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Percutaneous Coronary Intervention Technique

  • Author: George A Stouffer, III, MD; Chief Editor: Karlheinz Peter, MD, PhD  more...
Updated: Jun 25, 2015


Coronary angiography and percutaneous coronary intervention (PCI) are more commonly performed via the femoral or the radial artery and less commonly performed via the brachial or ulnar artery. Overall, the femoral artery is the most common route of access for these procedures; however, the use of radial access is increasing.

Two randomized, controlled trials reported lower mortality with transradial access than with femoral access in ST-segment elevation myocardial infarction (STEMI) patients undergoing PCI. In the RIFLE STEACS (Radial Versus Femoral Randomized Investigation in ST-Elevation Acute Coronary Syndrome) study, a multicenter randomized trial involving 1001 STEMI patients, radial access was associated with significantly lower rates of cardiac mortality (5.2% vs 9.2%) and bleeding (7.8% vs 12.2%) than femoral access was.[75]

The RIVAL (Radial Versus Femoral Access for Coronary Intervention) trial compared the efficacy and bleeding outcomes of radial and femoral access separately in patients with STEMI and non-STEMI (NSTEMI).[76] Radial access was associated with reduced all-cause mortality (1.3% vs 3.2%) and reduced death/myocardial infarction (MI)/stroke (2.7% vs 4.6%) in STEMI patients but not in NSTEMI patients. In both STEMI and NSTEMI groups, radial access was associated with significantly reduced ACUITY major bleeding and major vascular access site complications.

The European Society of Cardiology guidelines on STEMI patients recommend preference of radial over femoral access, if performed by an experienced radial operator (class IIa, level B). The Society for Cardiovascular Angiography and Interventions released a consensus statement on best practices for the use of radial access for diagnosing and treating coronary artery disease (CAD), focusing on avoiding radial artery occlusion, reducing radiation exposure, and using the transradial approach in STEMI.[77]

Recommendations for STEMI patients include the following:

  • Before integrating the radial approach into practice, clinicians should gain experience with at least 100 elective radial procedures and have a femoral crossover rate lower than 4%
  • Practitioners should start with easier cases and ensure that all laboratory personnel are comfortable with the procedure
  • A bailout approach to either contralateral radial or femoral access should be prepared in advance


The patient is prepared as described earlier (see Patient Preparation).

For transradial catheterization, an arteriotomy is made approximately 2 cm proximal to the radial styloid process so as to avoid the distal bifurcation and diminutive vessels. While palpation is being done, the radial artery is punctured with a micropuncture needle, and a hydrophilic sheath is placed by means of the modified Seldinger technique.

Once the sheath is in place, an intra-arterial vasodilator is given (nicardipine 500 µg or verapamil 5 mg), with half the dose administered at the beginning of the procedure and the other half at the end. Intravenous (IV) heparin dramatically reduces the risk of radial artery occlusion and is therefore often used in transradial catheterization (usual dose, 50 units/kg; maximum total dose, 5000 units).

For transfemoral catheterization, the arteriotomy site is the common femoral artery, above its bifurcation into the deep femoral artery (profunda femoris) and the superficial femoral artery and below the inferior epigastric artery. Because the skin crease can sometimes be misleading, a combination of various other anatomic landmarks may be used, such as bony landmarks (aiming 2 cm below the center of the inguinal ligament) and the point of maximal palpable impulse.

Fluoroscopy is often used to mark the femoral head, and the target zone for the arteriotomy is the middle of the femoral head. A micropuncture (21-gauge) or 18-gauge needle is used to puncture the femoral artery, and a sheath is placed with the modified Seldinger technique. Sheath size varies according to the preference of the operator; in general, it is in the range of 4-6 French.

Once access is obtained, catheters are advanced over a 0.035-in. J-tip guide wire into the ascending aorta. Various different catheter shapes are available; the choice depends on the operator’s preference and the patient’s anatomy. Selective coronary angiography is performed in different views (at least two orthogonal views for each segment of the coronary) using hand or power injections of iohexol.

Guide catheters have the same external diameter as diagnostic catheters but a larger lumen and are used for PCI. Once the catheter has engaged the coronary ostium and diagnostic angiograms have been obtained, weight-based IV anticoagulant (unfractionated heparin [UFH], bivalirudin, or low-molecular-weight heparin [LMWH]) therapy may be administered. If the patient is not on long-term dual antiplatelet therapy (DAPT), a loading dose of a P2Y12 inhibitor is also given. As noted above, all patients should have been pretreated with aspirin.

A 0.014-in. guide wire is then advanced into the coronary artery across the stenotic lesion. All balloon catheters and other devices will be tracked over this wire. In some cases, direct stenting of the lesion can be done; however, in most cases, vessel preparation with either predilation with a semicompliant balloon or an atherectomy device is performed. The balloon is then withdrawn, and a stent of appropriate length and diameter is advanced over the coronary guide wire, positioned across the lesion, and deployed.

