procedure begins with arterial access, typically via the femoral or radial artery. A 6 French (6F) or larger guiding catheter is used to engage the coronary ostium, ensuring adequate support, facilitating device delivery, and allowing contrast injection. Proper catheter selection is essential for optimal vessel alignment and procedural success.

Anticoagulation

Systemic anticoagulation is critical to minimize the risk of thrombus formation during the intervention. Unfractionated heparin, enoxaparin, or bivalirudin is administered to achieve an activated clotting time (ACT) greater than 250 seconds, with anticoagulation maintained throughout the procedure.

Coronary Guidewires

After engaging the coronary artery, a 0.014-inch coronary guidewire is advanced across the lesion. The guidewire serves as a rail for delivering balloons and stents to the treatment site. Different types of guidewires are available, including "workhorse" wires, hydrophilic-coated wires for navigating tortuous vessels, and extra-support wires designed for complex lesions.

Balloon Delivery Systems and Stent Deployment

After crossing the lesion, a stent mounted on a balloon catheter is delivered to the target site. The stent delivery balloon is inflated to high atmospheric pressures using an insufflator device, which is manually operated by the technician or interventionalist. This inflation deploys the stent, embedding it within the vessel wall and restoring luminal patency.

Stent Types and Materials

Stent platforms have evolved significantly to address issues such as in-stent restenosis, thrombosis, and delayed healing. Several categories of stents are approved by the US Food and Drug Administration (FDA), as listed below.

• Bare-metal stents: Stainless steel platforms provide mechanical support but are prone to restenosis due to neointimal hyperplasia.
• Durable polymer drug-eluting stents: These stents are constructed from cobalt-chromium or platinum-chromium platforms and incorporate antiproliferative agents such as everolimus or zotarolimus. By releasing these drugs locally, DES inhibit SMC proliferation and reduce neointimal hyperplasia.
• Bioabsorbable polymer drug-eluting stents: These stents are designed to gradually resorb over time, minimizing long-term polymer exposure while continuing to deliver antiproliferative agents.
• Polymer-free drug-coated stents: These stents use microstructured surfaces to hold drugs such as biolimus directly on the stent platform, which may allow for shorter durations of DAPT.
• Bioresorbable scaffolds: These scaffolds are fully resorbed after fulfilling their purpose, eliminating the long-term presence of metal within the vessel.
• Drug-eluting balloons: These balloons are coated with antiproliferative drugs, lack a permanent stent structure, and are particularly useful for treating specific lesion subsets.[18]

DES consists of 3 components—a metallic stent platform, an active pharmacological drug agent, and a carrier vehicle. Stainless steel or cobalt-chromium is the most commonly used metal, providing long-term mechanical stability to counteract vascular recoil. Commonly used drugs work by blocking signal transduction and cell cycle progression at various phases, thereby inhibiting SMC proliferation or intimal hyperplasia at the stented arterial site. Rapamycin agents bind to the intracellular protein FKBP-12, which inhibits the protein kinase mTOR. Rapamycin agents bind to the intracellular protein, FKBP-12, which inhibits the protein kinase mTOR. This intracellular complex increases the expression of p27 and blocks the progression of the cell cycle from the G1 phase to the S phase (DNA synthesis). Taxanes are another class of drugs that interfere with microtubule function, which is necessary for the M phase (mitosis). As a result, cells are arrested in the G2 phase of the cell cycle.

A carrier vehicle matrix or polymer coating is used to facilitate sufficient drug loading and long-term release to increase surface area. The polymer coating consists of repeating units of biodegradable poly-L-lactide, poly-D, and L-lactic-co-glycolic acid in a regular pattern. These components are broken down into lactic acid and glycolic acid, which are ultimately converted into water and carbon dioxide. First-generation DES features a coating of sirolimus or paclitaxel on a stainless steel base. In contrast, second-generation DES utilizes zotarolimus or everolimus on a biocompatible cobalt-chromium or platinum-chromium platform. Drug release occurs through diffusion via pores in the polymeric coating.

