The two failure modes of balloon angioplasty, abrupt closure and restenosis, have stimulated development of myriad devices, all with the goal of reducing the risk of the procedure, the risk of restenosis, or both. Only coronary stents have been shown to be advantageous over balloon angioplasty, except in cases of severely calcified lesions (Table 20-4). There are numerous coronary stent designs, but the majority of those in current use consist of a stainless steel (or alloy, such as cobalt chromium) cylinder that has been “carved,” creating a so-called slotted-tube design. Stent expansion creates a series of interlocking cells, resembling a cylindrical meshwork (Fig. 20-3). Stents are thus deformable, but when expanded, they maintain sufficient rigidity to act as scaffolding after deflation of the angioplasty balloon. Intimal disruption is contained and far less likely to propagate and occlude the treated vessel. In addition, the rigid framework left behind becomes part of the vessel wall, addressing the issue of remodeling, which is one of the mechanisms of restenosis.
Table 20-4 Devices Used for Coronary Angioplasty ||Download (.pdf)
Table 20-4 Devices Used for Coronary Angioplasty
|Experience||Ease of use||Complications||Efficacy||Lesion type|
|POBA||+ + + +||+ + + +||+||+ + +||Any|
|Cutting balloon||+||+ +||+ +||+ + +||Calcified lesion, ISR, bifurcation|
|Rotational atherectomy||+ + +||+||+ + +||+ + +||Heavily calcified, nondilatable ISR|
|Directional atherectomy||+||+||+ + +||+||Bifurcation, ostial lesion|
|Laser atherectomy||+ +||+ +||+ +||+ +||Calcification, ISR, thrombus|
|Aspiration (mechanical)||+ +||+||+||+ +||Thrombus|
|Aspiration (manual)||+||+ + +||+||+ +||Thrombus|
The coronary stent is a metallic “meshwork” that increases its rigidity when cold-worked by balloon expansion. Buttressing of the vascular wall, propagation of dissection, and early vascular recoil are reduced significantly. (Reprinted by permission from Texas Heart Institute, www.texasheart.org.)
Stents allow safe expansion of the vessel beyond that typically achieved with PTCA at the time of balloon expansion; however, stent use increases thrombotic and inflammatory responses of the vessel wall. The increased injury and a foreign-body response to stent struts result in a more intense and prolonged local inflammatory response.22 As a result, stent placement paradoxically exacerbates intimal hyperplasia.23,24 Using the late (6- or 9-month) loss in lumen diameter after stent implantation as a measure of intimal hyperplasia, even the most modern stent designs fall within a range of about 0.8 mm, more than twice the loss incurred after PTCA (0.32 mm). As a result, when examining restenosis after angioplasty, the impact of stent for percutaneous coronary revascularization (PCR) is rather small in comparison with that of PTCA.23,24 The bulk of intimal hyperplasia and risk of restenosis are functions of the size of the treated lumen on completion of the procedure, length of the treated lesion, and presence of unstable angina, hypertension, and diabetes mellitus (Table 20-5).25–27 Long-term follow-up studies suggest that a stent that does not reocclude during the first 6 to 9 months after implantation is not subject to late, rapid disease progression.28–32
Table 20-5 Approximate Risk of Restenosis Based on Final Lumen Diameter and Stent Length ||Download (.pdf)
Table 20-5 Approximate Risk of Restenosis Based on Final Lumen Diameter and Stent Length
|Final lumen diameter (mm)|
|Stent length (mm)||Percent risk|
By reducing the likelihood of both abrupt closure requiring emergency coronary artery bypass surgery and restenosis, stent-assisted angioplasty is more effective than routine balloon angioplasty for virtually any type of coronary artery lesion. Registry data describe a risk for emergency surgery of only 0.3 to 1.1%, and a procedural mortality of less than 1%.33–36 The likelihood of procedural complications may be estimated on the basis of lesion characteristics (Table 20-6).37 Depending on lesion characteristics and the number of lesions treated, after 1 year, 5 to 10% of patients require coronary artery bypass surgery, and 15 to 20% undergo a second PTCR procedure.38–41 After 5 years, 10 to 15% of patients require another revascularization procedure because of the development of severe stenosis at an untreated site.32 Diabetes increases the risk for adverse outcomes by increasing the risk of restenosis and disease progression at untreated sites.