Depending on the angiographic appearance of the stent, postdilation of the stent may or may not be performed with a noncompliant balloon. An intravascular imaging tool, such as intravascular ultrasonography (IVUS) or optical coherence tomography (OCT) (see Anatomic and Physiologic Assessment), can be used for further delineation and assessment of the anatomy including plaque burden, vessel size, and stent deployment.

After the PCI result is deemed adequate, the coronary wire is removed and final angiograms are taken.

Access sheath removal

In transradial catheterization, the sheath is removed immediately after the procedure, and a compression band is applied to the wrist. With a goal of patent hemostasis, this band is left inflated for 90-120 minutes and then gradually deflated.

In transfemoral catheterization, hemostasis is achieved either by the use of vascular closure devices (inserted at the end of the case) or by manual compression (a few hours later when activated clotting time [ACT] is in the appropriate range).


Anatomic and Physiologic Assessment

Intravascular ultrasonography

Although coronary angiography provides a display of luminal narrowing in multiple planes and is useful in guiding PCI, it provides only limited information about the vessel wall, which is where the atherosclerotic process resides.

IVUS (see the image below) was developed to provide information about the plaque, the vessel wall, and the degree of luminal narrowing. It provides a tomographic cross-section of the vessel, allowing operators to gather significant qualitative and quantitative information that is potentially valuable for assessing stenosis severity and determining the true extent of atherosclerotic involvement.

Example of an intravascular ultrasound (IVUS) imag Example of an intravascular ultrasound (IVUS) image in percutaneous transluminal coronary angioplasty (PTCA).

The lumen border and the media-adventitia interface are the key landmarks that should be identified during interrogation. Plaque can be distinguished from the lumen on the basis of differences in echogenicity. In addition to providing information about the amount and distribution of plaque, IVUS can identify features of plaque composition (eg, calcification and lipid collections) that may not be appreciated by angiography alone.

Frequent uses of IVUS include assessment of indeterminate lesions and evaluation of adequate stent deployment. The latter is particularly important, in that proper deployment of drug-eluting stents (DESs) is critical for reducing thrombosis rates. Developments in ultrasonography (eg, virtual histology) and other technologies (eg, OCT and plaque thermography) have led to ways of characterizing and identifying vulnerable segments of plaque that may pose a risk for future cardiac events.

Optical coherence tomography

OCT uses light-based imaging to capture micrometer-resolution images of the artery wall. It has 10 times higher resolution than IVUS does but is unable to penetrate as deep into the vessel wall. OCT’s high resolution enables it to better evaluate stent strut apposition and neointimal stent strut coverage.

Coronary physiologic assessment

Intracoronary Doppler pressure wires are used to characterize coronary lesion physiology and estimate lesion hemodynamic severity. Comparison of the pressure distal to a lesion with aortic pressure at maximal coronary hyperemia enables determination of fractional flow reserve (FFR) (see the image below).

Fractional flow ratio (FFR). Pressure wire is adva Fractional flow ratio (FFR). Pressure wire is advanced across left anterior descending (LAD) stenosis and intracoronary adenosine is given. FFR ratio is recorded at baseline and then after adenosine push is given. Here, LAD lesion and FFR postadenosine is shown.

An FFR measurement lower than 0.80 during maximal hyperemia (induced via administration of adenosine) is consistent with a hemodynamically significant lesion. This determination is useful in deciding whether to perform PCI in an angiographic intermediate lesion. Clinical data—namely, the findings from the DEFER (Deferral of Percutaneous Coronary Intervention) study—support using this approach; a low event rate was seen in medically managed patients with angina and an FFR measurement greater than 0.75.

The FAME (Fractional Flow Reserve versus Angiography for Guiding PCI in Patients with Multivessel Coronary Artery Disease) trial showed that routine measurement of FFR during angioplasty reduced the risk of death, MI, or repeat revascularization by 30% and the risk of death or MI by 35%, compared with the current practice of using angiography to guide stenting decisions.[78]

In this study, a cutoff FFR value of 0.80 was used to define a nonischemic lesion. A 2-year follow-up of the FAME trial showed continuing significant reductions in the combined endpoint of death and MI with the use of FFR in comparison with standard angiography-guided PCI.[79]

The FAME 2 trial randomly assigned patients with stable CAD who had at least one stenosis with an FFR less than 0.8 to receive either FFR-guided PCI plus optimal medical therapy or optimal medical therapy alone.[80] The occurrence of the primary endpoint—a composite of any-cause mortality, nonfatal MI, or urgent revascularization within 2 years—was significantly lower in the PCI group than in the medical therapy group (8.1% vs 19.5%).