While drug-eluting balloons have only an antiproliferative drug coating without an underlying metallic stent structure, bioresorbable scaffolds are also free of metal and are fully resorbed within a few months after serving their purpose. Other specialized stents, such as bifurcation stents and covered stents, are designed for specific circumstances, such as lesions over vascular bifurcations or coronary artery perforations, respectively.[19][20]

A major drawback of BMS is in-stent restenosis due to intimal layer injury. Neo-intimal hyperplasia is the underlying mechanism, where intimal injury leads to increased SMC migration and proliferation, resulting in restenosis. DES are designed to locally deliver anti-restenotic drugs that inhibit SMC migration and proliferation at the stent site, without causing systemic adverse drug effects. The efficacy of the drug depends on factors such as diffusion rate, tissue accumulation, distribution, and local vascular toxicity. Achieving a balance between adequate drug delivery and minimal local vascular toxicity is crucial. The rate of diffusion is influenced by several factors, including coating thickness, drug load, drug-to-polymer ratio, and the partition coefficient of the drug. The partition coefficient is directly proportional to the rate of diffusion.

Drug release follows an initial rapid phase due to the immediate dissolution of the drug from the outermost layer of the polymer coating. This fast-phase release follows first-order kinetics, with the majority of the total available dose being released within the first few days. Subsequently, a sustained, slower-release phase occurs, primarily driven by diffusion-mediated release. A higher loading dose typically results in a greater release during the initial fast-release phase.

The transport and distribution of a drug in arterial tissue are influenced by its hydrophobic, hydrophilic, or lipophilic properties. Hydrophilic drugs readily mix with blood, allowing for wider distribution in and around local arterial tissue but resulting in lower local drug concentrations. In contrast, hydrophobic drugs tend to accumulate more homogeneously within arterial tissue, leading to higher local drug concentrations and slower clearance. Lipophilic drugs exhibit a slower release rate.[21]

Studies have shown that rapamycin and paclitaxel can enhance the expression of prothrombotic factors, such as tissue factor and plasminogen activator inhibitor-1. When local drug toxicity occurs at the stent site, leading to delayed re-endothelialization, the acidic byproducts (lactic acid and glycolic acid) from polymer degradation, along with these prothrombotic factors, can increase the risk of stent thrombosis due to platelet activation. This risk is more pronounced when antithrombotic drugs are discontinued postoperatively. Additionally, hypersensitivity to polymer coatings has been reported, further contributing to chronic inflammation at the stent site.[22][23][2]

Evolution of Stent Technology

• First-generation drug-eluting stents: The TAXUS study demonstrated that the use of first-generation DES reduced the rate of target vessel revascularization (TVR) by 50% over a 5-year period compared to BMS. However, the major issue with first-generation DES was the occurrence of very late stent thrombosis events. Long-term follow-up of patients in the TAXUS study revealed an increase in myocardial infarction rates over the 5-year period, attributed to these late thrombosis events. This was suspected to be partly due to the polymer used for drug delivery in first-generation DES, as well as the fact that up to 60% of the stent surface area never fully endothelialized. The drug and polymer combination in these early stents effectively prevented neointimal hyperplasia, but it also hindered endothelialization at the stent site, contributing to the occurrence of very late stent thrombosis.[24][25]

• Second-generation drug-eluting stents: Second-generation DES were developed to address the issues and limitations of first-generation stents. These stents feature thinner struts, promoting faster healing and endothelialization of the coronary arteries while reducing inflammation and injury to the vessel wall. Unlike the stainless steel base of first-generation stents, second-generation DES are made from cobalt-chromium, which enhances their malleability and ease of delivery. Second-generation stents feature fluorinated polymers, which enhance biocompatibility and provide thromboresistant properties. Everolimus and zotarolimus are the primary drugs used to inhibit neointimal hyperplasia in these stents. The SPIRIT II, III, and IV and COMPARE trials demonstrated that everolimus-eluting stents significantly reduced major adverse cardiovascular events (MACE)—including cardiac death, myocardial infarction, and ischemic target vessel revascularization—by 30% to 40% over 24 months compared to paclitaxel-eluting stents. Additionally, these second-generation DES lowered the incidence of very late stent thrombosis by approximately 70%.[26][27]