Table 20-6 Risk Factors for Ischemic Events after Stent Placement ||Download (.pdf)
Table 20-6 Risk Factors for Ischemic Events after Stent Placement
|Nonchronic total occlusion|
|Moderately strong correlates|
|Length ≥ 10 mm|
|Large filling defect|
|Calcium ± angle ≥45|
|SVG age ≥10 years|
|Group||Definition||Death/MI emergency CABG|
|Highest risk||Either of the strongest correlates||12.7%|
|High risk||≥3 moderate correlates||8.2%|
|Moderate risk||1-2 moderate correlates||3.4%|
|Low risk||No risk factors||2.1%|
As noted in the description of the guidewire, iron components of stent struts attract fibrinogen and offer a site for platelet attachment and thrombosis. The increased risk of thrombosis at the treated site persists until endothelialization is complete. As a result, more intense antithrombotic therapy is required during the procedure and for up to 1 year afterward.42,43
Stents may be used as a drug-delivery system. However, rather than simply applying a drug to the stent surface, from which it will dissipate quickly, drug delivery is controlled by using a surface polymer or by altering the design or the material used to construct the stent.44 This method of drug delivery, called a drug-eluting stent (DES), allows the drug to be applied at high concentrations at the site of interest and reduces the probability of systemic toxicity.
Drug-eluting stents reduce the primary determinant of restenosis by 50 to 100%, as determined by quantitation of late lumen loss after angioplasty (Fig. 20-4). Studies examining the efficacy of the DES introduced new nomenclature to the follow-up end points. The most useful follow-up end point is termed target vessel failure (TVF), signified by cardiac death, MI, or repeat revascularization of the treated vessel. One year after the procedure, TVF is reduced from 19.4 to 21% with a bare-metal stent (BMS) to 8.8 to 10% with a paclitaxel or sirolimus DES.38,41
The effect of various stents on intimal hyperplasia in randomized trials is shown. A bare-metal stent's intimal hyperplasia thickness, or late loss, shown on the left, is compared with the late loss of drug-eluting stents shown at the right. BMS = Bare-metal stent.
Reduced rates of repeat intervention after DES placement have been reported for every type of lesion studied, except bifurcation lesions, in which the risk of restenosis remains significant, and the risk of potentially fatal early thrombosis is as high as 3.5% (Table 20-7).38,45–52 However, the impact of DESs on failure of long-term treatment and repeat procedures does not translate to a reduced risk of procedure-related complications.53 In addition, incomplete healing, a response to the eluting polymer, or both, confer an increased risk of stent thrombosis that extends beyond 1 year. As a result, dual antiplatelet therapy should be continued for at least 1 year after the procedure in all patients and indefinitely in patients with complex lesions.
Table 20-7 The Clinical Impact of Drug-Eluting Stents ||Download (.pdf)
Table 20-7 The Clinical Impact of Drug-Eluting Stents
|Population||End point||BMS (%)||DES (%)|
|Diabetes mellitus117||MACE 9 mo||27.2-36.3||11.3-15|
|Insulin-treated118||MACE 9 mo||31.5||19.6|
|Myocardial infarction119||TVR 8 mo||32||18|
|“Complex” lesions120||TLR 12 mo||29.8||2.4|
|Long lesion small vessel121-123||MACE 9 mo||18.3-22.6||4-8|
|Small vessel45||MACE 8 mo||31.3||9.3|
|Bifurcation46,124-126||TVR 6 mos.||13.3-38||8.6-19|
|Restenosis127||TVR 6 mos.||33||8-19|
|Saphenous vein graft lesion47||MACE 6 mos.||28.1||11.5|
Before the routine use of coronary stents, abrupt closure owing to dissection could be treated with repeat balloon inflation and, if unsuccessful, coronary artery bypass surgery. Prolonged balloon inflation generally was necessary for successful restoration of patency, but in the event of failure, transport for emergency surgery often was accompanied by severe ischemia of the treated territory. As a result, balloon catheters with a short third-lumen opening just proximal and distal to the balloon were developed. These catheters, or “perfusion balloons,” allowed for prolonged balloon inflation with far less ischemia and could be used to ameliorate the severity of ischemia during transport for surgery after an unsuccessful procedure. Since the introduction of the coronary stent, perfusion balloons rarely are used.