However, it is important to note that this difference in primary endpoint was primarily driven by a reduction in the rate of urgent revascularization in the PCI group (4% vs 16.3); there were no significant between-group differences in mortality and MI rate.[80]

The FAME 3 study, currently under way, is a multinational multicenter trial designed to compare FFR-guided PCI (using second-generation DESs) with coronary artery bypass grafting (CABG) in patients with multivessel CAD.

Currently, the use of FFR is recommended to assess the hemodynamic significance of angiographically intermediate (40-70%) stenosis. Both FFR and IVUS have shown favorable outcomes when used to assess angiographically intermediate lesions; however, the data on FFR are more robust.


Adjunctive Therapies in Catheterization Laboratory

Antithrombotic therapy

Aspirin and heparin have been the traditional adjunctive medical therapies for patients undergoing coronary angioplasty and have been shown to decrease complications after the procedure. Since 1994, several antithrombotic drugs have been developed that have advantages over standard heparin. Although heparin is an effective anticoagulant, it has several limitations, including variable pharmacokinetics requiring careful monitoring, inhibition by substances released from activated platelets, and inability to inhibit fibrin-bound thrombin.

To address these limitations, several direct thrombin inhibitors have been developed. Hirudin and bivalirudin were evaluated in multicenter trials,[24, 81, 82, 83] and both agents were found to be slightly better than heparin in preventing ischemic complications during balloon angioplasty, though they had no effect on restenosis rates.

At some centers, LMWHs are being substituted for standard heparin in the treatment of patients with acute coronary syndrome (ACS) and during coronary interventions. Factor IX and factor Xa inhibitors are being evaluated as potential alternative anticoagulants; however, trials have failed to show a significant difference in efficacy of factor Xa inhibition between these agents and UFH.

In the HORIZONS-AMI (Harmonizing Outcomes With Revascularization and Stents in Acute Myocardial Infarction) trial,[84] 3602 patients presenting with STEMI and undergoing PCI were treated with bivalirudin and had substantially lower 30-day rates of major hemorrhagic complications and lower rates of net adverse clinical events (ie, major bleeding or composite major adverse cardiovascular events [death, reinfarction, target-vessel revascularization for ischemia, or stroke]) than patients treated with heparin plus a glycoprotein (GP) IIb/IIIa inhibitor.

The investigators continued to follow patients for 1 year.[84] Data were available for 1696 patients in the bivalirudin group and 1702 patients in the heparin plus GPIIb/IIIa inhibitor group. At 1 year, the bivalirudin group continued to have reduced rates for major bleeding and adverse events as compared with the heparin plus GPIIb/IIIa inhibitor group. Death, reinfarction, target-vessel revascularization for ischemia, and stroke rates were similar in the two groups.

The Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) trial,[85] which studied the impact of age on outcomes in moderate- and high-risk non–ST-segment elevation ACS (NSTE-ACS), found that patients aged 75 years or older who were treated with bivalirudin alone had similar ischemic outcomes but significantly lower bleeding rates as compared with those who were treated with heparin plus GPIIb/IIIa inhibitors, both overall and in the PCI subset.

In this trial, outcomes were analyzed at 30 days and at 1 year in four age groups, overall, and in those undergoing PCI.[85] Of the 13,819 patients studied, 3655 (26.4%) were younger than 55 years, 3940 (28.5%) were aged 55-64 years, 3783 (27.4%) were aged 65-74 years, and 2441 (17.7%) were 75 years or older. Older patients had more cardiovascular risk factors and had a higher acuity at presentation.

In the NAPLES (Novel Approaches for Preventing or Limiting Events) trial, Tavano et al compared bivalirudin with UFH plus a GPIIb/IIIa inhibitor (ie, tirofiban) during PCI in 335 patients with diabetes mellitus and concluded that elective PCI with bivalirudin monotherapy is safe and feasible in patients with diabetes.[86]

The bivalirudin group experienced significantly less in-hospital bleeding (8.4% vs 20.8%).[86] Non–Q-wave MI rates were similar in the two groups (10.2% for bivalirudin vs 12.5% for UFH-tirofiban. In the early days of stenting, multiple antiplatelet agents and warfarin were used in an attempt to prevent stent thrombosis, but thrombosis continued to occur in approximately 6% of patients.

The EUROMAX (European Ambulance Acute Coronary Syndrome Angiography) trial randomly assigned 2218 STEMI patients to receive either bivalirudin or UFH or LMWH with optional GP IIb/IIIa inhibitors.[87] The bivalirudin group had a lower risk of the primary outcome, which was a composite of death or major bleeding not associated with CABG (5.1% vs 8.5%). It also had a lower rate of the principal secondary outcome, a composite of death, reinfarction, or non-CABG major bleeding (6.6% vs 9.2%).

These differences reported in the EUROMAX trial were primarily driven by a reduced risk of major bleeding (2.6% vs 6%); there were no significant differences in the rates of death or reinfarction.[87] The bivalirudin group had higher rates of acute stent thrombosis (1.1% vs 0.2%).