• Third-generation drug-eluting stents: Third-generation DES, currently under development, feature thinner struts and may incorporate bioabsorbable polymers, no polymer at all, or scaffolds that degrade over time. In the BIOFLOW V trial, a 60-micron thin-strut, bioabsorbable third-generation DES was compared to a current DES with 82-micron struts and durable fluoropolymer. The results showed a significant reduction in target lesion failure and event rates in the thinner strut group, likely due to the lower profile of the thinner stent. A meta-analysis by Bangalore and Stone compared ultra-thin stents (<70 microns) with thicker strut second-generation stents, revealing a trend toward better outcomes in the thinner stent group, driven by reduced target lesion failure and stent thrombosis. Another meta-analysis by Palmerini compared bioabsorbable polymer-based DES with durable polymer-based DES, showing a slight trend toward lower cardiac death and myocardial infarction compared to BMS. Additionally, there was less TVR in the bioabsorbable stent group compared to BMS, although no significant benefit was observed over the current durable polymer DES. In the EVOLVE II trial, which compared a bioabsorbable stent to a durable polymer DES after 36 months, no significant difference in target lesion failure was observed between the 2 stents.[28][29][30][31]

Another promising development in third-generation stents is polymer-free, drug-coated stents. These 120-micron-thick stainless steel stents feature microstructured surfaces that hold the antiproliferative drug on an abluminal surface. Polymer-free stents may enable shorter dual antiplatelet therapy durations and eliminate potential issues related to nonuniform drug elution from polymer coatings. Specifically, one such stent releases biolimus, which is 10 times more lipophilic than sirolimus, everolimus, and zotarolimus, allowing it to remain in the surface layers of cells and self-elute over time.

In the LEADERS FREE trial, the drug-coated stent significantly reduced target lesion failure compared to a BMS, as well as lowered rates of myocardial infarction and cardiac death. However, stent thrombosis rates were similar between the 2 groups. The similar stent thrombosis rates may be attributed to the large stent structure (120 microns). A newer version of this stent, featuring more malleable, thinner struts, is expected to address this issue. Another promising concept for the future involves thin-strut drug-filled stents with an outer cobalt alloy layer, a middle tantalum layer, and an inner core material removed, creating a lumen filled with antiproliferative medication. This design was tested in the RevElution trial and showed less in-stent late loss over a 9-month period.[32][33][34][35][36][37]

Additional Specialized Stents

Specialty stents, such as bifurcation and covered stents, are designed for complex anatomical challenges, including vessel bifurcations or to seal coronary artery perforations.[19][20]

Personnel

The successful execution of coronary stenting procedures requires a skilled, multidisciplinary healthcare team, with each member contributing expertise to ensure optimal patient outcomes.

• Interventional cardiologist 
• Cardiovascular nursing specialist
• Cardiovascular or radiology-trained technologist
• Advanced practice provider (physician assistant or cardiac nurse practitioner)
• Ancillary staff, including clinical pharmacists and technical assistants 
• Anesthesia personnel (when necessary)

Preparation

Preparation for coronary stent placement (PCI) begins with a comprehensive pre-procedural evaluation, emphasizing the patient’s cardiovascular history, comorbid conditions, and current medications. A detailed review of prior cardiac events, existing CAD, heart failure, arrhythmias, and bleeding risks is essential, along with screening for allergies to contrast agents. Patients are typically required to remain NPO (nothing by mouth) for 6 to 8 hours before an elective procedure to minimize the risk of aspiration if sedation is used. DAPT, consisting of aspirin and a P2Y12 inhibitor such as clopidogrel, should be initiated or confirmed before the procedure, with loading doses administered as needed. Laboratory tests, including a complete blood count, metabolic panel, coagulation studies, and type and screen, are conducted to establish baselines and assess procedural risk. A baseline electrocardiogram (ECG) and review of any recent imaging, such as echocardiograms or coronary computed tomography (CT) angiograms, help guide procedural planning.

On the day of the procedure, patients should continue most cardiac medications but may be advised to withhold nephrotoxic drugs or certain diabetes medications, such as metformin, to reduce the risk of contrast-induced nephropathy. Intravenous (IV) hydration may be administered, particularly in patients with CKD, to help preserve renal function. Informed consent is obtained after discussing the procedure’s purpose, steps, and potential risks, including bleeding, vascular complications, arrhythmias, stroke, myocardial infarction, and the possibility of emergency coronary artery bypass surgery. The requirement for prolonged DAPT post-stenting is also reviewed. The access approach—radial or femoral—is selected based on patient anatomy and comorbidities, with radial access often preferred to minimize bleeding risk.