When introduced, the concept of reducing the bulk of the obstructing atheroma was quite attractive. The idea was to reduce vessel wall thickness or “debulk,” allowing for balloon expansion at a lower pressure. With less force applied for lumen expansion, theoretically the likelihood of abrupt closure would be reduced, as would the degree of arterial injury at the time of treatment. Several devices used for debulking have been developed and studied, including directional coronary atherectomy, percutaneous transluminal rotational ablation, and laser ablation. Unfortunately, when subjected to rigorous examination, debulking devices provide no incremental gain over plain balloon angioplasty in achieving procedural success or avoiding restenosis.54–57 Although each device has developed a specific niche (see Table 20-4), their routine use generally is associated with an increased risk of procedural complications, including perforation and MI.57–59
Rotational atherectomy requires additional discussion because, unlike the other types of atherectomy, it is still commonly used. The Rotablator (Boston Scientific Corporation, Natick, MA) is an olive-shaped device that is coated with diamond chips. It is attached to an electrical motor, which causes the device to rotate at high speeds. The device is designed to abrade a rigid atherosclerotic intima, creating microemboli that are small enough to pass through the coronary microcirculation without incident. It is also useful as an initial treatment method for very rigid, heavily calcified lesions. However, the concept is not without failings. Microembolization is likely to exacerbate ischemia and therefore is contraindicated when there are thrombotic lesions, if there is impaired microcirculatory flow associated with a recent MI, or if the treated vessel is the last remaining patent vessel. Use of this device is also associated with an increased risk of perforation in highly angulated lesions.
A number of coronary aspiration devices are available to reduce the risk of distal embolization and diminish the local concentration of prothrombotic and vasoactive substances. These devices range from a simple end-hole catheter attached to a syringe to a complex suction catheter with or without an associated mechanical disrupter. These devices forcibly extract components of the thrombus or atheroma.60 Their use may improve flow after treatment of thrombus-laden lesions or saphenous vein grafts (Fig. 20-5).61
In a patient with ongoing inferior myocardial infarction, the right coronary artery is occluded by thrombus (A). After passage of a guidewire followed by aspiration at the site of occlusion, thrombus is withdrawn, restoring antegrade blood flow (B). A stent then is placed at the site of the culprit lesion to complete the procedure (C).