The single-center HEAT PPCI (How Effective Are Antithrombotic Therapies in Primary PCI) trial randomly assigned 1812 STEMI patients to receive either bivalirudin or UFH and compared the two regimens with respect to primary efficacy outcome (composite of all-cause mortality, cerebrovascular accident, reinfarction, or unplanned target-lesion revascularization) and primary safety outcome (incidence of major bleeding).[88]

In this trial, heparin reduced the incidence of major adverse ischemic events as compared with bivalirudin (5.7% for heparin vs 8.7% for bivalirudin).[88] There was no increase in the rate of bleeding complications with heparin (3.5% vs 3.1% for bivalirudin).The results of the HEAT PPCI trial differed from those of previous trials and suggested that bleeding risk is not increased with heparin. These results will have to be replicated before a conclusive decision is made on the safest and most effective approach to anticoagulation during PCI.

In summary, several trials have shown lower bleeding with bivalirudin than with heparin with or without GPIIb/IIIa inhibitors. However, some of these trials involved frequent use of GPIIb/IIIa inhibitors, which is no longer a routine strategy but is reserved for use as a bailout measure or when thrombus burden is high or P2Y12 inhibitor loading is inadequate. Some of the bleeding results can thus be attributed to GPIIb/III inhibitor use.

The HEAT PPCI results were in favor of heparin, and the significant cost difference between heparin and bivalirudin (heparin is substantially cheaper) has once again raised interest in heparin as the anticoagulant for PCI. One limitation of HEAT PPCI, however, was that it was a single-center trial; therefore, data from currently ongoing large multicenter trials addressing this question are needed to address this issue definitively.

Antiplatelet therapy

The most feared complication of intracoronary stents has been thrombotic occlusion of a freshly deployed metallic endoprosthesis. Aggressive antiplatelet therapy has been shown to significantly reduce the risk of stent thrombosis and is required in all patients receiving a stent.

Patients receiving stents are now treated with a combination of aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel, ticagrelor, or cangrelor); with this DAPT, the development of less thrombogenic stents and improvements in stent deployment technology, the incidence of subacute thrombosis currently is approximately 1%.

Today, DAPT is provided to all stent patients for a minimum of 4 weeks after a bare-metal stent is placed and for a minimum of 12 months when a DES is used. Several trials have suggested that a shorter duration of P2Y12 inhibitor administration may be safe in patients with second-generation DESs, but the guidelines still recommend 12 months of DAPT.

Issues remain as to whether the duration of aspirin and P2Y12 inhibitor therapy should be longer in patients who received first-generation DESs. In the authors’ view, aspirin therapy with a baby aspirin should be maintained for life in all DES patients, and lifetime P2Y12 inhibitor therapy should be considered unless bleeding contraindications restrict its use. Currently, there are multiple ongoing studies designed to evaluate the question of optimal DAPT duration for second-generation DESs.

In elective situations, clopidogrel is most effective when given before PCI; prasugrel and ticagrelor have been studied in patients with ACS but not in stable patients. In acute situations, this approach may not be practical, and thus, the P2Y12 inhibitor is often given after PCI.

Concerns still exist regarding the risk of bleeding and platelet transfusion requirements in patients taking a P2Y12 inhibitor who require urgent CABG. Because emergency CABG is rare, there may be time to risk-stratify patients and to give a P2Y12 inhibitor before cardiac catheterization. If CABG is required, the effect of a P2Y12 inhibitor usually diminishes within 5 days.

Another important consideration is the clopidogrel loading dose. American College of Cardiology (ACC)/American Heart Association (AHA) guidelines recommend giving 600 mg within the 6 hours preceding PCI with stenting.[5]

Results of the HORIZONS-AMI study also indicated that a 600-mg loading dose of clopidogrel yielded better clinical outcomes than a 300-mg dose.[89] The 2158 patients in the 600-mg group had significantly lower unadjusted 30-day mortality than the 1153 in the 300-mg group (1.9% vs 3.1%), as well as lower rates of reinfarction (1.3% vs 2.3%) and stent thrombosis (1.7% vs 2.8%). Bleeding rates did not differ. Similar differences were shown in patients who received either bivalirudin or UFH plus a GP inhibitor.

The GRAVITAS (Gauging Responsiveness with A VerifyNow Assay—Impact on Thrombosis And Safety) study, which enrolled 2214 patients with high on-treatment reactivity 12-24 hours after PCI, found that high-dose clopidogrel (600 mg initially, 150 mg/day thereafter) provided a 22% absolute reduction in the rate of high on-treatment reactivity at 30 days in comparison with standard treatment (no additional loading dose, 75 mg/day).[90]

However, the GRAVITAS investigators noted no difference in the primary endpoint of 6-month incidence of death from cardiovascular causes, nonfatal MI, or stent thrombosis.[90] Severe or moderate bleeding according to the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) definition was lower in the standard group, but the decrease did not reach statistical significance.