During the procedure, proper vessel preparation is essential before stent deployment. Balloon angioplasty is typically performed first to assess the lesion’s ability to expand and refine measurements of its length. This step also serves a diagnostic purpose, as inadequate lesion expansion may indicate significant calcification or resistant plaque. Simple balloon angioplasty may be insufficient in heavily calcified vessels, making stent delivery technically challenging or even impossible without additional intervention. In such cases, vessel modification techniques, such as rotational or orbital atherectomy, are used to debulk and remodel the calcified plaque, enhancing vessel compliance and facilitating the successful delivery and deployment of the stent.[38][39]

Throughout the procedure, contrast use and radiation exposure are minimized to reduce the risk of complications, particularly in patients with preexisting renal impairment. Sedation is typically light to moderate, ensuring patients remain conscious but comfortable. After the procedure, patients are monitored for bleeding, vascular complications, arrhythmias, and signs of myocardial ischemia, with particular attention to renal function in the hours following contrast exposure. They receive counseling on the necessity of continued DAPT, lifestyle modifications, and routine follow-up care to enhance long-term outcomes.

Technique or Treatment

Once the patient is adequately prepared, continuous vital sign monitoring is initiated, along with IV fluid administration and appropriate anticoagulation to reduce thrombotic risk during the intervention. Vascular access is obtained—typically via the radial or femoral artery—based on operator preference and patient anatomy. Multiple anatomical sites are cleaned, sterilized, and draped in preparation. After access is secured, diagnostic coronary angiography is performed to identify significant coronary lesions requiring intervention. Once a critical lesion is confirmed, the procedure transitions to PCI.

A guiding catheter is advanced under fluoroscopic guidance to the ostium of the affected coronary artery, and a flexible coronary guidewire is navigated across the target lesion. This guidewire serves as the rail for subsequent devices. Initial lesion preparation typically involves balloon angioplasty to predilate the narrowed segment, assess lesion compliance, and refine lesion length measurements. If the lesion is significantly calcified or resistant to dilation, adjunctive plaque modification techniques, such as rotational or orbital atherectomy, may be used to improve vessel compliance and facilitate stent delivery.

Once the lesion is adequately prepared, an appropriately sized intracoronary stent—usually a DES—mounted on a balloon catheter is advanced over the guidewire. Under continuous fluoroscopic guidance, the stent is carefully positioned to ensure full lesion coverage, with proximal and distal landing zones in healthy vessel segments. Intravascular imaging techniques, such as IVUS or OCT, may be utilized at this stage to confirm optimal stent sizing, lesion length, and morphology.

Once the stent is in the correct position, the balloon catheter is connected to an insufflator device and inflated to high pressures to deploy the stent against the vessel wall. This process embeds the stent into the arterial wall, restoring vessel patency. After deployment, additional intravascular imaging may be performed to confirm proper stent expansion, apposition, and to check for any significant edge dissections or complications. If needed, postdilation with a high-pressure, noncompliant balloon may be performed to further optimize stent expansion, particularly in calcified or tortuous vessels. Once a satisfactory result is confirmed, the equipment is removed, hemostasis is achieved at the access site, and the patient continues DAPT to reduce the risk of in-stent thrombosis and promote endothelialization of the stent.

Complications

Complications related to intracoronary stent placement can arise both during the procedure and in the short or long term after stent deployment. Procedural risks include vessel dissection and coronary perforation, which are also possible with balloon angioplasty. Although rare, coronary perforation is a severe complication that can increase 30-day mortality by 5-fold. This is typically caused by balloon or stent oversizing relative to the vessel wall but can also occur in calcified arteries or higher-risk patients, such as those with prior CABG, advanced age, or female sex.[40] Dissection of the coronary artery, another potential procedural complication, involves disruption of the vessel wall, which can compromise blood flow, lead to ischemia, or even result in myocardial infarction.