Embolic Protection Devices
During balloon angioplasty, mechanical dissolution of thrombus, if present, may result in macroembolization and distal vessel occlusion. The high-pressure manipulation of an atheromatous lesion also may free cholesterol crystals and other components of the lesion, resulting in distal microembolization, thrombosis, and slow- or no-reflow phenomenon. Several devices have been developed to reduce the frequency or impact of distal embolization. These devices may be placed distal or proximal to the treated lesion. Distal devices are mounted on the guidewire and use either a suspended micropore filter to trap particulate matter of 100 to 150 μm or larger or balloon occlusion of the treated vessel with posttreatment aspiration to capture embolized material. Proximally placed devices temporarily interrupt flow and aspirate the treated vessel. The PercuSurge GuardWire Plus (Medtronic, Minneapolis, MN) is a balloon occlusion and aspiration device that underwent testing in vein grafts in the Saphenous Vein Graft Angioplasty Free of Emboli Randomized (SAFER) trial.62 The trial demonstrated a 42% reduction in creatine kinase (CK) elevations and more than a 50% reduction in the no-reflow phenomenon.62 Unfortunately, these results did not apply to patients with MI.63
Angiographic imaging allows imaging of the coronary lumen but may be unreliable in the setting of severe calcification, difficult branching patterns, or previously placed coronary stents. Furthermore, a thrombus that may increase the risk of PCR may go undetected by standard angiographic imaging. Therefore, a number of alternative imaging methods have been developed to improve diagnosis, plan revascularization efforts, and evaluate the success of such efforts. Angioscopy or fiberoptic imaging requires occlusion of the imaged vessel and perfusion with saline. Although a useful tool to investigate the presence or components of thrombus within coronary vessels, angioscopy has not been a useful adjunct to PCR. In contrast, intracoronary ultrasound imaging has proved especially useful. Ultrasound imaging allows accurate determination of vessel size, luminal reduction, lesion components, and progress associated with revascularization attempts. Ultrasound guidance for stent implantation is associated with a greater than 30% reduction in the need for repeat procedures.64 Of equal importance, intracoronary ultrasound is an invaluable research tool used to investigate the accuracy of contrast angiography and the impact of mural lesion components on complications and outcomes after angioplasty.
Devices that Measure Lesion Severity
The hemodynamic significance of coronary lesions, the appropriateness of a treatment, and the success of treatment may be determined by the following two means: a guidewire that measures the velocity of blood flow within coronary arteries or a calculation that measures pressure distal to a coronary lesion.
A miniaturized Doppler-equipped guidewire with a 12-MHz transducer uses a pulsed interrogation that samples 5.2 mm beyond the guidewire tip at an angle of 14 degrees on either side. Assuming that the cross-sectional area of the interrogated vessel remains constant during all measurements, the ratio of velocities measured reflects the ratio of blood flow between any two measurements. The most important and reliable parameter that a flow probe measures is the ratio of resting flow to vasodilated coronary flow, a value known as coronary flow reserve. When measured using the Doppler probe, the value is termed coronary velocity reserve (CVR). As a coronary lesion becomes flow limiting, attempts to normalize tissue perfusion by autoregulation result in arteriolar dilatation at rest. Therefore, the administration of an arteriolar vasodilator such as adenosine will have little additional effect on flow velocity. The absence of an appropriate increase in velocity during adenosine- or dipyridamole-induced arteriolar vasodilation produces abnormal flow reserve. A CVR less than 2.0 indicates hemodynamically significant lesions.
CVR measurement reflects changes in flow relative to an assumed normal baseline state but is subject to error when baseline flow is abnormal. Examples of abnormal states include left ventricular (LV) hypertrophy, fibrosis, and perhaps anemia. In addition, abnormally large or small driving pressure gradients may fall outside the range of normal coronary autoregulation, altering the basal-to-hyperemic ratio. Failure to achieve arteriolar dilatation in response to adenosine or dipyridamole will produce an abnormal calculated flow reserve. Examples that affect arteriolar dilatation include diabetes mellitus, amyloidosis, and recent caffeine or theophylline ingestion.
An alternative to flow measurement is pressure measurement, proximally and distally to the lesion in question. Under normal conditions, epicardial vessels present little detectable resistance to flow. Therefore, driving pressure (PAo) and arteriolar resistance pressure (PRA) determine maximal coronary blood flow. The presence of a flow-limiting coronary lesion will cause some of the driving pressure to be lost, so maximal flow will depend on the distal coronary pressure (Pd) -to-PRA gradient and arteriolar resistance. Therefore, the fraction of maximal basal flow that remains possible in the presence of the lesion is
Canceling resistance and assuming that right atrial pressure remains constant results in a very simple relationship:
This ratio, called the myocardial fractional flow reserve (FFR), is obtained after the administration of adenosine. An FFR of 0.75 or less identifies a hemodynamically significant lesion. Routine use of FFR to ensure the necessity of PCI reduces the risk of adverse events both immediately and at 1 year.65