Use of newer intravenous (IV) antiplatelet agents such as cangrelor may help overcome these issues. In June 2015, cangrelor was approved by the US Food and Drug Administration (FDA) for use in adults undergoing PCI. Aspirin 325 mg should be given before all PCIs and then maintained at a dosage of 81 mg/day.

Clopidogrel is the most frequently utilized P2Y12 inhibitor. Numerous studies have shown the inconsistency in the metabolism of this drug as a result of variations in the CYP2C19 pathway. Clopidogrel is a prodrug that is metabolized to an active form by the cytochrome (CYP) 450 enzyme system in the liver. Research has demonstrated that genetic variation at the CYP450 2C19 locus results in decreased metabolic activation of clopidogrel and increased risk of stent thrombosis and ischemic events.

This finding led to an update to the package insert for clopidogrel, which now includes a “black box” warning for use in patients who are “poor metabolizers” (ie, those who have two abnormal alleles at the CYP 2C19 locus; approximately 2-4% of white patients fall into this category).

Individuals with a single abnormal allele have intermediate metabolism of clopidogrel to the active metabolite. In a meta-analysis of nine studies and almost 10,000 patients, Mega et al found that the presence of even one reduced-function CYP2C19 allele in patients treated with clopidogrel after PCI was associated with a significantly increased risk of major adverse cardiovascular events (MACE), particularly stent thrombosis.[91]

Studies of platelet function testing have shown variability in the pharmacodynamic response to clopidogrel, and studies of genetic testing have identified genetic polymorphisms that affect its absorption (ABCB1), metabolism (eg, CYP2C19) and ultimately its pharmacodynamic effects. Genetic testing for CYP2C19 polymorphisms has potentially important prognostic implications.

In population-based studies, patients with high on-treatment platelet reactivity have had an increased risk of MACE. Unfortunately, studies have not shown that measuring platelet reactivity in an individual patient (primarily with the VerifyNow assay) is useful for identifying those at risk. Currently, measurement of platelet reactivity is still reserved for use as a research tool.[92, 93]

Besides genetic polymorphisms, there are clinical factors to consider, such as obesity and diabetes mellitus, as well as potential drug interactions, such as those with calcium-channel blockers and proton pump inhibitors (PPIs). In particular, omeprazole was implicated in clopidogrel hyporesponsiveness. However, the COGENT trial demonstrated that there was no increase in MACE in patients who took clopidogrel plus a PPI as compared with clopidogrel alone.[94]

Prasugrel is a thienopyridine adenosine diphosphate (ADP) receptor inhibitor that inhibits platelet aggregation. It has been shown to reduce new and recurrent MIs.[95] The loading dose is 60 mg orally given once, and the maintenance dosage is 10 mg/day orally (given with aspirin 75-325 mg/day).

Prasugrel is indicated for reducing thrombotic cardiovascular events (including stent thrombosis) in patients with an ACS that is managed with PCI. It is used specifically for unstable angina or NSTEMI or for acute STEMI that is managed with primary or delayed PCI.

TRITON TIMI (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel—Thrombolysis in Myocardial Infarction) 38 analyzed whether the type, size, and timing of MI affected prasugrel’s ability to reduce new or recurrent MI.[95] Compared with clopidogrel, prasugrel significantly reduced the overall risk of any type of MI (eg, procedure-related, nonprocedural, and consistently across MI size). Significant, sometimes fatal, bleeding occurred more often with prasugrel than with clopidogrel.

Ticagrelor, a cyclopentyl-triazolo-pyrimidine, is an oral P2Y12 receptor antagonist that reversibly inhibits platelets. It does not require hepatic bioactivation, because it is an active drug. The PLATO (Platelet Inhibition and Patient Outcomes) trial, looking at 18,264 patients with ACS (35% STEMI), showed that ticagrelor reduced the composite primary efficacy event (death, MI, or stroke) in comparison with clopidogrel (9.8% vs 11.7%) but increased non–CABG-related major bleeding (2.8% vs 2.2%) and fatal intracranial hemorrhage.[96]

Potential disadvantages of ticagrelor include side effects such as dyspnea, ventricular pauses, significantly greater cost than generic clopidogrel, and increased concentration of uric acid and creatinine.

On the basis of the benefit observed in these trials, current NSTE-ACS guidelines state that it is reasonable to use ticagrelor in preference to clopidogrel for DAPT in patients with NSTE-ACS who undergo an early invasive or ischemia-guided strategy. Prasugrel (at the time of PCI) may be chosen over clopidogrel for DAPT in patients with NSTE-ACS who undergo PCI and are not at high risk for bleeding complications.