Device-related complications also present significant risks. Although rare, stent embolization can occur if the stent dislodges from its delivery balloon during advancement. In such cases, the stent may either be deployed at its unintended location or retrieved using a snare device. Another mechanical complication is longitudinal stent deformity, which is more commonly observed with newer-generation, thinner chromium or platinum stents. While these stents offer improved radial strength and flexibility, they may lack longitudinal integrity, leading to deformation, strut protrusion into the lumen, malapposition, and an increased risk of thrombosis.[40] Failure of stent deployment, more common with first-generation stents, is another serious procedural complication, occurring in 2% to 8.3% of cases. Stent dislodgment from the balloon tip can lead to embolization and procedural failure. However, advancements in stent design, particularly with second- and third-generation stents, have significantly reduced the incidence of this complication.[41]

One of the most severe and life-threatening complications is stent thrombosis, which can lead to acute myocardial infarction or death. Stent thrombosis is classified by timing—acute (within hours), subacute (within 30 days), and late (after 1 year, typically with DES). Premature discontinuation of DAPT is a major risk factor for stent thrombosis.[42] Although exceedingly rare, stent infection is another catastrophic complication that can result in coronary artery perforation or the formation of a mycotic aneurysm.[43]

Other potential complications include the formation of coronary artery aneurysms—rare but mostly associated with DES—as well as myocardial ischemia or infarction, arrhythmias, access site bleeding, retroperitoneal hematoma, atheroembolism, AKI from contrast exposure, hypersensitivity reactions, and stroke. Each of these complications highlights the importance of careful patient selection, meticulous technique, and vigilant post-procedural monitoring during coronary stent placement.

Clinical Significance

The evolution of coronary stents has been central to the advancement of PCI, significantly improving outcomes in patients with CAD. Beginning with Andreas Grüntzig's introduction of balloon angioplasty in 1977, PCI revolutionized the treatment of obstructive coronary lesions by eliminating the need for open thoracotomy, providing a life-saving option for acute myocardial infarction.[44] However, early balloon angioplasty was hindered by issues such as abrupt vessel closure, elastic recoil, and restenosis.

The development of BMS in 1986 addressed these limitations by preventing acute vessel recoil and dissection. BMS rapidly became the standard of care, especially when combined with optimized implantation techniques and DAPT. However, despite their early success, BMS induced vascular SMC proliferation, leading to neointimal hyperplasia and in-stent restenosis in up to 30% of patients, which presents a significant clinical challenge.[45] The Belgium Netherlands Stent Arterial Revascularization Therapies Study (BENESTENT) and the North American Stent Restenosis Study (STRESS) are the 2 pivotal randomized controlled trials that demonstrated that BMS reduced restenosis and the need for repeat revascularization compared to balloon angioplasty in patients with stable CAD. These findings led to the widespread adoption of BMS by the late 1990s.[46][47]

DES were introduced in the early 2000s to reduce restenosis, and they incorporate antiproliferative agents within a polymer-coated metallic framework. First-generation DES, such as the CYPHER^® sirolimus-eluting and TAXUS^® paclitaxel-eluting stents, significantly reduced neointimal hyperplasia. Clinical trials, such as RAVEL and TAXUS-IV, showed superior outcomes with DES over BMS in reducing restenosis and target lesion revascularization.[50] Large meta-analyses further confirmed substantial reductions in revascularization rates with DES compared to BMS, reporting hazard ratios for TVR of 0.45 (95% CI, 0.37-0.54) in randomized trials and 0.54 (95% CI, 0.48-0.61) in observational studies. However, first-generation DES were associated with delayed healing and an increased risk of stent thrombosis, particularly early after placement. This necessitated prolonged DAPT, which in turn increased bleeding risks. Systematic reviews by the European Society of Cardiology (ESC) and the European Association for Percutaneous Cardiovascular Interventions (EAPCI) confirmed the early benefits of DES in reducing target lesion revascularization compared to BMS, but also underscored the need for safety improvements.

The development of newer-generation DES addressed many of these issues. These stents feature thinner struts (50-90 μm versus 130-150 μm in earlier models), which improve hemodynamics, reduce vessel injury, and lower thrombogenicity. New stent platforms incorporate biocompatible or biodegradable polymers, such as vinylidene-fluoride hexafluoropropylene copolymers or lactic or glycolic acid derivatives, enhancing safety and ensuring more consistent drug delivery. Additionally, some newer DES eliminate polymers completely, directly releasing drugs from the stent surface to minimize inflammatory responses.