Glycoprotein inhibitor therapy

PCI results in disruption of the coronary endothelium, which leads to platelet activation. Activated platelets bind to the vessel wall (adhesion) and to each other (aggregation) and release numerous vasoactive compounds.

Aspirin blocks the cyclooxygenase pathway and reduces thrombotic complications after balloon angioplasty. However, despite heparin and aspirin therapy, thrombotic complications are not eliminated. Studies identified the importance of the GPIIb/IIIa receptor, which binds fibrinogen and mediates platelet cross-linking and aggregation. The introduction of GP IIb/IIIa inhibitors had a major influence on PCI treatment strategies in the 1990s, but these drugs are now used much less frequently than they once were.

Early studies of GPIIb/IIIa inhibitors showed the following:

  • Abciximab, tirofiban, and eptifibatide are capable of reducing ischemic complications in patients undergoing balloon angioplasty and coronary stenting
  • In primary PCI, GPIIb/IIIa inhibitors can improve flow and perfusion and reduce adverse events
  • Abciximab may improve outcomes in patients when given before arrival in the catheterization laboratory for primary PCI [97]
  • A meta-analysis of GPIIb/IIIa inhibitor trials showed a significant reduction in early mortality when these agents are used during coronary intervention; the combined endpoint of death or MI was also reduced significantly at 30 days
  • The EVA-AMI (Eptifibatide vs Abciximab in Primary PCI for Acute ST Elevation Myocardial Infarction) trial, which compared the efficacy of two GPIIb/IIIa inhibitors as adjuncts to PCI in 427 patients with STEMI, showed that double-bolus eptifibatide followed by a 24-hour infusion was as effective as single-bolus abciximab followed by a 12-hour infusion for ST-segment resolution [98]
  • These agents are effective at reducing ischemic complications of PCI; however, they have not been shown to improve outcome in saphenous vein graft PCI
  • A meta-analysis of 22 studies including 10,123 patients evaluated the use of GPIIb/IIIa inhibitors during elective PCI in patients pretreated with clopidogrel determined that GPIIb/IIIa inhibitors had no effect on mortality or major bleeding but were associated with a decrease in the incidence of nonfatal MI and an increase in the rate of minor bleeding [99]

The evidence supporting the use of GPIIb/IIIa inhibitors derives largely from a the time before the use of oral P2Y12 inhibitors. Several studies have failed to show a benefit with upstream administration of GPIIb/IIIa inhibitors. In view of these findings, coupled with the increased risk of bleeding, routine use of these agents is no longer recommended. GPIIb/IIIa inhibitors may be used as an adjunctive therapy at the time of PCI, on an individual basis, for large thrombus burden or inadequate P2Y12 receptor antagonist loading.



The common complications of PCI are bleeding, hematoma, and pseudoaneurysm at the access site. To minimize the risk of these complications, extreme care must be taken in obtaining access at the beginning of the procedure.

Bleeding avoidance strategies (eg, vascular closure devices, bivalirudin, the radial approach, and combinations thereof) appear to lower the risk of post-PCI bleeding for both men and women; however, such strategies may be of particular significance in female patients, in that the absolute differences in risk are substantially greater in women.[100]

A retrospective cohort analysis of data on 2,820,874 PCI procedures from the CathPCI registry demonstrated that the use of radial access for PCI (r-PCI) was on the increase and that the procedure was associated with a lower risk of bleeding and vascular complications than traditional transfemoral PCI, even after age, sex, and clinical presentation were accounted for.[101]

Anaphylaxis caused by the contrast agent can occur; therefore, a careful preprocedural history must be obtained. Patients with a prior anaphylactoid reaction to the contrast media should receive appropriate steroid prophylaxis before repeat contrast administration. Contrast administration is one of the leading causes of hospital-acquired acute kidney injury (AKI). The only strategies that have been shown to minimize the risk of AKI are hydration and minimizing the use of contrast.

Early registries of balloon angioplasty results showed complication rates that were much higher than those typically observed today. Reductions in the complication rate have been complemented by improvements in the acute success rate. Previously, registries such as the National Heart, Lung, and Blood Institute (NHLBI) Coronary Angioplasty Registry reported primary success rates of 61%. Today, with the use of stents and adjunctive pharmacotherapy, success rates range from 95% to 99%.

The mechanism by which balloon angioplasty or stenting improves luminal diameter is associated with significant local trauma to the vessel wall, which can, in turn, lead to occlusive complications in a minority of patients. Coronary artery dissection typically results from the vessel injury secondary to balloon expansion. Animal and postmortem human studies have shown that localized dissection at the site of balloon expansion is detected angiographically in as many as 50% of patients immediately after the procedure.

Such small dissections probably are necessary to obtain adequate lumen expansion; they rarely interfere with antegrade blood flow and are usually unimportant. Angiographic follow-up typically shows no residual evidence of a dissection as early as 6 weeks after angioplasty in most of the cases studied. However, larger dissections can lead to complications.

Often, these dissections are treated with a stent to cover the dissection flap. Coronary perforation or rupture is very rare (occurring in fewer than 1% of cases) and is typically associated with the use of ablative devices or oversized balloons. It can occur from the wire tip or at the culprit lesion. Wire perforations are typically small and usually do not warrant further intervention; perforations from balloon inflation or stent implantation can occasionally necessitate treatment with a covered stent graft.

Abrupt vessel closure may occur in as many as 5% of balloon angioplasty cases, usually developing when the true lumen is compressed by a large dissection flap, thrombus formation, superimposed coronary vasospasm, or a combination of these processes. The presence of large coronary dissections immediately after balloon angioplasty is associated with a fivefold increase in the risk of abrupt closure. This underscores the importance of a good postprocedural angiographic result for ensuring good clinical outcomes.

Since the introduction and implementation of intracoronary stents and newer antiplatelet drugs, the incidence of abrupt closure has decreased significantly, to less than 1%. Microembolization of plaque debris or adherent thrombus may also cause acute complications during angioplasty and may contribute to postprocedural cardiac enzyme elevation and chest pain in some patients.

In fewer than 1% of angioplasty patients, microembolization of the platelet-rich thrombus may cause diffuse distal arteriolar vasospasm secondary to release of vasoactive agents, resulting in no-reflow. This complication is difficult to treat but may respond to intracoronary calcium channel antagonists, adenosine, or nitroprusside. Patients undergoing balloon angioplasty of saphenous vein graft lesions and primary angioplasty in the setting of acute MI with a large amount of adherent thrombus are at greatest risk for distal embolization.

Restenosis (see below) after balloon angioplasty necessitating a second revascularization procedure is a major limitation that occurs in about 15-30% of patients, depending on the definition of restenosis applied. With the advent of DESs, restenosis rates have fallen to less than 10%.

Some of the very rare but serious complications of PCI are stroke, MI, and death. With advances in technique, technology, and adjuvant medical therapy, PCI is now associated with mortality and emergency bypass rates lower than 1%. The rate of nonfatal MI after coronary angioplasty ranges from 5% to 15%, whereas the rate after stent placement ranges from 2% to 5%.


After balloon angioplasty or stent implantation, the vessel wall undergoes a number of changes. Platelets and fibrin adhere to the site within minutes of vessel injury. Within hours to days, inflammatory cells infiltrate the site, and vascular smooth muscle cells begin to migrate toward the lumen.

The vascular smooth muscle cells then undergo hypertrophy and excrete an extensive extracellular matrix. During this period of vascular smooth muscle cell proliferation, endothelial cells colonize the surface of the lumen and regain their normal function.

Over the course of several weeks to months, multiple forces interact to cause remodeling of the vessel wall with either a decrease in lumen diameter (negative remodeling) or an increase in lumen diameter (positive remodeling). The amount of late loss in lumen diameter is dependent on the amount of neointimal proliferation and the degree of remodeling after intervention (see the image below). After 6 months, the repair process stabilizes and the risk of restenosis decreases significantly.

Mechanism of restenosis following percutaneous tra Mechanism of restenosis following percutaneous transluminal coronary angioplasty (PTCA).

Several studies have shown that the lumen diameter or area after treatment is one of the major predictors of restenosis. The use of coronary artery stents has decreased the rate of restenosis by improving the acute gain achieved and by minimizing negative remodeling.

Depending on the definition used, angiographic restenosis has been reported in as many as 50% of patients within 6 months after balloon angioplasty, necessitating repeat target-vessel revascularization in approximately 20-30% of patients. As noted (see above), DESs have reduced restenosis rates to less than 10%. Poststenting lumen diameter and lesion complexity are still the major predictors of restenosis with these newer stents.

Stent thrombosis

Although DESs have significantly reduced the incidence of restenosis, they are still linked with concerns regarding stent thrombosis. In fact, the thrombosis rate for a DES is virtually identical to that for a bare-metal stent at 1 year (0.5-0.7%). However, late stent thrombosis (>1 year) continues to occur with DESs, whereas it is exceedingly rare with bare-metal stents.

The factor that makes the greatest contribution to stent thrombosis is interruption of antiplatelet therapy. Current guidelines recommend a minimum of 1 year of DAPT for patients with DESs and a month for those with bare-metal stents.[6] DESs take longer to endothelialize on the coronary vessel wall than bare-metal stents do, and discontinuing DAPT may expose patients to an increased risk for stent thrombosis over time.

In some clinical situations (eg, before urgent noncardiac surgery in which antiplatelet therapy may have to be discontinued and when known or potential medicine compliance issues are present), implanting a bare-metal stent during PCI may be preferred to implanting a DES. Another important factor is final stent diameter and area.