Sirolimus and its analogs, including everolimus, zotarolimus, and biolimus, became the preferred antiproliferative agents, offering better efficacy than paclitaxel due to their mechanisms of action, which inhibit protein synthesis, cell cycle progression, and migration. Everolimus-eluting stents, such as XIENCE^®/Promus, now have the most extensive supporting trial data. The NORSTENT trial demonstrated that DES reduced restenosis rates (0.8% versus 1.2% in BMS, hazard ratio 0.64, 95% CI: 0.41-1.00, P = .0498). However, long-term mortality and myocardial infarction rates were similar, confirming that the principal benefit of DES is reducing repeat revascularization rather than impacting survival.[48] 

Despite these advances, DES still face challenges. Irregularities in polymer coatings can lead to inconsistent drug delivery and create thrombus-prone surfaces. Stent fractures and longitudinal deformation occur in 2% to 5% of cases, particularly in the right coronary artery, potentially compromising stent integrity and outcomes.[5] The permanent metallic nature of DES also alters vessel compliance, impairs cyclic strain, and reduces vasomotion, thereby contributing to long-term vessel dysfunction. Notably, neoatherosclerosis has emerged as a late complication, where lipid-laden plaques develop within the stent, thereby mimicking native atherosclerosis.[5]

Certain patient populations continue to present higher risks, which indicate further areas of innovation.

• Diabetes mellitus: Diabetic patients experience accelerated atherosclerosis and diffuse multivessel disease. Novel DES with enhanced anti-inflammatory and antiproliferative properties may improve outcomes for this group.[49]
• Acute myocardial infarction: Although DES are crucial in acute myocardial infarction management, challenges such as stent malapposition due to vasoconstriction and thrombus burden may persist. Self-expanding and mesh-covered stents are being explored to better adapt to vessel anatomy and prevent distal embolization.[50][51]
• Restoration of vascular physiology: Permanent stents impair normal vessel function. Fully bioresorbable stents are a promising solution, designed to temporarily support the vessel and fully degrade over time, potentially restoring normal physiology.[52]
• Complex lesions: Heavily calcified and bifurcation lesions remain challenging to treat. Ongoing development of specialized devices and techniques aims to reduce complications and improve long-term patency in these anatomically challenging cases.[5]

Clinically, DES has revolutionized the management of CAD by reducing restenosis, particularly in high-risk patients with complex lesions, left main disease, or diabetes. The EXCEL trial demonstrated the non-inferiority of PCI with new-generation DES compared to CABG in patients with low-to-moderate anatomical complexity (SYNTAX score <33) in terms of MACE over 3 years.[53] However, the NOBLE trial showed that CABG was superior in treating complex left main disease, emphasizing that surgical revascularization remains essential in selected cases.[54]

Enhancing Healthcare Team Outcomes

The management of CAD involves an interprofessional healthcare team, including nurses, pharmacists, therapists, and dietitians. As CAD is a progressive disorder, all treatments are considered palliative. Healthcare providers must address the process of atherosclerosis and work to halt its progression. Patient education on lifestyle changes is essential, as no treatment can be effective in the long term without these modifications

Nursing, Allied Health, and Interprofessional Team Interventions

An interprofessional healthcare team, comprising nursing staff, home health caregivers, and primary care physicians, should develop an integrated postoperative care plan in collaboration with the operating cardiologist. DAPT is indicated to prevent stent thrombosis for all patients, and medication compliance is crucial for ensuring optimal outcomes. 

Patients with BMS need at least 1 month of DAPT, whereas those with DES need 6 to 12 months. In patients with a low risk of bleeding complications, 18 to 24 months of DAPT is recommended. A recently published study found that 1 to 3 months of DAPT use did not increase the odds of postoperative stent-related complications but reduced the odds of bleeding by 30%. Stent thrombosis, a lethal complication of coronary artery stent placement, is mitigated by DAPT, which also reduces the risk of major adverse cardiac events such as cardiac death, myocardial infarction, or stroke. 

Pharmacy consultation should focus on medication safety instructions, emphasizing the importance of patient compliance. Additionally, home health care counseling should include guidance on diet and exercise modifications. Primary care physicians should be updated with accurate medication reconciliation upon discharge. The patient's medical records and care plan should be forwarded to the primary care physician to ensure continuity of care. A follow-up appointment should be scheduled within 3 days, with a cardiology follow-up within 1 to 2 weeks.