Underdeployment or incomplete apposition of the DES may also increase the risk of stent thrombosis. This is not to say that DESs are unsafe. In fact, there is no difference in long-term rates of death and MI between DESs and bare-metal stents; however, there is a striking reduction in restenosis.

Stone et al found that although stent thrombosis is infrequent, it results in higher rates of MI and death.[102] The greater frequency of target-vessel revascularization results in a lower rate of MI and death. Although late stent thrombosis is a risk with DESs, the noticeable reduction in restenosis may offset the risk.[102]

An analysis of data from 7090 consecutive PCI-treated patients in the ISAR-ASPI (Intracoronary Stenting and Antithrombotic Regimen-ASpirin and Platelet Inhibition) registry suggested that high platelet reactivity in patients on aspirin (HAPR) at the time of PCI was associated with a greater risk of death or stent thrombosis (6.2% vs 3.7% for non-HAPR) during the first year after PCI.[103] Moreover, HAPR independently predicted death or stent thrombosis at 1 year. These findings may support use of HAPR as a prognostic biomarker in PCI-treated patients.

Contributor Information and Disclosures

George A Stouffer, III, MD Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center

George A Stouffer, III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.


Josh W Todd, MD Interventional Cardiologist, Knoxville Heart Group

Josh W Todd, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Society for Cardiovascular Angiography and Interventions

Disclosure: Nothing to disclose.

Pradeep K Yadav, MD Interventional Cardiology Fellow, Department of Cardiology, University of North Carolina at Chapel Hill School of Medicine

Disclosure: Nothing to disclose.

Mian Atif Yousuf, MD Interventional Cardiology Fellow, Department of Cardiology, University of North Carolina at Chapel Hill School of Medicine

Mian Atif Yousuf, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Chief Editor

Karlheinz Peter, MD, PhD Professor of Medicine, Monash University; Head of Centre of Thrombosis and Myocardial Infarction, Head of Division of Atherothrombosis and Vascular Biology, Associate Director, Baker Heart Research Institute; Interventional Cardiologist, The Alfred Hospital, Australia

Karlheinz Peter, MD, PhD is a member of the following medical societies: American Heart Association, German Cardiac Society, Cardiac Society of Australia and New Zealand

Disclosure: Nothing to disclose.


Jeb Burchenal, MD Assistant Professor of Medicine, University of Colorado School of Medicine; Consulting Staff, South Denver Cardiology Associates

Jeb Burchenal, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

Jorge Davalos, MD Interventional Cardiology Fellow, University of North Carolina at Chapel Hill

Jorge Davalos, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Medical Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Robert Vincent Kelly, MD Consulting Staff, Division of Interventional Cardiology, University of North Carolina Hospital

Disclosure: Nothing to disclose.

James Maddux, MD Consulting Staff, Department of Cardiology, International Heart Institute

James Maddux, MD is a member of the following medical societies: American Medical Association and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Percutaneous transluminal coronary angioplasty (PTCA). The rotational atherectomy catheter (Rotablator) is a device designed for the removal of plaque from coronary arteries. This device, which has a diamond-studded burr at its tip, rotates at about 160,000 rpm and is particularly well suited for ablation of calcific or fibrotic plaque material.
Percutaneous transluminal coronary angioplasty (PTCA). TRISTAR stent.
Percutaneous transluminal coronary angioplasty (PTCA). NIR stent.
Percutaneous transluminal coronary angioplasty (PTCA). Wallstent.
Example of an intravascular ultrasound (IVUS) image in percutaneous transluminal coronary angioplasty (PTCA).
Mechanism of restenosis following percutaneous transluminal coronary angioplasty (PTCA).
Fractional flow ratio (FFR). Pressure wire is advanced across left anterior descending (LAD) stenosis and intracoronary adenosine is given. FFR ratio is recorded at baseline and then after adenosine push is given. Here, LAD lesion and FFR postadenosine is shown.
Table 1. Comparison of Surgical Therapy and Coronary Angioplasty
Endpoint Pocock et al* Pocock et al† BARI Study‡












Death (%) 0.3 1.9 2.8 3.1 10.7 13.7
Death or MI 4.5 7.2 8.5 8.1 11.7 10.9
Repeat CABG 1.4 16.0§ 0.8 18.3§ 0.7 20.5§
Repeat CABG or PTCA 3.6 30.5§ 3.2 34.5§ 8.0 54.0§
More than mild angina 6.5 14.6§ 12.1 17.8§ ... ...
*Meta-analysis of results of 3 trials at 1 year. Patients with single-vessel disease were studied.[22]

†Meta-analysis of results of 3 trials at 1 year. Patients with multivessel disease were studied.[22]

‡Reported results are for 5-year follow-up. Patients with multivessel disease were studied.[21]

§ P < .05.

BARI = Bypass Angioplasty Revascularization Investigation; CABG = coronary artery bypass grafting; MI = myocardial infarction; PTCA = percutaneous transluminal coronary angioplasty.

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